Depression as a Neuroendocrine Disorder: Emerging Neuropsychopharmacological Approaches beyond Monoamines

dc.contributor.authorChávez-Castillo, Mervin
dc.contributor.authorNúñez, Victoria
dc.contributor.authorNava, Manuel
dc.contributor.authorOrtega, Ángel
dc.contributor.authorRojas, Milagros
dc.contributor.authorBermúdez, Valmore
dc.contributor.authorRojas-Quintero, Joselyn
dc.date.accessioned2019-01-18T21:53:11Z
dc.date.available2019-01-18T21:53:11Z
dc.date.issued2019
dc.description.abstractDepression is currently recognized as a crucial problem in everyday clinical practice, in light of ever-increasing rates of prevalence, as well as disability, morbidity, and mortality related to this disorder. Currently available antidepressant drugs are notoriously problematic, with suboptimal remission rates and troubling side-effect profiles. Their mechanisms of action focus on the monoamine hypothesis for depression, which centers on the disruption of serotonergic, noradrenergic, and dopaminergic neurotransmission in the brain. Nevertheless, views on the pathophysiology of depression have evolved notably, and the comprehension of depression as a complex neuroendocrine disorder with important systemic implications has sparked interest in a myriad of novel neuropsychopharmacological approaches. Innovative pharmacological targets beyond monoamines include glutamatergic and GABAergic neurotransmission, brain-derived neurotrophic factor, various endocrine axes, as well as several neurosteroids, neuropeptides, opioids, endocannabinoids and endovanilloids. This review summarizes current knowledge on these pharmacological targets and their potential utility in the clinical management of depression.eng
dc.identifier.issn16876334
dc.identifier.urihttp://hdl.handle.net/20.500.12442/2457
dc.language.isoengeng
dc.publisherHindawieng
dc.rights.accessrightsinfo:eu-repo/semantics/openAccess
dc.rights.licenseLicencia de Creative Commons Reconocimiento-NoComercial-CompartirIgual 4.0 Internacionalspa
dc.sourceAdvances in Pharmacological Scienceseng
dc.source.urihttps://doi.org/10.1155/2019/7943481eng
dc.subjectDepressioneng
dc.subjectNeuroendocrine Disordereng
dc.titleDepression as a Neuroendocrine Disorder: Emerging Neuropsychopharmacological Approaches beyond Monoamineseng
dc.typearticleeng
dcterms.referencesH. A. Whiteford, A. J. Ferrari, L. Degenhardt, V. Feigin, and T. Vos, “2e global burden of mental, neurological and substance use disorders: an analysis from the global burden of disease study 2010,” PLoS One, vol. 10, no. 2, Article ID e0116820, 2015.eng
dcterms.referencesD. L. Hare, S. R. Toukhsati, P. Johansson, and T. Jaarsma, “Depression and cardiovascular disease: a clinical review,” European Heart Journal, vol. 35, no. 21, pp. 1365–1372, 2013.eng
dcterms.referencesP. E. Greenberg, A.-A. Fournier, T. Sisitsky, C. T. Pike, and R. C. Kessler, “2e economic burden of adults with major depressive disorder in the United States (2005 and 2010),” Ae Journal of Clinical Psychiatry, vol. 76, no. 2, pp. 155–162, 2015.eng
dcterms.referencesE. Dale, B. Bang-Andersen, and C. Sánchez, “Emerging mechanisms and treatments for depression beyond SSRIs and SNRIs,” Biochemical Pharmacology, vol. 95, no. 2, pp. 81–97, 2015.eng
dcterms.referencesS. J. Mathew, H. K. Manji, and D. S. Charney, “Novel drugs and therapeutic targets for severe mood disorders,” Neuropsychopharmacology, vol. 33, no. 9, pp. 2080–2092, 2008.eng
dcterms.referencesY. Agid, G. Buzsáki, D. M. Diamond et al., “How can drug discovery for psychiatric disorders be improved?,” Nature Reviews Drug Discovery, vol. 6, no. 3, pp. 189–201, 2007.eng
dcterms.referencesB. L. Roth, D. J. Sheffler, and W. K. Kroeze, “Magic shotguns versus magic bullets: selectively non-selective drugs for mood disorders and schizophrenia,” Nature Reviews Drug Discovery, vol. 3, no. 4, pp. 353–359, 2004.eng
dcterms.referencesT. M. Hillhouse and J. H. Porter, “A brief history of the development of antidepressant drugs: from monoamines to glutamate,” Experimental and Clinical Psychopharmacology, vol. 23, no. 1, pp. 1–21, 2015.eng
dcterms.referencesM. Hinz, A. Stein, and T. Uncini, “2e discrediting of the monoamine hypothesis,” International Journal of General Medicine, vol. 5, pp. 135–142, 2012.eng
dcterms.referencesU. E. Lang and S. Borgwardt, “Molecular mechanisms of depression: perspectives on new treatment strategies,” Cellular Physiology and Biochemistry, vol. 31, no. 6, pp. 761–777, 2013.eng
dcterms.referencesF. Caraci, G. M. Leggio, S. Salomone, and F. Drago, “New drugs in psychiatry: focus on new pharmacological targets,” F1000Research, vol. 6, p. 397, 2017.eng
dcterms.referencesA. Jansson, “Mood disorders and the brain: depression, melancholia, and the historiography of psychiatry,” Medical History, vol. 55, no. 3, pp. 393–399, 2012.eng
dcterms.referencesJ. Dean and M. Keshavan, “2e neurobiology of depression: an integrated view,” Asian Journal of Psychiatry, vol. 27, pp. 101–111, 2017.eng
dcterms.referencesF. Orrego and S. Villanueva, “2e chemical nature of the main central excitatory transmitter: a critical appraisal based upon release studies and synaptic vesicle localization,” Neuroscience, vol. 56, no. 3, pp. 539–555, 1993.eng
dcterms.referencesJ. H. Krystal, D. C. D’Souza, I. L. Petrakis et al., “NMDA agonists and antagonists as probes of glutamatergic dysfunction and pharmacotherapies in neuropsychiatric disorders,” Harvard Review of Psychiatry, vol. 7, no. 3, pp. 125–143, 1999.eng
dcterms.referencesJ. H. Krystal, G. Sanacora, and R. S. Duman, “Rapid-acting glutamatergic antidepressants: the path to ketamine and beyond,” Biological Psychiatry, vol. 73, no. 12, pp. 1133–1141, 2013.eng
dcterms.referencesS. D. Geddes, S. Assadzada, A. Sokolovski, R. Bergeron, S. Haj-Dahmane, and J.-C. B´e¨ıque, “Time-dependent modulation of glutamate synapses onto 5-HT neurons by antidepressant treatment,” Neuropharmacology, vol. 95, pp. 130–143, 2015.eng
dcterms.referencesD. C. Javitt, D. Schoepp, P. W. Kalivas et al., “Translating glutamate: from pathophysiology to treatment,” Science Translational Medicine, vol. 3, no. 102, p. 102mr2, 2011.eng
dcterms.referencesX. Fan, W. Y. Jin, and Y. T. Wang, “2e NMDA receptor complex: a multifunctional machine at the glutamatergic synapse,” Frontiers in Cellular Neuroscience, vol. 8, p. 160, 2014.eng
dcterms.referencesG. Perea, M. Sur, and A. Araque, “Neuron-glia networks: integral gear of brain function,” Frontiers in Cellular Neuroscience, vol. 8, p. 378, 2014.eng
dcterms.referencesN. Li, B. Lee, R.-J. Liu et al., “mTOR-dependent synapse formation underlies the rapid antidepressant effects of NMDA antagonists,” Science, vol. 329, no. 5994, pp. 959– 964, 2010.eng
dcterms.referencesI. A. Paul and P. Skolnick, “Glutamate and depression,” Annals of the New York Academy of Sciences, vol. 1003, no. 1, pp. 250–272, 2003.eng
dcterms.referencesR. Trullas and P. Skolnick, “Functional antagonists at the NMDA receptor complex exhibit antidepressant actions,” European Journal of Pharmacology, vol. 185, no. 1, pp. 1–10, 1990.eng
dcterms.referencesM. Kurdi, K. 2eerth, and R. Deva, “Ketamine: current applications in anesthesia, pain, and critical care,” Anesthesia: Essays and Researches, vol. 8, no. 3, p. 283, 2014.eng
dcterms.referencesC. A. Zarate, J. B. Singh, P. J. Carlson et al., “A randomized trial of an N-methyl-D-aspartate antagonist in treatmentresistant major depression,” Archives of General Psychiatry, vol. 63, no. 8, p. 856, 2006.eng
dcterms.referencesN. Diazgranados, L. Ibrahim, N. E. Brutsche et al., “A randomized add-on trial of an N-methyl-D-aspartate antagonist in treatment-resistant bipolar depression,” Archives of General Psychiatry, vol. 67, no. 8, pp. 793–802, 2010.eng
