Antidepressants and neuroplasticity

D’Sa, Carrol; Duman, Ronald S.

doi:10.1034/j.1399-5618.2002.01203.x

Cited by 460 publications

(283 citation statements)

References 92 publications

(161 reference statements)

Supporting

Mentioning

272

Contrasting

Unclassified

Order By: Relevance

“…Recent studies demonstrate that chronic stress alters dendritic morphology not only in the hippocampus, but also in the medial PFC (Cook and Wellman, 2004;. Parallel to these findings, a growing number of studies demonstrate that many of these stress-induced cellular changes can be reversed by antidepressant treatment (D'Sa and Duman, 2002;Dranovsky and Hen, 2006). It has been argued that these observations are likely to have human relevance as stressful life events are among the most potent factors known to trigger or induce major depressive episodes (Kendler et al, 1999).…”

Section: Introductionmentioning

confidence: 94%

Chronic Social Stress Inhibits Cell Proliferation in the Adult Medial Prefrontal Cortex: Hemispheric Asymmetry and Reversal by Fluoxetine Treatment

Czéh

Müller-Keuker

Ryguła

et al. 2006

Neuropsychopharmacol

316

221

View full text Add to dashboard Cite

Profound neuroplastic changes have been demonstrated in various limbic structures after chronic stress exposure and antidepressant treatment in animal models of mood disorders. Here, we examined in rats the effect of chronic social stress and concomitant antidepressant treatment on cell proliferation in the medial prefrontal cortex (mPFC). We also examined possible hemispheric differences. Animals were subjected to 5 weeks of daily social defeat by an aggressive conspecific and received concomitant, daily, oral fluoxetine (10 mg/kg) during the last 4 weeks. Bromodeoxyuridine (BrdU) labeling and quantitative stereological techniques were used to evaluate the treatment effects on proliferation and survival of newborn cells in limbic structures such as the mPFC and the hippocampal dentate gyrus, in comparison with nonlimbic structures such as the primary motor cortex and the subventricular zone. Phenotypic analysis showed that neurogenesis dominated the dentate gyrus, whereas in the mPFC most newborn cells were glia, with smaller numbers of endothelial cells. Chronic stress significantly suppressed cytogenesis in the mPFC and neurogenesis in the dentate gyrus, but had minor effect in nonlimbic structures. Fluoxetine treatment counteracted the inhibitory effect of stress. Hemispheric comparison revealed that the rate of cytogenesis was significantly higher in the left mPFC of control animals, whereas stress inverted this asymmetry, yielding a significantly higher incidence of newborn cells in the right mPFC. Fluoxetine treatment abolished hemispheric asymmetry in both control and stressed animals. These pronounced changes in gliogenesis after chronic stress exposure may relate to the abnormalities of glial cell numbers reported in the frontolimbic areas of depressed patients.

show abstract

Section: Introductionmentioning

confidence: 94%

Chronic Social Stress Inhibits Cell Proliferation in the Adult Medial Prefrontal Cortex: Hemispheric Asymmetry and Reversal by Fluoxetine Treatment

Czéh

Müller-Keuker

Ryguła

et al. 2006

Neuropsychopharmacol

316

221

View full text Add to dashboard Cite

show abstract

“…As noted above, in preliminary experiments, modafinil has been found to activate MAPK in cell culture as well as in vivo in the mouse cerebral cortex and to do so via stimulation of a 1 -receptors. It has also been found that administration of an a 2 -antagonist, yohimbine, which facilitates the release of brain catecholamines, increases the expression of nerve growth factor mRNA in the rat cortex (Stone et al, 1994), while catecholamines and/or indoleamines in cell culture (Ohta et al, 2002) as well as electroconvulsive shock and antidepressant drugs in vivo can induce the expression of BDNF, GDNF, and/or NT3 as well as elicit functional and neuroanatomical signs of neural plasticity (D'Sa and Duman, 2002).…”

Section: Trophic Actions Of a 1 -Receptorsmentioning

confidence: 99%

Emerging Evidence for a Central Epinephrine-Innervated α1-Adrenergic System that Regulates Behavioral Activation and is Impaired in Depression

