Abstract
There is accumulating evidence that the nucleus accumbens (NAc) plays an important role in the pathophysiology of depression. Given that clinical depression is marked by anhedonia (diminished interest or pleasure), dysfunction of the brain reward pathway has been suggested as contributing to the pathophysiology of depression. Since the NAc is the center of reward and learning, it is hypothesized that anhedonia might be produced by hampering the function of the NAc. Indeed, it has been reported that stress, drug exposure and drug withdrawal, all of which produce a depressive-phenotype, alter various functions within the NAc, leading to inhibited dopaminergic activity in the NAc. In this review, we describe various factors as possible candidates within the NAc for the initiation of depressive symptoms. First, we discuss the roles of several neurotransmitters and neuropeptides in the functioning of the NAc, including dopamine, glutamate, γ-aminobutyric acid (GABA), acetylcholine, serotonin, dynorphin, enkephaline, brain-derived neurotrophic factor (BDNF), cAMP response element-binding protein (CREB), melanin-concentrating hormone (MCH) and cocaine- and amphetamine-regulated transcript (CART). Second, based on previous studies, we propose hypothetical relationships among these substances and the shell and core subregions of the NAc.
Keywords: Depression, nucleus accumbens, glutamate, dopamine, γ-aminobutyric acid (GABA), acetylcholine, dynorphin, cAMP response element-binding protein (CREB)
Current Neuropharmacology
Title: Neurochemistry of the Nucleus Accumbens and its Relevance to Depression and Antidepressant Action in Rodents
Volume: 4 Issue: 4
Author(s): Yukihiko Shirayama and Shigeyuki Chaki
Affiliation:
Keywords: Depression, nucleus accumbens, glutamate, dopamine, γ-aminobutyric acid (GABA), acetylcholine, dynorphin, cAMP response element-binding protein (CREB)
Abstract: There is accumulating evidence that the nucleus accumbens (NAc) plays an important role in the pathophysiology of depression. Given that clinical depression is marked by anhedonia (diminished interest or pleasure), dysfunction of the brain reward pathway has been suggested as contributing to the pathophysiology of depression. Since the NAc is the center of reward and learning, it is hypothesized that anhedonia might be produced by hampering the function of the NAc. Indeed, it has been reported that stress, drug exposure and drug withdrawal, all of which produce a depressive-phenotype, alter various functions within the NAc, leading to inhibited dopaminergic activity in the NAc. In this review, we describe various factors as possible candidates within the NAc for the initiation of depressive symptoms. First, we discuss the roles of several neurotransmitters and neuropeptides in the functioning of the NAc, including dopamine, glutamate, γ-aminobutyric acid (GABA), acetylcholine, serotonin, dynorphin, enkephaline, brain-derived neurotrophic factor (BDNF), cAMP response element-binding protein (CREB), melanin-concentrating hormone (MCH) and cocaine- and amphetamine-regulated transcript (CART). Second, based on previous studies, we propose hypothetical relationships among these substances and the shell and core subregions of the NAc.
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Cite this article as:
Shirayama Yukihiko and Chaki Shigeyuki, Neurochemistry of the Nucleus Accumbens and its Relevance to Depression and Antidepressant Action in Rodents, Current Neuropharmacology 2006; 4 (4) . https://dx.doi.org/10.2174/157015906778520773
DOI https://dx.doi.org/10.2174/157015906778520773 |
Print ISSN 1570-159X |
Publisher Name Bentham Science Publisher |
Online ISSN 1875-6190 |
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