dcterms.referencesG. W. Valentine, G. F. Mason, R. Gomez et al., “2e antidepressant effect of ketamine is not associated with changes in occipital amino acid neurotransmitter content as measured by [1H]-MRS,” Psychiatry Research: Neuroimaging, vol. 191, no. 2, pp. 122–127, 2011.eng
dcterms.referencesR. M. Berman, A. Cappiello, A. Anand et al., “Antidepressant effects of ketamine in depressed patients,” Biological Psychiatry, vol. 47, no. 4, pp. 351–354, 2000.eng
dcterms.referencesS. A. Irwin and A. Iglewicz, “Oral ketamine for the rapid treatment of depression and anxiety in patients receiving hospice care,” Journal of Palliative Medicine, vol. 13, no. 7, pp. 903–908, 2010.eng
dcterms.referencesC. G. Zanicotti, D. Perez, and P. Glue, “Mood and pain responses to repeat dose intramuscular ketamine in a depressed patient with advanced cancer,” Journal of Palliative Medicine, vol. 15, no. 4, pp. 400–403, 2012.eng
dcterms.referencesK. A. B. Lapidus, C. F. Levitch, A. M. Perez et al., “A randomized controlled trial of intranasal ketamine in major depressive disorder,” Biological psychiatry, vol. 76, no. 12, pp. 970–976, 2014.eng
dcterms.referencesN. D. Iadarola, M. J. Niciu, E. M. Richards et al., “Ketamine and other N-methyl-D-aspartate receptor antagonists in the treatment of depression: a perspective review,” Aerapeutic advances in chronic disease, vol. 6, no. 3, pp. 97–114, 2015.eng
dcterms.referencesH. Homayoun and B. Moghaddam, “NMDA receptor hypofunction produces opposite effects on prefrontal cortex interneurons and pyramidal neurons,” Journal of Neuroscience, vol. 27, no. 43, pp. 11496–11500, 2007.eng
dcterms.referencesA. E. Autry, M. Adachi, E. Nosyreva et al., “NMDA receptor blockade at rest triggers rapid behavioural antidepressant responses,” Nature, vol. 475, no. 7354, pp. 91–95, 2011.eng
dcterms.referencesM. M. Harraz, R. Tyagi, P. Cortés, and S. H. Snyder, “Antidepressant action of ketamine via mTOR is mediated by inhibition of nitrergic Rheb degradation,” Molecular Psychiatry, vol. 21, no. 3, pp. 313–319, 2016.eng
dcterms.referencesN. Li, R.-J. Liu, J. M. Dwyer et al., “Glutamate N-methyl-Daspartate receptor antagonists rapidly reverse behavioral and synaptic deficits caused by chronic stress exposure,” Biological Psychiatry, vol. 69, no. 8, pp. 754–761, 2011.eng
dcterms.referencesJ. M. Witkin, D. E. Knutson, G. J. Rodriguez, and S. Shi, “Rapid-acting antidepressants,” Current Pharmaceutical Design, vol. 24, no. 22, pp. 2556–2563, 2018.eng
dcterms.referencesC. Yang, Y. Shirayama, J.-c. Zhang et al., “R-ketamine: a rapid-onset and sustained antidepressant without psychotomimetic side effects,” Translational Psychiatry, vol. 5, no. 9, p. e632, 2015.eng
dcterms.referencesK. Hashimoto and C. Yang, “Is (S)-norketamine an alternative antidepressant for esketamine?,” European Archives of Psychiatry and Clinical Neuroscience, vol. 268, 2018.eng
dcterms.referencesC. Yang, S. Kobayashi, K. Nakao et al., “AMPA receptor activation-independent antidepressant actions of ketamine metabolite (S)-norketamine,” Biological Psychiatry, vol. 84, no. 8, pp. 591–600, 2018.eng
dcterms.referencesJ. Moskal, J. Burgdorf, P. Stanton et al., “2e development of rapastinel (formerly GLYX-13), a rapid acting and long lasting antidepressant,” Current Neuropharmacology, vol. 15, no. 1, pp. 47–56, 2016.eng
dcterms.referencesC. I. Rodriguez, J. Zwerling, E. Kalanthroff et al., “Effect of a novel NMDA receptor modulator, rapastinel (formerly GLYX-13), in OCD: proof of concept,” American Journal of Psychiatry, vol. 173, no. 12, pp. 1239–1241, 2016.eng
dcterms.referencesM. E. d. S. Frizzo, L. P. Dall’Onder, K. B. Dalcin, and D. O. Souza, “Riluzole enhances glutamate uptake in rat astrocyte cultures,” Cellular and Molecular Neurobiology, vol. 24, no. 1, pp. 123–128, 2004.eng
dcterms.referencesM. Banasr, G. M. I. Chowdhury, R. Terwilliger et al., “Glial pathology in an animal model of depression: reversal of stress-induced cellular, metabolic and behavioral deficits by the glutamate-modulating drug riluzole,” Molecular Psychiatry, vol. 15, no. 5, pp. 501–511, 2008.eng
dcterms.referencesP. T¨urck and M. E. Frizzo, “Riluzole stimulates BDNF release from human platelets,” BioMed Research International, vol. 2015, Article ID 189307, 6 pages, 2015.eng
dcterms.referencesE. H. Wong, J. A. Kemp, T. Priestley, A. R. Knight, G. N. Woodruff, and L. L. Iversen, “2e anticonvulsant MK- 801 is a potent N-methyl-D-aspartate antagonist,” Proceedings of the National Academy of Sciences, vol. 83, no. 18, pp. 7104–7108, 1986.eng
dcterms.referencesS. Maeng, C. A. Zarate, J. Du et al., “Cellular mechanisms underlying the antidepressant effects of ketamine: role of α-amino-3-hydroxy-5-methylisoxazole-4-propionic acid receptors,” Biological Psychiatry, vol. 63, no. 4, pp. 349–352, 2008.eng
dcterms.referencesS. Chaki, Y. Ago, A. Palucha-Paniewiera, F. Matrisciano, and A. Pilc, “mGlu2/3 and mGlu5 receptors: potential targets for novel antidepressants,” Neuropharmacology, vol. 66, pp. 40–52, 2013.eng
dcterms.referencesA. Mahapatra and R. Gupta, “Role of psilocybin in the treatment of depression,” Aerapeutic Advances in Psychopharmacology, vol. 7, no. 1, pp. 54–56, 2016.eng
dcterms.referencesR. L. Carhart-Harris, L. Roseman, M. Bolstridge et al., “Psilocybin for treatment-resistant depression: fMRImeasured brain mechanisms,” Scientific Reports, vol. 7, no. 1, p. 13187, 2017.eng
dcterms.referencesR. L. Carhart-Harris, M. Bolstridge, C. M. J. Day et al., “Psilocybin with psychological support for treatmentresistant depression: six-month follow-up,” Psychopharmacology, vol. 235, no. 2, pp. 399–408, 2017.eng
dcterms.referencesM.-N. Quan, N. Zhang, Y.-Y. Wang, T. Zhang, and Z. Yang, “Possible antidepressant effects and mechanisms of memantine in behaviors and synaptic plasticity of a depression rat model,” Neuroscience, vol. 182, pp. 88–97, 2011.eng
dcterms.referencesE. J. Lenze, E. R. Skidmore, A. E. Begley, J. W. Newcomer, M. A. Butters, and E. M. Whyte, “Memantine for late-life depression and apathy after a disabling medical event: a 12- week, double-blind placebo-controlled pilot study,” International Journal of Geriatric Psychiatry, vol. 27, no. 9, pp. 974–980, 2011.eng
dcterms.referencesC. A. Zarate, J. B. Singh, J. A. Quiroz et al., “A double-blind, placebo-controlled study of memantine in the treatment of major depression,” American Journal of Psychiatry, vol. 163, no. 1, pp. 153–155, 2006.eng
dcterms.referencesS. J. Mathew, J. W. Murrough, M. aan het Rot, K. A. Collins, D. L. Reich, and D. S. Charney, “Riluzole for relapse prevention following intravenous ketamine in treatmentresistant depression: a pilot randomized, placebo-controlled continuation trial,” International Journal of Neuropsychopharmacology, vol. 13, no. 1, pp. 71–82, 2010.eng
dcterms.referencesL. Ibrahim, N. DiazGranados, J. Franco-Chaves et al., “Course of improvement in depressive symptoms to a single intravenous infusion of ketamine vs add-on riluzole: results from a 4-week, double-blind, placebo-controlled study,” Neuropsychopharmacology, vol. 37, no. 6, pp. 1526–1533, 2012.eng
dcterms.referencesM. J. Niciu, B. Kelmendi, and G. Sanacora, “Overview of glutamatergic neurotransmission in the nervous system,” Pharmacology Biochemistry and Behavior, vol. 100, no. 4, pp. 656–664, 2012.eng
dcterms.referencesC. A. Zarate, J. L. Payne, J. Quiroz et al., “An open-label trial of riluzole in patients with treatment-resistant major depression,” American Journal of Psychiatry, vol. 161, no. 1, pp. 171–174, 2004.eng
dcterms.referencesE. Salardini, A. Zeinoddini, P. Mohammadinejad et al., “Riluzole combination therapy for moderate-to-severe major depressive disorder: a randomized, double-blind, placebo-controlled trial,” Journal of Psychiatric Research, vol. 75, pp. 24–30, 2016.eng
