The neurobiology of depression

Palazidou, Eleni

doi:10.1093/bmb/lds004

Cited by 239 publications

(195 citation statements)

References 56 publications

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“…One of the prevalent hypotheses to explain depression, the monoamine hypothesis of depression, posits that this disorder is caused by a deficiency in monoamines (NA,and DA) in the brain, and that antidepressant drugs restore these molecules to normal levels (Palazidou, 2012). In the present study, we found a significant decrease in NA and 5-HT levels in the hippocampus of UCMS rats.…”

Section: Discussionsupporting

confidence: 58%

“…We did not observe any significant differences in the cortex (data not shown). The prefrontal cortex, the amygdala, and, particularly, the hippocampus are the brain structures that have been studied most widely in relation to depression (Palazidou, 2012). Therefore, we should extend our studies to the investigation of the levels of neurotransmitter and BDNF, 5-HT systemic gene expression in other brain regions, such as the prefrontal cortex and the amygdala.…”

Section: Discussionmentioning

confidence: 98%

“…Recently, several lines of evidence suggest that a deficiency in neurotransmitters in the brain alter BDNF expression, leading to brain diseases, which indicates a complex modulatory relationship between BDNF and the serotonin system (Ivy et al, 2003;Palazidou, 2012;Pezet & Malcangio, 2004). BDNF can augment 5-HT signaling; in turn, 5-TH stimulates BDNF expression (Goggi et al, 2002;Juric et al, 2006;Mamounas et al, 2000;Mattson et al, 2004;Siuciak et al, 1996).…”

Section: Discussionmentioning

confidence: 99%

“…In addition, an increasing number of studies have proven that the expression of the brain-derived nerve factor (BDNF) mRNA, particularly within the hippocampus, is regulated by stress and by therapeutic agents, such as antidepressants (Coppell et al, 2003;Lindvall et al, 1994;Molteni et al, 2006;Nibuya et al, 1995;Smith et al, 1995). Neurotransmitters have been implicated in the regulation of BDNF mRNA expression (Ivy et al, 2003;Juric et al, 2006;Lindholm et al, 1994;Palazidou et al, 2012;Thoenen et al, 1991).…”

Section: Introductionmentioning

confidence: 99%

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Involvement of norepinephrine and serotonin system in antidepressant-like effects of hederagenin in the rat model of unpredictable chronic mild stress-induced depression

Liang

Huang

Wang

et al. 2014

Pharmaceutical Biology

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Objective: This study compared the antidepressant ability of FAE with that of HG in mice and further investigated the antidepressant-like effects and potential mechanisms of HG in rats subjected to unpredictable chronic mild stress (UCMS). Materials and methods: Mice received FAE (50 mg/kg) and HG (20 mg/kg) once a day via intragastric administration (i.g.) for 3 weeks. The anxiolytic and antidepressant activities of FAE and HG were compared using elevated plus maze (EPM) and behavioral despair tests including tail suspension test (TST) and forced swimming test (FST), respectively. Antidepressant effects of HG (5 mg/kg) were assessed using the UCMS depressive rat model. Moreover, the levels of monoamine neurotransmitters and relevant gene expression in UCMS rats' hippocampi were determined through high-performance liquid chromatography with electrochemical detection and real-time polymerase chain reaction techniques. Results: The results of our preliminary screening test suggest that HG at 20 mg/kg, while not FAE at 50 mg/kg, significantly decreased the immobility in both TST and FST compared with the vehicle group when administered chronically; however, there were no significant differences observed between the HG and the FAE group. Chronic administration of HG failed to significantly reverse the altered crossing and rearing behavioral performance, time spent in the open arm and closed entries in the EPM, even if they showed an increased tendency, but HG significantly increased the percent of sucrose preference in the sucrose preference test (SPT) and decreased the immobility time in the FST. HG showed that significant increases of norepinephrine and serotonin levels and exhibited a tendency to increase the expression of 5-hydroxytryptamine (serotonin) 1A receptor mRNA, and to significantly decrease the expression of the mRNA for the serotonin transporter (5-HTT). However, there were no significant differences in the expression of the brain-derived neurotrophic factor. Conclusion: These findings confirm the antidepressant-like effects of HG in a behavioral despair test and UCMS rat model, which may be associated with monoamine neurotransmitters and 5-HTT mRNA expression.

