Neuronal plasticity and survival in mood disorders

Duman, Ronald S.; Malberg, Jessica E.; Nakagawa, Shin; D’Sa, Carrol

doi:10.1016/s0006-3223(00)00935-5

Cited by 583 publications

(398 citation statements)

References 44 publications

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“…There is one report that activation of the cAMP pathway in cultured progenitor cells increases neuronal differentiation (Palmer et al 1997). The potential role of the cAMP-CREB cascade in neurogenesis is of particular interest because of our previous studies demonstrating that antidepressant treatment up-regulates this pathway (Figure 2) (see Duman et al 1997Duman et al , 2000. One piece of evidence of particular interest was discovered when we were studying the influence of antidepressants on CREB phosphorylation.…”

Section: Role Of the Camp-creb Cascade In Adult Neurogenesismentioning

confidence: 99%

“…This has led to the discovery that repeated long-term antidepressant administration up-regulates the cAMP-CREB (cAMP response element binding protein) cascade and expression of brain derived neurotrophic factor (BDNF) in hippocampus ( Figure 2) (Nibuya et al 1995(Nibuya et al , 1996Thome et al 2000). Both CREB and BDNF are known to play a role in synaptic plasticity as well as neuronal survival (see Finkbeiner 2000;Duman et al 2000). Based on these findings, studies were initiated to determine if antidepressants influence neuronal remodeling, particularly neurogenesis.…”

Section: Antidepressant Treatment Increases Adult Neurogenesismentioning

confidence: 99%

“…Antidepressant treatment up-regulates the cAMP cascade at several intracellular sites, including increased coupling of Gs, the stimulatory GTPbinding protein, with adenylyl cyclase, increased levels cAMP-dependent protein kinase (PKA), and increased function and expression of cAMP response element binding protein (CREB) (see Duman et al 2000). CREB can also be regulated by Ca 2ϩ -dependent or microtubule-associated protein (MAP) kinases.…”

Section: Figurementioning

confidence: 99%

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Regulation of Adult Neurogenesis by Antidepressant Treatment

Duman

Nakagawa

Malberg

2001

Neuropsychopharmacology

428

249

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Demonstration of neurogenesis in adult brainOur understanding of how the brain functions and undergoes adaptation and plasticity has changed dramatically over the past several years. A great deal of work has demonstrated that altered levels of neurotransmitters, second messenger pathways, and gene expression profiles underlie cellular and behavioral plasticity. This includes models of learning and memory as well as models of depression, anxiety, and psychosis, and the long-term actions of psychotropic drugs. However, it is now becoming increasing evident that changes in cellular morphology and even more pronounced alterations in brain structure also contribute to neural plasticity or remodeling. At the cellular level these changes can occur in the form of up or down-regulation of synapse formation and spine density or extension and retraction of dendrites. Another very dramatic example is up or down-regulation of neurogenesis in adult brain. Studies in recent years demonstrate that new cell birth occurs in adult brain and that the rate of neurogenesis and the survival of new neurons is regulated by a number of environmental, endocrine, and pharmacological treatments.In this paper we discuss the evidence that structural remodeling may be involved in the pathophysiology and treatment of mood disorders. The potential role of neurogenesis is also discussed as well as the molecular mechanisms which underlie antidepressant regulation of new cell birth and survival. The studies to date suggest an exciting possibility for the role of neurogenesis

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Section: Role Of the Camp-creb Cascade In Adult Neurogenesismentioning

confidence: 99%

Section: Antidepressant Treatment Increases Adult Neurogenesismentioning

confidence: 99%

Section: Figurementioning

confidence: 99%

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Regulation of Adult Neurogenesis by Antidepressant Treatment

Duman

Nakagawa

Malberg

2001

Neuropsychopharmacology

428

249

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“…BDNF is also thought to play a role in the cellular and behavioral responses to stress (Duman et al , 2000. Exposure to physical stress, such as immobilization, downregulates BDNF expression in the hippocampus (Smith et al 1995, Vaidya et al 1997 (Duman et al , 2000.…”