dcterms.referencesJ. Du, K. Suzuki, Y. Wei et al., “2e anticonvulsants lamotrigine, riluzole, and valproate differentially regulate AMPA receptor membrane localization: relationship to clinical effects in mood disorders,” Neuropsychopharmacology, vol. 32, no. 4, pp. 793–802, 2006.eng
dcterms.referencesA. Pałucha-Poniewiera and A. Pilc, “Involvement of mGlu5 and NMDA receptors in the antidepressant-like effect of acamprosate in the tail suspension test,” Progress in Neuro- Psychopharmacology and Biological Psychiatry, vol. 39, no. 1, pp. 102–106, 2012.eng
dcterms.referencesE. R. Hascup, K. N. Hascup, M. Stephens et al., “Rapid microelectrode measurements and the origin and regulation of extracellular glutamate in rat prefrontal cortex,” Journal of Neurochemistry, vol. 115, no. 6, pp. 1608–1620, 2010.eng
dcterms.referencesJ. M. Dwyer, A. E. Lepack, and R. S. Duman, “mGluR2/3 blockade produces rapid and long-lasting reversal of anhedonia caused by chronic stress exposure,” Journal of Molecular Psychiatry, vol. 1, no. 1, p. 15, 2013.eng
dcterms.referencesJ. M. Dwyer, A. E. Lepack, and R. S. Duman, “mTOR activation is required for the antidepressant effects of mGluR2/ 3 blockade,” Ae International Journal of Neuropsychopharmacology, vol. 15, no. 4, pp. 429–434, 2011.eng
dcterms.referencesA. Pałucha-Poniewiera, B. Szewczyk, and A. Pilc, “Activation of the mTOR signaling pathway in the antidepressant-like activity of the mGlu5 antagonist MTEP and the mGlu7 agonist AMN082 in the FST in rats,” Neuropharmacology, vol. 82, pp. 59–68, 2014.eng
dcterms.referencesM. L. Furey, A. Khanna, E. M. Hoffman, and W. C. Drevets, “Scopolamine produces larger antidepressant and antianxiety effects in women than in men,” Neuropsychopharmacology, vol. 35, no. 12, pp. 2479–2488, 2010.eng
dcterms.referencesB. Voleti, A. Navarria, R.-J. Liu et al., “Scopolamine rapidly increases mammalian target of rapamycin complex 1 signaling, synaptogenesis, and antidepressant behavioral responses,” Biological Psychiatry, vol. 74, no. 10, pp. 742–749, 2013.eng
dcterms.referencesM. Amar, E. Lucas-Meunier, G. Baux, and P. Fossier, “Blockade of different muscarinic receptor subtypes changes the equilibrium between excitation and inhibition in rat visual cortex,” Neuroscience, vol. 169, no. 4, pp. 1610–1620, 2010.eng
dcterms.referencesM. L. Furey and W. C. Drevets, “Antidepressant efficacy of the antimuscarinic drug scopolamine,” Archives of General Psychiatry, vol. 63, no. 10, p. 1121, 2006.eng
dcterms.referencesA. Alt, E. S. Nisenbaum, D. Bleakman, and J. M. Witkin, “A role for AMPA receptors in mood disorders,” Biochemical Pharmacology, vol. 71, no. 9, pp. 1273–1288, 2006.eng
dcterms.referencesW. C. Drevets and M. L. Furey, “Replication of scopolamine’s antidepressant efficacy in major depressive disorder: a randomized, placebo-controlled clinical trial,” Biological Psychiatry, vol. 67, no. 5, pp. 432–438, 2010.eng
dcterms.referencesJ. C. Gillin, L. Sutton, C. Ruiz et al., “2e effects of scopolamine on sleep and mood in depressed patients with a history of alcoholism and a normal comparison group,” Biological Psychiatry, vol. 30, no. 2, pp. 157–169, 1991.eng
dcterms.referencesK. M. Kantak, “Magnesium deficiency alters aggressive behavior and catecholamine function,” Behavioral Neuroscience, vol. 102, no. 2, pp. 304–311, 1988.eng
dcterms.referencesH. Murck, “Magnesium and affective disorders,” Nutritional Neuroscience, vol. 5, no. 6, pp. 375–389, 2013.eng
dcterms.referencesN. Singewald, C. Sinner, A. Hetzenauer, S. B. Sartori, and H. Murck, “Magnesium-deficient diet alters depression- and anxiety-related behavior in mice-influence of desipramine and Hypericum perforatum extract,” Neuropharmacology, vol. 47, no. 8, pp. 1189–1197, 2004.eng
dcterms.referencesG. A. Eby and K. L. Eby, “Rapid recovery from major depression using magnesium treatment,” Medical Hypotheses, vol. 67, no. 2, pp. 362–370, 2006.eng
dcterms.referencesG. K. Kirov, N. J. Birch, P. Steadman, and R. G. Ramsey, “Plasma magnesium levels in a population of psychiatric patients: correlations with symptoms,” Neuropsychobiology, vol. 30, no. 2-3, pp. 73–78, 2008.eng
dcterms.referencesA. Zieba, R. Kata, D. Dudek, M. Schlegel-zawadzka, and G. Nowak, “Serum trace elements in animal models and human depression: Part III. Magnesium. Relationship with copper,” Human Psychopharmacology: Clinical and Experimental, vol. 15, no. 8, pp. 631–635, 2001.eng
dcterms.referencesM. Watanabe, K. Maemura, K. Kanbara, T. Tamayama, and H. Hayasaki, “GABA and GABA receptors in the central nervous system and other organs,” International Review of Cytology, vol. 213, pp. 1–47, 2002.eng
dcterms.referencesE. Sigel and M. E. Steinmann, “Structure, function, and modulation of GABAAReceptors,” Journal of Biological Chemistry, vol. 287, no. 48, pp. 40224–40231, 2012.eng
dcterms.referencesB. Bettler, K. Kaupmann, J. Mosbacher, and M. Gassmann, “Molecular structure and physiological functions of GABABReceptors,” Physiological Reviews, vol. 84, no. 3, pp. 835–867, 2004.eng
dcterms.referencesG. Sanacora, G. F. Mason, and J. H. Krystal, “Impairment of GABAergic transmission in depression: new insights from neuroimaging studies,” Critical Reviews in Neurobiology, vol. 14, no. 1, pp. 23–45, 2000.eng
dcterms.referencesJ. Fischell, A. M. Van Dyke, M. D. Kvarta, T. A. LeGates, and S. M. 2ompson, “Rapid antidepressant action and restoration of excitatory synaptic strength after chronic stress by negative modulators of alpha5-containing GABAA receptors,” Neuropsychopharmacology, vol. 40, no. 11, pp. 2499–2509, 2015.eng
dcterms.referencesK. G. Lloyd, F. 2uret, and A. Pilc, “Upregulation of gammaaminobutyric acid (GABA) B binding sites in rat frontal cortex: a common action of repeated administration of different classes of antidepressants and electroshock,” J Pharmacol Exp Aer, vol. 235, no. 1, pp. 191–199, 1985.eng
dcterms.referencesJ. A. Cross and R. W. Horton, “Effects of chronic oral administration of the antidepressants, desmethylimipramine and zimelidine on rat cortical GABAB binding sites: a comparison with 5-HT2 binding site changes,” British Journal of Pharmacology, vol. 93, no. 2, pp. 331–336, 2012.eng
dcterms.referencesT. R. Berigan, “Psychiatric uses of newer anticonvulsants,” Ae Primary Care Companion to Ae Journal of Clinical Psychiatry, vol. 3, no. 2, pp. 82–84, 2001.eng
dcterms.referencesA. Foster and J. Kemp, “Glutamate- and GABA-based CNS therapeutics,” Current Opinion in Pharmacology, vol. 6, no. 1, pp. 7–17, 2006.eng
dcterms.referencesP. Zanos, M. E. Nelson, J. N. Highland et al., “A negative allosteric modulator for α5 subunit-containing GABA receptors exerts a rapid and persistent antidepressant-like action without the side effects of the NMDA receptor antagonist ketamine in mice,” eNeuro, vol. 4, no. 1, article ENEURO.0285-16.2017, 2017.eng
dcterms.referencesT. Duka and D. N. Stephens, “Potentiation of the Propunishment, but not the convulsant action of the β-carboline DMCM by naltrexone,” Pharmacology Biochemistry and Behavior, vol. 25, no. 3, pp. 595–598, 1986.eng
dcterms.referencesE. Castrén, “Neurotrophins and psychiatric disorders,” Neurotrophic Factors, vol. 220, pp. 461–479, 2014.eng
dcterms.referencesO. Berton and E. J. Nestler, “New approaches to antidepressant drug discovery: beyond monoamines,” Nature Reviews Neuroscience, vol. 7, no. 2, pp. 137–151, 2006.eng
dcterms.referencesG. Ochs, R. D. Penn, M. York et al., “A phase I/II trial of recombinant methionyl human brain derived neurotrophic factor administered by intrathecal infusion to patients with amyotrophic lateral sclerosis,” Amyotrophic Lateral Sclerosis and Other Motor Neuron Disorders, vol. 1, no. 3, pp. 201–206, 2009.eng
dcterms.referencesH. Toenen and M. Sendtner, “Neurotrophins: from enthusiastic expectations through sobering experiences to rational therapeutic approaches,” Nature Neuroscience, vol. 5, pp. 1046–1050, 2002.eng