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Section: Discussionsupporting

confidence: 58%

Section: Discussionmentioning

confidence: 98%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

Involvement of norepinephrine and serotonin system in antidepressant-like effects of hederagenin in the rat model of unpredictable chronic mild stress-induced depression

Liang

Huang

Wang

et al. 2014

Pharmaceutical Biology

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“…Najbolje istražen dio mozga povezan s depresijom je hipokampus, ponajviše zbog toga što ima ključnu ulogu u učenju i pamćenju. Dodatno, poremećaji u ovom dijelu mozga mogu biti odgovorni za neprikladne emocionalne reakcije na podražaje iz okoline 7 . Istraživanja pokazuju da promjene u plastičnosti sinapsi, u specifičnim dijelovima središnjeg živčanog sustava, posebno u hipokampusu, mogu biti ključan čimbenik u razvoju depresije 8 .…”

Section: Definicija Klinička Slika I Dijagnozaunclassified

Epigenetics and major depression disorder

2017

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Sažetak. Veliki depresivni poremećaj (MDD, od engl. Major Depressive Disorder) jedan je od najčešćih psihosomatskih poremećaja, sa snažnom tendencijom porasta broja oboljelih. Do 2020. godine mogao bi postati drugi najveći zdravstveni svjetski problem. Uzroci nastanaka bolesti, kao i klinička slika, vrlo su složeni. Ovakva složenost posljedica je aktivnosti velikog broja gena, od kojih svaki "pridonosi" nastanku i izražaju bolesti s relativno malim udjelom. Sve veći broj rezultata mnogih studija upućuje na važnost epigenetičkih mehanizama regulacije aktivnosti gena, kao poveznicu bioloških i drugih čimbenika koji se povezuju s nastankom depresije. Većina istraživanja pokazuje uzročno-posljedičnu vezu između različitih bioloških i psihosocijalnih čimbenika, s jedne strane, te međuovisne promjene obrazaca metilacije/demetilacije molekule DNK i promjene koda histona, s druge strane. Sve je više podataka o značajnoj ulozi različitih nekodirajućih molekula RNK u nastanku depresivnog poremećaja. Konačno, pokazalo se da mnogi antidepresivi djeluju na epigenom. Ovaj učinak otvara potpuno novo poglavlje u razumijevanju patogeneze i epigenetičke podloge liječenja depresivnog poremećaja.Ključne riječi: antidepresivi; epigenetika; stres; veliki depresivni poremećaj Abstract. Major Depressive Disorder (MDD) represents one of the most common psychosomatic disorders with a pronounced increasing incidence. It is expected to become the number two major world health problem by 2020. The causes of MDD as well as its clinical features are very complex. The probable reason for such complexity relates to a large number of genes, being involved in a condition where each gene makes only a minor contribution to the MDD etiology and clinic phenotypes. An increasing number of studies published during last decade have pointed out the importance of epigenetic regulatory mechanisms in affecting gene activity as well as constituting a possible link between biological and other factors related to MDD. Most of the studies have shown causality between different, MDD related biological and psycho-social factors. They have also described mutually controlled processes involved in the regulation of DNA methylation and establishment of histone code. There is a growing body of evidence on the significant role of non-coding RNA molecules in the ethiopathogenesis of MDD. Finally, it was shown that many antidepressive agents exert much influence on the epigenome. Such activity opens a new chapter in understanding the MDD pathogenesis and the basis for epigenome-reshaping related therapy.

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Music therapy for depression

Aalbers

Fusar-Poli

Freeman

et al. 2017

Cochrane Database of Systematic Reviews

406

238

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Findings of the present meta-analysis indicate that music therapy provides short-term beneficial effects for people with depression. Music therapy added to treatment as usual (TAU) seems to improve depressive symptoms compared with TAU alone. Additionally, music therapy plus TAU is not associated with more or fewer adverse events than TAU alone. Music therapy also shows efficacy in decreasing anxiety levels and improving functioning of depressed individuals.Future trials based on adequate design and larger samples of children and adolescents are needed to consolidate our findings. Researchers should consider investigating mechanisms of music therapy for depression. It is important to clearly describe music therapy, TAU, the comparator condition, and the profession of the person who delivers the intervention, for reproducibility and comparison purposes.

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The neurobiology of depression

Cited by 239 publications

References 56 publications

Involvement of norepinephrine and serotonin system in antidepressant-like effects of hederagenin in the rat model of unpredictable chronic mild stress-induced depression

Involvement of norepinephrine and serotonin system in antidepressant-like effects of hederagenin in the rat model of unpredictable chronic mild stress-induced depression

Epigenetics and major depression disorder

Music therapy for depression

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