Section: This Study Examined the Effects Of Footshock Stress And Reexmentioning

confidence: 99%

“…Thus, through a variety of mechanisms in different brain regions, BDNF has been implicated in emergent phenomena such as learning and memory (Patterson et al 1996;Mu et al 1999) and even contributes to the modulation of overt behaviors such as aggression (Lyons et al 1999). The ability of BDNF to influence these processes is related, in part, to the activity dependent regulation of BDNF expression in adult brain (Lewin and Barde 1996).BDNF is also thought to play a role in the cellular and behavioral responses to stress (Duman et al , 2000. Exposure to physical stress, such as immobilization, downregulates BDNF expression in the hippocampus (Smith et al 1995, Vaidya et al 1997 (Duman et al , 2000.…”

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confidence: 99%

Downregulation of BDNF mRNA in the Hippocampal Dentate Gyrus after Re-exposure to Cues Previously Associated with Footshock,

Rasmusson

Shi

Duman

2002

Neuropsychopharmacology

235

109

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This study examined the effects of footshock stress and reexposure to cues previously associated with footshock on expression of brain-derived neurotrophic factor (BDNF) mRNA in the hippocampus of male rats. Exposure to twenty 0.5-s 0.4-mA footshocks co-terminating withBrain-derived neurotrophic factor (BDNF) is a member of the neurotrophin family of growth factors, which also includes nerve growth factor and neurotrophins 3 and 4. BDNF as well as these other neurotrophins, plays an important role in neuronal growth and differentiation during development, and also contributes to the survival, function, and plasticity of neurons in the adult brain (Lewin and Barde 1996). Thus, through a variety of mechanisms in different brain regions, BDNF has been implicated in emergent phenomena such as learning and memory (Patterson et al. 1996;Mu et al. 1999) and even contributes to the modulation of overt behaviors such as aggression (Lyons et al. 1999). The ability of BDNF to influence these processes is related, in part, to the activity dependent regulation of BDNF expression in adult brain (Lewin and Barde 1996).BDNF is also thought to play a role in the cellular and behavioral responses to stress (Duman et al. , 2000. Exposure to physical stress, such as immobilization, downregulates BDNF expression in the hippocampus (Smith et al. 1995, Vaidya et al. 1997 (Duman et al. , 2000. Moreover, downregulation of BDNF could contribute to the hippocampal pathology observed in psychiatric disorders such as post-traumatic stress disorder (PTSD) and depression (Bremner et al. 2000;Mervaala et al. 2000;Vakili et al. 2000). This possibility is supported by the observation that these disorders are sensitive to stressful experiences (Breslau et al. 1995;Kendler et al. 2000). Based on these observations and findings, we became interested in determining whether psychological stress has a measurable impact on hippocampal BDNF expression similar to the effects of physical stressors that have been reported.We therefore tested the effects of psychological stress produced by exposures to cues previously paired with footshock on BDNF mRNA levels in the dentate gyrus of the hippocampus. We hypothesized that re-exposure to cues associated with footshock stress, as well as footshock itself, would decrease BDNF mRNA in the dentate gyrus. The results demonstrate that this type of psychological stress produces a heightened sensitivity to previously neutral cues that results in downregulation of BDNF, and suggest that psychological stress, such as that experienced in association with PTSD and depression, as well as other disorders, could result in decreased neurotrophic support of the hippocampus. MATERIAL AND METHODS AnimalsAdult male Sprague-Dawley rats were kept in a 12:12 h light-dark cycle (lights on at 7:00 A . M .) for 7-10 days before each experiment. The animals were housed two or three per cage and fed ad libitum. Experiments were conducted between 9:00 A . M . and 6:00 P . M . To control for possible effects of diurnal variation on hippoca...

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