dcterms.referencesP. D. O’Leary and R. A. Hughes, “Design of potent peptide mimetics of brain-derived neurotrophic factor,” Journal of Biological Chemistry, vol. 278, no. 28, pp. 25738–25744, 2003.eng
dcterms.referencesS.-W. Jang, X. Liu, M. Yepes et al., “A selective TrkB agonist with potent neurotrophic activities by 7,8-dihydroxyflavone,” Proceedings of the National Academy of Sciences, vol. 107, no. 6, pp. 2687–2692, 2010.eng
dcterms.referencesC. Liu, C. B. Chan, and K. Ye, “7,8-dihydroxyflavone, a small molecular TrkB agonist, is useful for treating various BDNFimplicated human disorders,” Translational Neurodegeneration, vol. 5, no. 1, p. 2, 2016.eng
dcterms.referencesX. Liu, C.-B. Chan, Q. Qi et al., “Optimization of a small tropomyosin-related kinase B (TrkB) agonist 7,8-dihydroxyflavone active in mouse models of depression,” Journal of Medicinal Chemistry, vol. 55, no. 19, pp. 8524– 8537, 2012.eng
dcterms.referencesX. Liu, Q. Qi, G. Xiao, J. Li, H. R. Luo, and K. Ye, “Omethylated metabolite of 7,8-dihydroxyflavone activates TrkB receptor and displays antidepressant activity,” Pharmacology, vol. 91, no. 3-4, pp. 185–200, 2013.eng
dcterms.referencesJ. C. Zhang, J. Wu, Y Fujita et al., “Antidepressant effects of TrkB ligands on depression-like behavior and dendritic changes in mice after inflammation,” Int J Neuropsychopharmacol, vol. 18, no. 4, 2014.eng
dcterms.referencesM. Cazorla, J. Pr´emont, A. Mann, N. Girard, C. Kellendonk, and D. Rognan, “Identification of a low-molecular weight TrkB antagonist with anxiolytic and antidepressant activity in mice,” Journal of Clinical Investigation, vol. 121, no. 5, pp. 1846–1857, 2011.eng
dcterms.referencesG. Tamagno and J. Epelbaum, “Editorial: neurological and psychiatric disorders in endocrine diseases,” Frontiers in Endocrinology, vol. 6, p. 75, 2015.eng
dcterms.referencesA. Badhan, H. Sareen, and J. Trivedi, “Endocrine dysfunctions and psychiatric disorders: understanding an interface,” Indian Journal of Behavioural Sciences, vol. 18, no. 2, pp. 50–64, 2008.eng
dcterms.referencesM. Altemus, “Hormone-specific psychiatric disorders: do they exist?,” Archives of Women’s Mental Health, vol. 13, no. 1, pp. 25-26, 2010.eng
dcterms.referencesD. Stenzel and W. B. Huttner, “Role of maternal thyroid hormones in the developing neocortex and during human evolution,” Frontiers in Neuroanatomy, vol. 7, p. 19, 2013.eng
dcterms.referencesK. N. Fountoulakis, S. Kantartzis, M. Siamouli et al., “Peripheral thyroid dysfunction in depression,” Ae World Journal of Biological Psychiatry, vol. 7, no. 3, pp. 131–137, 2009.eng
dcterms.referencesD. Ordas and L. Labbate, “Routine screening of thyroid function in patients hospitalized for major depression or dysthymia?,” Annals of Clinical Psychiatry, vol. 7, no. 4, pp. 161–165, 1995.eng
dcterms.referencesJ. D. Davis, R. A. Stern, and L. A. Flashman, “Cognitive and neuropsychiatric aspects of subclinical hypothyroidism: significance in the elderly,” Current Psychiatry Reports, vol. 5, no. 5, pp. 384–390, 2003.eng
dcterms.referencesS. Gulseren, L. Gulseren, Z. Hekimsoy, P. Cetinay, C. Ozen, and B. Tokatlioglu, “Depression, anxiety, health-related quality of life, and disability in patients with overt and subclinical thyroid dysfunction,” Archives of Medical Research, vol. 37, no. 1, pp. 133–139, 2006.eng
dcterms.referencesV. B. Chueire, J. H. Romaldini, and L. S. Ward, “Subclinical hypothyroidism increases the risk for depression in the elderly,” Archives of Gerontology and Geriatrics, vol. 44, no. 1, pp. 21–28, 2007.eng
dcterms.referencesC. Fekete and R. M. Lechan, “Central regulation of hypothalamic-pituitary-thyroid Axis under physiological and pathophysiological conditions,” Endocrine Reviews, vol. 35, no. 2, pp. 159–194, 2014.eng
dcterms.referencesM. P. Hage and S. T. Azar, “2e link between thyroid function and depression,” Journal of Ayroid Research, vol. 2012, Article ID 590648, 8 pages, 2012.eng
dcterms.referencesY. Mizoguchi, T. A. Kato, Y. Seki et al., “Brain-derived neurotrophic factor (BDNF) induces sustained intracellular Ca2+Elevation through the up-regulation of surface transient receptor potential 3 (TRPC3) channels in rodent microglia,” Journal of Biological Chemistry, vol. 289, no. 26, pp. 18549–18555, 2014.eng
dcterms.referencesT. A. Kato, Y. Yamauchi, H Horikawa et al., “Neurotransmitters, psychotropic drugs and microglia: clinical implications for psychiatry,” Current Medicinal Chemistry, vol. 20, no. 3, pp. 331–344, 2013.eng
dcterms.referencesS. Honda, Y. Sasaki, K. Ohsawa et al., “Extracellular ATP or ADP induce chemotaxis of cultured microglia through Gi/ocoupled P2Y receptors,” Ae Journal of Neuroscience, vol. 21, no. 6, pp. 1975–1982, 2001.eng
dcterms.referencesH. Kalyanaraman, R. Schwappacher, J. Joshua et al., “Nongenomic thyroid hormone signaling occurs through a plasma membrane-localized receptor,” Science Signaling, vol. 7, no. 326, p. ra48, 2014.eng
dcterms.referencesY. Mori, D. Tomonaga, A. Kalashnikova et al., “Effects of 3,3′,5-triiodothyronine on microglial functions,” Glia, vol. 63, no. 5, pp. 906–920, 2015.eng
dcterms.referencesR. T. Joffe, “Is the thyroid still important in major depression?,” Journal of Psychiatry and Neuroscience, vol. 31, no. 6, pp. 367-368, 2006.eng
dcterms.referencesO. Agid and B. Lerer, “Algorithm-based treatment of major depression in an outpatient clinic: clinical correlates of response to a specific serotonin reuptake inhibitor and to triiodothyronine augmentation,” Ae International Journal of Neuropsychopharmacology, vol. 6, no. 1, pp. 41–49, 2003.eng
dcterms.referencesL. L. Altshuler, M. A. Frye, and M. J. Gitlin, “Acceleration and augmentation strategies for treating bipolar depression,” Biological Psychiatry, vol. 53, no. 8, pp. 691–700, 2003.eng
dcterms.referencesS. Pridmore and Y. Turnier-Shea, “Medication options in the treatment of treatment-resistant depression,” Australian and New Zealand Journal of Psychiatry, vol. 38, no. 4, pp. 219– 225, 2004.eng
dcterms.referencesB. Demartini, R. Ranieri, A. Masu, V. Selle, S. Scarone, and O. Gambini, “Depressive symptoms and major depressive disorder in patients affected by subclinical hypothyroidism,” Ae Journal of Nervous and Mental Disease, vol. 202, no. 8, pp. 603–607, 2014.eng
dcterms.referencesS. J. Claes, “CRH, stress, and major depression: a psychobiological interplay,” Vitamins & Hormones, vol. 69, pp. 117–150, 2004.eng
dcterms.referencesF. Holsboer, “Stress, hypercortisolism and corticosteroid receptors in depression: implicatons for therapy,” Journal of Affective Disorders, vol. 62, no. 1-2, pp. 77–91, 2001.eng
dcterms.referencesF. Holsboer and N. Barden, “Antidepressants and hypothalamic-pituitary-adrenocortical regulation,” Endocrine Reviews, vol. 17, no. 2, pp. 187–205, 1996.eng
dcterms.referencesK. Van Pett, V. Viau, J. C. Bittencourt et al., “Distribution of mRNAs encoding CRF receptors in brain and pituitary of rat and mouse,” Ae Journal of Comparative Neurology, vol. 428, no. 2, pp. 191–212, 2000.eng
dcterms.referencesZ. Liu, F. Zhu, G. Wang et al., “Association of corticotropinreleasing hormone receptor1 gene SNP and haplotype with major depression,” Neuroscience Letters, vol. 404, no. 3, pp. 358–362, 2006.eng
dcterms.referencesM. L. Wong, J. Licinio, K. I. Pasternak, and P. W. Gold, “Localization of corticotropin-releasing hormone (CRH) receptor mRNA in adult rat brain by in situ hybridization histochemistry,” Endocrinology, vol. 135, no. 5, pp. 2275– 2278, 1994.eng
dcterms.referencesA. W. Zobel, T. Nickel, H. E. K¨unzel et al., “Effects of the high-affinity corticotropin-releasing hormone receptor 1 antagonist R121919 in major depression: the first 20 patients treated,” Journal of Psychiatric Research, vol. 34, no. 3, pp. 171–181, 2000.eng