Stone

Yang

Rosengarten

et al. 2003

Neuropsychopharmacol

View full text Add to dashboard Cite

Currently, most basic and clinical research on depression is focused on either central serotonergic, noradrenergic, or dopaminergic neurotransmission as affected by various etiological and predisposing factors. Recent evidence suggests that there is another system that consists of a subset of brain a 1B -adrenoceptors innervated primarily by brain epinephrine (EPI) that potentially modulates the above three monoamine systems in parallel and plays a critical role in depression. The present review covers the evidence for this system and includes findings that brain a 1 -adrenoceptors are instrumental in behavioral activation, are located near the major monoamine cell groups or target areas, receive EPI as their neurotransmitter, are impaired or inhibited in depressed patients or after stress in animal models, and are restored by a number of antidepressants. This 'EPI-a 1 system' may therefore represent a new target system for this disorder.

show abstract

“…Recent data suggest that antidepressants facilitate activity-dependent selection of functional synaptic connections in brain and, through their neurotrophic effects, improve information processing within neuronal networks compromised in mood disorders. 58 In fact, an increasing number of studies suggest that it is the ability to modify synaptic plasticity that is the crucial feature of clinically effective antidepressants, rather than the enhancement of neuronal survival alone. The emerging pharmacological profile of tianeptine suggests that this antidepressant may serve to organize synaptic function, thereby allowing the chemical signal to reinstate the optimal functioning of critical circuits necessary for normal affective functioning.…”

Section: Neurobiological Properties Of Tianeptinementioning

confidence: 99%

“…22 Several other studies have shown protective effects of antidepressants in different models, and mostly in the hippocampus. 58,86 In a maternal deprivation and a prenatal restraint stress model, alterations in granule cell number and neurogenesis as well as apoptosis occur 87,88 and these changes could be normalized by fluoxetine treatment.…”

Section: Cytoprotective Effectsmentioning

confidence: 99%

Neurobiology of mood, anxiety, and emotions as revealed by studies of a unique antidepressant: tianeptine

McEwen

Olie

2005

Mol Psychiatry

View full text Add to dashboard Cite

Recent studies have provided evidence that structural remodeling of certain brain regions is a feature of depressive illness, and the postulated underlying mechanisms contribute to the idea that there is more to antidepressant actions that can be explained exclusively by a monoaminergic hypothesis. This review summarizes recent neurobiological studies on the antidepressant, tianeptine (S-1574, [3-chloro-6-methyl-5,5-dioxo-6,11-dihydro-(c,f)-dibenzo-(1,2-thiazepine)-11-yl) amino]-7 heptanoic acid, sodium salt), a compound with structural similarities to the tricyclic antidepressant agents, the efficacy and good tolerance of which have been clearly established. These studies have revealed that the neurobiological properties of tianeptine involve the dynamic interplay between numerous neurotransmitter systems, as well as a critical role of structural and functional plasticity in the brain regions that permit the full expression of emotional learning. Although the story is far from complete, the schema underlying the effect of tianeptine on central plasticity is the most thoroughly studied of any antidepressants. Effects of tianeptine on neuronal excitability, neuroprotection, anxiety, and memory have also been found. Together with clinical data on the efficacy of tianeptine as an antidepressant, these actions offer insights into how compounds like tianeptine may be useful in the treatment of neurobiological features of depressive disorders. Molecular Psychiatry (2005) 10, 525-537.

show abstract

Antidepressants and neuroplasticity

Cited by 460 publications

References 92 publications

Chronic Social Stress Inhibits Cell Proliferation in the Adult Medial Prefrontal Cortex: Hemispheric Asymmetry and Reversal by Fluoxetine Treatment

Chronic Social Stress Inhibits Cell Proliferation in the Adult Medial Prefrontal Cortex: Hemispheric Asymmetry and Reversal by Fluoxetine Treatment

Emerging Evidence for a Central Epinephrine-Innervated α1-Adrenergic System that Regulates Behavioral Activation and is Impaired in Depression

Neurobiology of mood, anxiety, and emotions as revealed by studies of a unique antidepressant: tianeptine

Contact Info

Product

Resources

About