dcterms.referencesF. Holsboer and M. Ising, “Central CRH system in depression and anxiety - evidence from clinical studies with CRH1 receptor antagonists,” European Journal of Pharmacology, vol. 583, no. 2-3, pp. 350–357, 2008.eng
dcterms.referencesB. Binneman, D. Feltner, S. Kolluri, Y. Shi, R. Qiu, and T. Stiger, “A 6-week randomized, placebo-controlled trial of CP-316,311 (a selective CRH1Antagonist) in the treatment of major depression,” American Journal of Psychiatry, vol. 165, no. 5, pp. 617–620, 2008.eng
dcterms.referencesM. Ising, U. S. Zimmermann, H. E. K¨unzel et al., “Highaffinity CRF1 receptor antagonist NBI-34041: preclinical and clinical data suggest safety and efficacy in attenuating elevated stress response,” Neuropsychopharmacology, vol. 32, no. 9, pp. 1941–1949, 2007.eng
dcterms.referencesR. Sanghvi, E. Mogalian, S. G. Machatha et al., “Preformulation and pharmacokinetic studies on antalarmin: a novel stress inhibitor,” Journal of Pharmaceutical Sciences, vol. 98, no. 1, pp. 205–214, 2009.eng
dcterms.referencesM. B. Solomon and J. P. Herman, “Sex differences in psychopathology: of gonads, adrenals and mental illness,” Physiology & Behavior, vol. 97, no. 2, pp. 250–258, 2009.eng
dcterms.referencesG. B. Parker and H. L. Brotchie, “From diathesis to dimorphism,” Ae Journal of Nervous and Mental Disease, vol. 192, no. 3, pp. 210–216, 2004.eng
dcterms.referencesS. L. Douma, C. Husband, M. E. OʼDonnell, B. N. Barwin, and A. K. Woodend, “Estrogen-related mood disorders,” Advances in Nursing Science, vol. 28, no. 4, pp. 364–375, 2005.eng
dcterms.referencesR. C. Kessler, O. Demler, R. G. Frank et al., “Prevalence and treatment of mental disorders, 1990 to 2003,” New England Journal of Medicine, vol. 352, no. 24, pp. 2515–2523, 2005.eng
dcterms.referencesM. H. J. Bekker and J. van Mens-Verhulst, “Anxiety disorders: sex differences in prevalence, degree, and background, but gender-neutral treatment,” Gender Medicine, vol. 4, pp. S178–S193, 2007.eng
dcterms.referencesM. ¨ Osterlund, G.J.M. Kuiper, J.- ˚ A. Gustafsson, and Y. L. Hurd, “Differential distribution and regulation of estrogen receptor-α and -β mRNA within the female rat brain,” Molecular Brain Research, vol. 54, no. 1, pp. 175–180, 1998.eng
dcterms.referencesS. Grigoriadis and S. H. Kennedy, “Role of estrogen in the treatment of depression,” American Journal of Aerapeutics, vol. 9, no. 6, pp. 503–509, 2002.eng
dcterms.referencesP. J. Schmidt, L. Nieman, M. A. Danaceau et al., “Estrogen replacement in perimenopause-related depression: a preliminary report,” American Journal of Obstetrics and Gynecology, vol. 183, no. 2, pp. 414–420, 2000.eng
dcterms.referencesE. L. Klaiber, D. M. Broverman, W. Vogel, and Y. Kobayashi, “Estrogen therapy for severe persistent depressions in women,” Archives of general psychiatry, vol. 36, no. 5, pp. 550–554, 1979.eng
dcterms.referencesC. E. Gleason, N. M. Dowling, W. Wharton et al., “Effects of hormone therapy on cognition and mood in recently postmenopausal women: findings from the randomized, controlled KEEPS-cognitive and affective study,” PLoS Medicine, vol. 12, no. 6, article e1001833, 2015.eng
dcterms.referencesJ. M. Whedon, A. KizhakkeVeettil, N. A. Rugo, and K. A. Kieffer, “Bioidentical estrogen for menopausal depressive symptoms: a systematic review and meta-analysis,” Journal of Women’s Health, vol. 26, no. 1, pp. 18–28, 2017.eng
dcterms.referencesS. J. Jung, A. Shin, and D. Kang, “Hormone-related factors and post-menopausal onset depression: results from KNHANES (2010-2012),” Journal of Affective Disorders, vol. 175, pp. 176–183, 2015.eng
dcterms.referencesS. Brummelte and L. A. M. Galea, “Postpartum depression: etiology, treatment and consequences for maternal care,” Hormones and Behavior, vol. 77, pp. 153–166, 2016.eng
dcterms.referencesL. Andréen, S. Nyberg, S. Turkmen, G. van Wingen, G. Fernández, and T. B¨ackström, “Sex steroid induced negative mood may be explained by the paradoxical effect mediated by GABAA modulators,” Psychoneuroendocrinology, vol. 34, no. 8, pp. 1121–1132, 2009.eng
dcterms.referencesA. Ahokas, J. Kaukoranta, K. Wahlbeck, and M. Aito, “Estrogen deficiency in severe postpartum depression: successful treatment with sublingual physiologic 17betaestradiol: a preliminary study,” Journal of Clinical Psychiatry, vol. 62, no. 5, pp. 332–336, 2001.eng
dcterms.referencesK. L. Wisner, D. K. Y. Sit, E. L. Moses-Kolko et al., “Transdermal estradiol treatment for postpartum depression: a pilot, randomized trial,” Journal of Clinical Psychopharmacology, vol. 35, no. 4, pp. 389–395, 2015.eng
dcterms.referencesS. Kanes, H. Colquhoun, H. Gunduz-Bruce et al., “Brexanolone (SAGE-547 injection) in post-partum depression: a randomised controlled trial,” Ae Lancet, vol. 390, no. 10093, pp. 480–489, 2017.eng
dcterms.referencesE. E. Baulieu and P. Robel, “Neurosteroids: a new brain function?,” Ae Journal of Steroid Biochemistry and Molecular Biology, vol. 37, no. 3, pp. 395–403, 1990.eng
dcterms.referencesR. C. Melcangi, L. M. Garcia-Segura, and A. G. Mensah- Nyagan, “Neuroactive steroids: state of the art and new perspectives,” Cellular and Molecular Life Sciences, vol. 65, no. 5, pp. 777–797, 2008.eng
dcterms.referencesR. Rupprecht, “Neuroactive steroids: mechanisms of action and neuropsychopharmacological properties,” Psychoneuroendocrinology, vol. 28, no. 2, pp. 139–168, 2003.eng
dcterms.referencesB. O. Dubrovsky, “Steroids, neuroactive steroids and neurosteroids in psychopathology,” Progress in Neuro- Psychopharmacology and Biological Psychiatry, vol. 29, no. 2, pp. 169–192, 2005.eng
dcterms.referencesD. Eser, C. Sch¨ule, T. C. Baghai, E. Romeo, D. P. Uzunov, and R. Rupprecht, “Neuroactive steroids and affective disorders,” Pharmacology Biochemistry and Behavior, vol. 84, no. 4, pp. 656–666, 2006.eng
dcterms.referencesJ. McHenry, N. Carrier, E. Hull, and M. Kabbaj, “Sex differences in anxiety and depression: role of testosterone,” Frontiers in Neuroendocrinology, vol. 35, no. 1, pp. 42–57, 2014.eng
dcterms.referencesA. H. Ford, B. B. Yeap, L. Flicker et al., “Prospective longitudinal study of testosterone and incident depression in older men: the health in men study,” Psychoneuroendocrinology, vol. 64, pp. 57–65, 2016.eng
dcterms.referencesC. J. DiBlasio, J. Hammett, J. B. Malcolm et al., “Prevalence and predictive factors for the development of de novo psychiatric illness in patients receiving androgen deprivation therapy for prostate cancer,” Ae Canadian Journal of Urology, vol. 15, no. 5, pp. 4249–4256, 2008.eng
dcterms.referencesH. G. Pope, R. Amiaz, B. P. Brennan et al., “Parallel-group placebo-controlled trial of testosterone gel in men with major depressive disorder displaying an incomplete response to standard antidepressant treatment,” Journal of Clinical Psychopharmacology, vol. 30, no. 2, pp. 126–134, 2010.eng
dcterms.referencesK. K. Miller, R. H. Perlis, G. I. Papakostas et al., “Low-dose transdermal testosterone augmentation therapy improves depression severity in women,” CNS Spectrums, vol. 14, no. 12, pp. 688–694, 2009.eng
dcterms.referencesJ. Durdiakova, D. Ostatnikova, and P. Celec, “Testosterone and its metabolites–modulators of brain functions,” Acta Neurobiologiae Experimentalis, vol. 71, no. 4, pp. 434–454, 2011.eng
dcterms.referencesU. D. Rohr, “2e impact of testosterone imbalance on depression and women’s health,” Maturitas, vol. 41, no. 1, pp. 25–46, 2002.eng
dcterms.referencesA. Locci and G. Pinna, “Neurosteroid biosynthesis downregulation and changes in GABA A receptor subunit composition: a biomarker axis in stress-induced cognitive and emotional impairment: neurosteroids and GABA: biomarkers for emotions,” British Journal of Pharmacology, vol. 174, no. 19, pp. 3226–3241, 2017.eng
dcterms.referencesT. Bäckström, M. Bixo, M. Johansson et al., “Allopregnanolone and mood disorders,” Progress in Neurobiology, vol. 113, pp. 88–94, 2014.eng
dcterms.referencesC. C. Smith, T. T. Gibbs, and D. H. Farb, “Pregnenolone sulfate as a modulator of synaptic plasticity,” Psychopharmacology, vol. 231, no. 17, pp. 3537–3556, 2014.eng
dcterms.referencesM. Schumacher, C. Mattern, A. Ghoumari et al., “Revisiting the roles of progesterone and allopregnanolone in the nervous system: resurgence of the progesterone receptors,” Progress in Neurobiology, vol. 113, pp. 6–39, 2014.eng
dcterms.referencesC. E. Schiller, P. J. Schmidt, and D. R. Rubinow, “Allopregnanolone as a mediator of affective switching in reproductive mood disorders,” Psychopharmacology, vol. 231, no. 17, pp. 3557–3567, 2014.eng
dcterms.referencesC. Schüle, C. Nothdurfter, and R. Rupprecht, “2e role of allopregnanolone in depression and anxiety,” Progress in Neurobiology, vol. 113, pp. 79–87, 2014.eng
dcterms.referencesNational Library of Medicine, A Study to Evaluate SAGE-217 in Subjects with Moderate to Severe Major Depressive Disorder, ClinicalTrials.gov NCT03000530, National Library of Medicine, Bethesda, MD, USA, 2018, http://clinicaltrials. gov/show/NCT03000530.eng
dcterms.referencesH. Kische, S. Gross, H. Wallaschofski et al., “Associations of androgens with depressive symptoms and cognitive status in the general population,” in PLoS One, B. He, Ed., vol. 12, no. 5, Article ID e0177272, 2017.eng
dcterms.referencesB. Weber, S. Lewicka, M. Deuschle, M. Colla, and I. Heuser, “Testosterone, androstenedione and dihydrotestosterone concentrations are elevated in female patients with major depression,” Psychoneuroendocrinology, vol. 25, no. 8, pp. 765–771, 2000.eng
dcterms.referencesT. R. Insel, “2e challenge of translation in social neuroscience: a review of oxytocin, vasopressin, and affiliative behavior,” Neuron, vol. 65, no. 6, pp. 768–779, 2010.eng
dcterms.referencesI. D. Neumann and R. Landgraf, “Balance of brain oxytocin and vasopressin: implications for anxiety, depression, and social behaviors,” Trends in Neurosciences, vol. 35, no. 11, pp. 649–659, 2012.eng
dcterms.referencesJ. A. Barraza and P. J. Zak, “Empathy toward strangers triggers oxytocin release and subsequent generosity,” Annals of the New York Academy of Sciences, vol. 1167, no. 1, pp. 182–189, 2009.eng
dcterms.referencesV. Morhenn, J. Park, E. Piper, and P. Zak, “Monetary sacrifice among strangers is mediated by endogenous oxytocin release after physical contact,” Evolution and Human Behavior, vol. 29, no. 6, pp. 375–383, 2008.eng
dcterms.referencesB. Leuner, J. M. Caponiti, and E. Gould, “Oxytocin stimulates adult neurogenesis even under conditions of stress and elevated glucocorticoids,” Hippocampus, vol. 22, no. 4, pp. 861–868, 2012.eng
dcterms.referencesK. W. Yuen, J. P. Garner, D. S. Carson et al., “Plasma oxytocin concentrations are lower in depressed vs. healthy control women and are independent of cortisol,” Journal of Psychiatric Research, vol. 51, pp. 30–36, 2014.eng
dcterms.referencesR. J. McQuaid, O. A. McInnis, A. Abizaid, and H. Anisman, “Making room for oxytocin in understanding depression,” Neuroscience & Biobehavioral Reviews, vol. 45, pp. 305–322, 2014.eng
dcterms.referencesG. Meynen, U. A. Unmehopa, M. A. Hofman, D. F. Swaab, and W. J. G. Hoogendijk, “Hypothalamic oxytocin mRNA expression and melancholic depression,” Molecular Psychiatry, vol. 12, no. 2, pp. 118-119, 2007.eng
dcterms.referencesM. R. Melis, T. Melis, C. Cocco et al., “Oxytocin injected into the ventral tegmental area induces penile erection and increases extracellular dopamine in the nucleus accumbens and paraventricular nucleus of the hypothalamus of male rats: ventral tegmental area, oxytocin and penile erection,” European Journal of Neuroscience, vol. 26, no. 4, pp. 1026– 1035, 2007.eng
dcterms.referencesJ. M. Cantor, Y. M. Binik, and J. G. Pfaus, “Chronic fluoxetine inhibits sexual behavior in the male rat: reversal with oxytocin,” Psychopharmacology, vol. 144, no. 4, pp. 355–362, 1999.eng
dcterms.referencesM. Lancel, S. Krömer, and I. D. Neumann, “Intracerebral oxytocin modulates sleep-wake behaviour in male rats,” Regulatory Peptides, vol. 114, no. 2–3, pp. 145–152, 2003.eng
dcterms.referencesP. Mak, C. Broussard, K. Vacy, and J. H. Broadbear, “Modulation of anxiety behavior in the elevated plus maze using peptidic oxytocin and vasopressin receptor ligands in the rat,” Journal of Psychopharmacology, vol. 26, no. 4, pp. 532–542, 2012.eng
dcterms.referencesM. Birnbaumer, “Vasopressin receptors,” Trends in Endocrinology & Metabolism, vol. 11, no. 10, pp. 406–410, 2000.eng
dcterms.referencesJ. Roper, A.-M. O’Carroll, W. Young, and S. Lolait, “2e vasopressin Avpr1b receptor: molecular and pharmacological studies,” Stress, vol. 14, no. 1, pp. 98–115, 2011.eng
dcterms.referencesS. Jard, C. Barberis, S. Audigier, and E. Tribollet, “Neurohypophyseal hormone receptor systems in brain and periphery,” Progress in Brain Research, vol. 72, pp. 173–187, 1987.eng
dcterms.referencesM. 2ibonnier, P. Coles, A. 2ibonnier, and M. Shoham, “2e basic and clinical pharmacology of nonpeptide vasopressin receptor antagonists,” Annual Review of Pharmacology and Toxicology, vol. 41, no. 1, pp. 175–202, 2001.eng
dcterms.referencesN. G. Simon, C. Guillon, K. Fabio et al., “Vasopressin antagonists as anxiolytics and antidepressants: recent developments,” Recent Patents on CNS Drug Discovery, vol. 3, no. 2, pp. 77–93, 2008.eng
dcterms.referencesG. Griebel and F. Holsboer, “Neuropeptide receptor ligands as drugs for psychiatric diseases: the end of the beginning?,” Nature Reviews Drug Discovery, vol. 11, no. 6, pp. 462–478, 2012.eng
dcterms.referencesR. Landgraf, M. S. Keßler, M. Bunck et al., “Candidate genes of anxiety-related behavior in HAB/LAB rats and mice: focus on vasopressin and glyoxalase-I,” Neuroscience & Biobehavioral Reviews, vol. 31, no. 1, pp. 89–102, 2007.eng
dcterms.referencesD. Katz, C. Locke, N. Greco, W. Liu, and K. Tracy, “Hypothalamic- pituitary- adrenal axis and depression symptom effects on an arginine vasopressin type 1B receptor antagonist in a one-week randomized Phase 1b trial,” Brain and Behavior, vol. 7, no. 3, article e00628, 2017.eng
dcterms.referencesM. S. Kramer, N. Cutler, J. Feighner et al., “Distinct mechanism for antidepressant activity by blockade of central substance P receptors,” Science, vol. 281, no. 5383, pp. 1640–1645, 1998.eng
dcterms.referencesM. Keller, S. Montgomery, W. Ball et al., “Lack of efficacy of the substance p (neurokinin1 receptor) antagonist aprepitant in the treatment of major depressive disorder,” Biological Psychiatry, vol. 59, no. 3, pp. 216–223, 2006.eng
dcterms.referencesE. Ratti, P. Bettica, R. Alexander et al., “Full central neurokinin-1 receptor blockade is required for efficacy in depression: evidence from orvepitant clinical studies,” Journal of Psychopharmacology, vol. 27, no. 5, pp. 424–434, 2013.eng
dcterms.referencesD. F. Ionescu and G. I. Papakostas, “Experimental medication treatment approaches for depression,” Translational Psychiatry, vol. 7, no. 3, p. e1068, 2017.eng
dcterms.referencesE. Ratti, K. Bellew, P. Bettica et al., “Results from 2 randomized, double-blind, placebo-controlled studies of the novel NK1 receptor antagonist casopitant in patients with major depressive disorder,” Journal of Clinical Psychopharmacology, vol. 31, no. 6, pp. 727–733, 2011.eng
dcterms.referencesF. Reichmann and P. Holzer, “Neuropeptide Y: a stressful review,” Neuropeptides, vol. 55, pp. 99–109, 2016.eng
dcterms.referencesN. M. Enman, E. L. Sabban, P. McGonigle, and E. J. Van Bockstaele, “Targeting the neuropeptide Y system in stress-related psychiatric disorders,” Neurobiology of Stress, vol. 1, pp. 33–43, 2015.eng
dcterms.referencesJ. P. Redrobe, Y. Dumont, and R. Quirion, “Neuropeptide Y (NPY) and depression: from animal studies to the human condition,” Life Sciences, vol. 71, no. 25, pp. 2921–2937, 2002.eng
dcterms.referencesH. Hashimoto, “Plasma neuropeptide Y in patients with major depressive disorder,” Neuroscience Letters, vol. 216, no. 1, pp. 57–60, 1996.eng
dcterms.referencesM. Heilig, “Decreased cerebrospinal fluid neuropeptide Y (NPY) in patients with treatment refractory unipolar major depression: preliminary evidence for association with preproNPY gene polymorphism,” J. Psychiatr. Res.vol. 38, no. 2, pp. 113–121, 2004.eng
dcterms.referencesS. Ozsoy, O. Olguner Eker, and U. Abdulrezzak, “2e effects of antidepressants on neuropeptide Y in patients with depression and anxiety,” Pharmacopsychiatry, vol. 49, no. 1, pp. 26–31, 2016.eng
dcterms.referencesJ. Redrobe, “2e neuropeptide Y (NPY) Y1 receptor subtype mediates NPY- induced antidepressant-like activity in the mouse forced swimming test,” Neuropsychopharmacology, vol. 26, no. 5, pp. 615–624, 2002.eng
dcterms.referencesJ. P. Redrobe, “Role of serotonin (5-HT) in the antidepressant-like properties of neuropeptide Y (NPY) in the mouse forced swim test,” Peptides, vol. 26, no. 8, pp. 1394–1400, 2005.eng
dcterms.referencesK. A. Stogner and P. V. Holmes, “Neuropeptide-Y exerts antidepressant-like effects in the forced swim test in rats,” European Journal of Pharmacology, vol. 387, no. 2, pp. R9– R10, 2000.eng
dcterms.referencesH. Ishida, “Infusion of neuropeptide Y into CA3 region of hippocampus produces antidepressant-like effect via Y1 receptor,” Hippocampus, vol. 17, no. 4, pp. 271–280, 2007.eng
dcterms.referencesE. Painsipp, H. Herzog, and P. Holzer, “Implication of neuropeptide-Y Y2 receptors in the effects of immune stress on emotional, locomotor and social behavior of mice,” Neuropharmacology, vol. 55, no. 1, pp. 117–126, 2008.eng
dcterms.referencesR. O. Tasan, “Increased novelty-induced motor activity and reduced depression-like behavior in neuropeptide Y (NPY)- Y4 receptor knockout mice,” Neuroscience, vol. 158, no. 4, pp. 1717–1730, 2009.eng
dcterms.referencesX. Zhao, R. R. Seese, K. Yun, T. Peng, and Z. Wang, “2e role of galanin system in modulating depression, anxiety, and addiction-like behaviors after chronic restraint stress,” Neuroscience, vol. 246, pp. 82–93, 2013.eng
dcterms.referencesE. Kuteeva, T. H¨okfelt, T. Wardi, and S. O. Ogren, “Galanin, Galanin Receptor Subtypes and Depression-Like Behaviour,” in Experientia Supplementum, vol. 102, pp. 163–181, 2010.eng
dcterms.referencesC. Millón, A. Flores-Burgess, M. Narváez et al., “2e neuropeptides Galanin and Galanin(1–15) in depression-like behaviours,” Neuropeptides, vol. 64, pp. 39–45, 2017.eng
dcterms.referencesG. Juhasz, G. Hullam, N. Eszlari et al., “Brain galanin system genes interact with life stresses in depression-related phenotypes,” Proceedings of the National Academy of Sciences, vol. 111, no. 16, pp. E1666–E1673, 2014.eng
dcterms.referencesY.-J. Wang, Y.-T. Yang, H. Li, P.-Z. Liu, C.-Y. Wang, and Z.-Q. D. Xu, “Plasma galanin is a biomarker for severity of major depressive disorder,” Ae International Journal of Psychiatry in Medicine, vol. 48, no. 2, pp. 109–119, 2014.eng
dcterms.referencesA. Flores-Burgess, C. Mill´on, B. Gago et al., “Galanin (1-15) enhancement of the behavioral effects of Fluoxetine in the forced swimming test gives a new therapeutic strategy against depression,” Neuropharmacology, vol. 118, pp. 233– 241, 2017.eng
dcterms.referencesI. Saar, J. Lahe, K. Langel et al., “Novel systemically active galanin receptor 2 ligands in depression-like behavior,” Journal of Neurochemistry, vol. 127, no. 1, pp. 114–123, 2013.eng
dcterms.referencesI. Saar, J. Runesson, J. J¨arv, K. Kurrikoff, and ¨U Langel, “Novel galanin receptor subtype specific ligand in depression like behavior,” Neurochemical Research, vol. 38, no. 2, pp. 398–404, 2013.eng
dcterms.referencesA. M. Barr, J. W. Kinney, M. N. Hill et al., “A novel, systemically active, selective galanin receptor type-3 ligand exhibits antidepressant-like activity in preclinical tests,” Neuroscience Letters, vol. 405, no. 1-2, pp. 111–115, 2006.eng
dcterms.referencesC. J. Swanson, T. P. Blackburn, X. Zhang et al., “From the Cover: anxiolytic- and antidepressant-like profiles of the galanin-3 receptor (Gal3) antagonists SNAP 37889 and SNAP 398299,” Proceedings of the National Academy of Sciences, vol. 102, no. 48, pp. 17489–17494, 2005.eng
dcterms.referencesS. N. Haber and B. Knutson, “2e reward circuit: linking primate anatomy and human imaging,” Neuropsychopharmacology, vol. 35, no. 1, pp. 4–26, 2010.eng
dcterms.referencesA. Alcaro, R. Huber, and J. Panksepp, “Behavioral functions of the mesolimbic dopaminergic system: an affective neuroethological perspective,” Brain Research Reviews, vol. 56, no. 2, pp. 283–321, 2007.eng
dcterms.referencesS. J. Russo and E. J. Nestler, “2e brain reward circuitry in mood disorders,” Nature Reviews Neuroscience, vol. 14, no. 9, pp. 609–625, 2013.eng
dcterms.referencesM. Heshmati and S. J. Russo, “Anhedonia and the brain reward circuitry in depression,” Current Behavioral Neuroscience Reports, vol. 2, no. 3, pp. 146–153, 2015.eng
dcterms.referencesE. J. Nestler, “Role of the brain’s reward circuitry in depression: transcriptional mechanisms,” International Review of Neurobiology, vol. 124, pp. 151–170, 2015.eng
dcterms.referencesB. W. Dunlop and C. B. Nemeroff, “2e role of dopamine in the pathophysiology of depression,” Archives of General Psychiatry, vol. 64, no. 3, p. 327, 2007.eng
dcterms.referencesK. C. Berridge, C.-Y. Ho, J. M. Richard, and A. G. DiFeliceantonio, “2e tempted brain eats: pleasure and desire circuits in obesity and eating disorders,” Brain Research, vol. 1350, pp. 43–64, 2010.eng
dcterms.referencesL. Perogamvros and S. Schwartz, “2e roles of the reward system in sleep and dreaming,” Neuroscience & Biobehavioral Reviews, vol. 36, no. 8, pp. 1934–1951, 2012.eng
dcterms.referencesP. Robledo, F. Berrendero, A. Ozaita, and R. Maldonado, “Advances in the field of cannabinoid-opioid cross-talk: advances in cannabinoid-opioid cross-talk,” Addiction Biology, vol. 13, no. 2, pp. 213–224, 2008.eng
dcterms.referencesA. Perchuk, S. M. Bierbower, A. Canseco-Alba et al., “Developmental and behavioral effects in neonatal and adult mice following prenatal activation of endocannabinoid receptors by capsaicin,” Acta Pharmacologica Sinica, 2018.eng
dcterms.referencesA. T. Knoll and W. A. Carlezon, “Dynorphin, stress, and depression,” Brain Research, vol. 1314, pp. 56–73, 2010.eng
dcterms.referencesP.-E. Lutz and B. L. Kieffer, “Opioid receptors: distinct roles in mood disorders,” Trends in Neurosciences, vol. 36, no. 3, pp. 195–206, 2013.eng
dcterms.referencesP. L. Tenore, “Psychotherapeutic benefits of opioid agonist therapy,” Journal of Addictive Diseases, vol. 27, no. 3, pp. 49–65, 2008.eng
dcterms.referencesJ. Le Merrer, J. A. J. Becker, K. Befort, and B. L. Kieffer, “Reward processing by the opioid system in the brain,” Physiological Reviews, vol. 89, no. 4, pp. 1379–1412, 2009.eng
dcterms.referencesE. Berrocoso, P. Sánchez-Blázquez, J. Garzón, and J. A. Mico, “Opiates as antidepressants,” Current Pharmaceutical Design, vol. 15, no. 14, pp. 1612–1622, 2009.eng
dcterms.referencesS. Scarone, O. Gambini, G. Calabrese et al., “Asymmetrical distribution of beta-endorphin in cerebral hemispheres of suicides: preliminary data,” Psychiatry Research, vol. 32, no. 2, pp. 159–166, 1990.eng
dcterms.referencesS. E. Kennedy, R. A. Koeppe, E. A. Young, and J.-K. Zubieta, “Dysregulation of endogenous opioid emotion regulation circuitry in major depression in women,” Archives of General Psychiatry, vol. 63, no. 11, p. 1199, 2006.eng
dcterms.referencesJ.-K. Zubieta, T. A. Ketter, J. A. Bueller et al., “Regulation of human affective responses by anterior cingulate and limbic μ-opioid neurotransmission,” Archives of General Psychiatry, vol. 60, no. 11, p. 1145, 2003.eng
dcterms.referencesG. Zalsman, A. Molcho, Y. Huang, A. Dwork, S. Li, and J. J. Mann, “Postmortem mu-opioid receptor binding in suicide victims and controls,” Journal of Neural Transmission, vol. 112, no. 7, pp. 949–954, 2005.eng
dcterms.referencesS. C. Ribeiro, S. E. Kennedy, Y. R. Smith, C. S. Stohler, and J.-K. Zubieta, “Interface of physical and emotional stress regulation through the endogenous opioid system and μ-opioid receptors,” Progress in Neuro-Psychopharmacology and Biological Psychiatry, vol. 29, no. 8, pp. 1264–1280, 2005.eng
dcterms.referencesJ. F. Scherrer, J. Salas, L. A. Copeland et al., “Increased risk of depression recurrence after initiation of prescription opioids in noncancer pain patients,” Ae Journal of Pain, vol. 17, no. 4, pp. 473–482, 2016.eng
dcterms.referencesA. Grattan, M. D. Sullivan, K. W. Saunders, C. I. Campbell, and M. R. Von Korff, “Depression and prescription opioid misuse among chronic opioid therapy recipients with no history of substance abuse,” Ae Annals of Family Medicine, vol. 10, no. 4, pp. 304–311, 2012.eng
dcterms.referencesJ. O. Merrill, M. Von Korff, C. J. Banta-Green et al., “Prescribed opioid difficulties, depression and opioid dose among chronic opioid therapy patients,” General Hospital Psychiatry, vol. 34, no. 6, pp. 581–587, 2012.eng
dcterms.referencesJ. F. Scherrer, D. M. Svrakic, K. E. Freedland et al., “Prescription opioid analgesics increase the risk of depression,” Journal of General Internal Medicine, vol. 29, no. 3, pp. 491–499, 2014.eng
dcterms.referencesE. Berrocoso, K. Ikeda, I. Sora, G. R. Uhl, P. Sánchez- Blázquez, and J. A. Mico, “Active behaviours produced by antidepressants and opioids in the mouse tail suspension test,” Ae International Journal of Neuropsychopharmacology, vol. 16, no. 1, pp. 151–162, 2013.eng
dcterms.referencesR. Vergura, G. Balboni, B. Spagnolo et al., “Anxiolytic- and antidepressant-like activities of H-Dmt-Tic-NH-CH(CH2- COOH)- Bid (UFP-512), a novel selective delta opioid receptor agonist,” Peptides, vol. 29, no. 1, pp. 93–103, 2008.eng
dcterms.referencesC. Contet, B. L. Kieffer, and K. Befort, “Mu opioid receptor: a gateway to drug addiction,” Current Opinion in Neurobiology, vol. 14, no. 3, pp. 370–378, 2004.eng
dcterms.referencesM. Fava, A. Memisoglu, M. E. 2ase et al., “Opioid modulation with buprenorphine/samidorphan as adjunctive treatment for inadequate response to antidepressants: a randomized double-blind placebo-controlled trial,” American Journal of Psychiatry, vol. 173, no. 5, pp. 499–508, 2016.eng
dcterms.referencesZ. Benyhe, G. Toth, M. Wollemann et al., “Effects of synthetic analogues of human opiorphin on rat brain opioid receptors,” Journal of Physiology and Pharmacology, vol. 65, no. 4, pp. 525–530, 2014.eng
dcterms.referencesH. Javelot, M. Messaoudi, S. Garnier, and C. Rougeot, “Human opiorphin is a naturally occurring antidepressant acting selectively on enkephalin-dependent delta-opioid pathways,” Journal of Physiology and Pharmacology, vol. 61, no. 3, pp. 355–362, 2010.eng
dcterms.referencesQ.-Z. Yang, S.-S. Lu, X.-Z. Tian, A.-M. Yang, W.-W. Ge, and Q. Chen, “The antidepressant- like effect of human opiorphin via opioid-dependent pathways in mice,” Neuroscience Letters, vol. 489, no. 2, pp. 131–135, 2011.eng
dcterms.referencesV. Di Marzo, A. Fontana, H. Cadas et al., “Formation and inactivation of endogenous cannabinoid anandamide in central neurons,” Nature, vol. 372, no. 6507, pp. 686–691, 1994.eng
dcterms.referencesT. Sugiura, S. Kondo, A. Sukagawa et al., “Enzymatic synthesis of anandamide, an endogenous cannabinoid receptor ligand, through N-acylphosphatidylethanolamine pathway in testis: involvement of Ca2+-dependent transacylase and phosphodiesterase activities,” Biochemical and Biophysical Research Communications, vol. 218, no. 1, pp. 113–117, 1996.eng
dcterms.referencesZ. E. Zajkowska, A. Englund, and P. A. Zunszain, “Towards a personalized treatment in depression: endocannabinoids, inflammation and stress response,” Pharmacogenomics, vol. 15, no. 5, pp. 687–698, 2014.eng
dcterms.referencesA. Agrawal, E. C. Nelson, A. K. Littlefield et al., “Cannabinoid receptor genotype moderation of the effects of childhood physical abuse on anhedonia and depression,” Archives of General Psychiatry, vol. 69, no. 7, pp. 732–740, 2012.eng
dcterms.referencesM. Mitjans, C. Gastó, R. Catalán, L. Fañanás, and B. Arias, “Genetic variability in the endocannabinoid system and 12- week clinical response to citalopram treatment: the role of the CNR1, CNR2 and FAAH genes,” Journal of Psychopharmacology, vol. 26, no. 10, pp. 1391–1398, 2012.eng
dcterms.referencesL. Colino, J. Herranz-Herrer, E. Gil-Benito et al., “Cannabinoid receptors, mental pain and suicidal behavior: a systematic review,” Current Psychiatry Reports, vol. 20, no. 3, p. 19, 2018.eng
dcterms.referencesL. Kranaster, C. Hoyer, S. S. Aksay et al., “Electroconvulsive therapy enhances endocannabinoids in the cerebrospinal fluid of patients with major depression: a preliminary prospective study,” European Archives of Psychiatry and Clinical Neuroscience, vol. 267, no. 8, pp. 781–786, 2017.eng
dcterms.referencesS. Jeon and Y.-K. Kim, “Molecular neurobiology and promising new treatment in depression,” International Journal of Molecular Sciences, vol. 17, no. 3, p. 381, 2016.eng
dcterms.referencesK. Starowicz, L. Cristino, and V. Di Marzo, “TRPV1 receptors in the central nervous system: potential for previously unforeseen therapeutic applications,” Current Pharmaceutical Design, vol. 14, no. 1, pp. 42–54, 2008.eng
dcterms.referencesN. Khairatkar-Joshi and A. Szallasi, “TRPV1 antagonists: the challenges for therapeutic targeting,” Trends in Molecular Medicine, vol. 15, no. 1, pp. 14–22, 2009.eng
dcterms.referencesE. E. Benarroch, “2e locus ceruleus norepinephrine system: functional organization and potential clinical significance,” Neurology, vol. 73, no. 20, pp. 1699–1704, 2009.eng
dcterms.referencesI. J. You, Y. H. Jung, M. J. Kim et al., “Alterations in the emotional and memory behavioral phenotypes of transient receptor potential vanilloid type 1-deficient mice are mediated by changes in expression of 5-HT1 A, GABA(A), and NMDA receptors,” Neuropharmacology, vol. 62, no. 2, pp. 1034–1043, 2012.eng
dcterms.referencesS. S. Manna and S. N. Umathe, “A possible participation of transient receptor potential vanilloid type 1 channels in the antidepressant effect of fluoxetine,” European Journal of Pharmacology, vol. 685, no. 1–3, pp. 81–90, 2012.eng
dcterms.referencesT. Hayase, “Differential effects of TRPV1 receptor ligands against nicotine-induced depression-like behaviors,” BMC Pharmacology, vol. 11, no. 1, p. 6, 2011.eng
dcterms.referencesNational Library of Medicine, Low Dose Intravenous Ketamine in Treatment Resistant Depression Patients (Ketamine), ClinicalTrials.gov. NCT02935595, http:// clinicaltrials.gov/show/NCT02935595, National Library of Medicine, Bethesda, MD, USA, 2018.eng
dcterms.referencesNational Library of Medicine, Study of Oral Ketamine Versus Placebo for Treating Depression in Patients Undergoing Treatment for Cancer, ClinicalTrials.gov. NCT02836288, http://clinicaltrials.gov/show/NCT02836288, National Library of Medicine, Bethesda, MD, USA, 2018.eng

Archivos

Bloque original
Mostrando 1 - 1 de 1
Cargando...
Miniatura
Nombre:
Depression as a Neuroendocrine Disorder_Emerging.pdf
Tamaño:
4.01 MB
Formato:
Adobe Portable Document Format
Descripción:
PDF
Bloque de licencias
Mostrando 1 - 1 de 1
No hay miniatura disponible
Nombre:
license.txt
Tamaño:
368 B
Formato:
Item-specific license agreed upon to submission
Descripción:

Colecciones