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The Neuroscientist The Neuroscientist http://nro.sagepub.com/ Review : Stress, Antidepressant Treatments, and Neurotrophic Factors: Molecular and Cellular Mechanisms Ronald S. Duman, Vidita A. Vaidya, Masashi Nibuya, Shigeru Morinobu and Laura Rydelek Fitzgerald Neuroscientist 1995 1: 351 DOI: 10.1177/107385849500100607 The online version of this article can be found at: http://nro.sagepub.com/content/1/6/351 Published by: http://www.sagepublications.com Additional services and information for The Neuroscientist can be found at: Email Alerts: http://nro.sagepub.com/cgi/alerts Subscriptions: http://nro.sagepub.com/subscriptions Reprints: http://www.sagepub.com/journalsReprints.nav Permissions: http://www.sagepub.com/journalsPermissions.nav Citations: http://nro.sagepub.com/content/1/6/351.refs.html >> Version of Record - Nov 1, 1995 What is This? Downloaded from nro.sagepub.com at HOMI BHABHA CENT SCI EDUC on January 31, 2013 Stress, Antidepressant Treatments, and Neurotrophic Factors: Molecular and Cellular Mechanisms RONALD S. DUMAN, VIDITA A. VAIDYA, MASASHI NIBUYA, SHIGERU MORINOBU, and LAURA RYDELEK FITZGERALD Laboratory of Molecular Psychiatry Departments of Psychiatry and Pharmacology Yale University School of Medicine Connecticut Mental Health Center New Haven, Connecticut Repeated stress or an excess of glucocorticoids can exacerbate neuronal damage in response to insults and, in severe cases, can lead to neuronal atrophy and death. These effects are thought to be related to the actions of stress and glucocorticoids on glutamate function, neuronal metabolism, and the generation of cytotoxic free radicals. Recent studies demonstrate that the regulation of neurotrophic factors may contribute to the actions of stress on neuronal function. Acute or chronic stress decreases the expression of brain derived neurotrophic factor, the most abundant neurotrophin in the brain, in specific regions of the hippocampus, and other forebrain regions. In addition, chronic stress increases the expression of neurotrophin-3 in certain regions of the hippocampus and may, thereby, help to protect these regions from the neurotoxic effects of chronic stress. The deleterious effects of stress may contribute to psy- chiatric illnesses, such as depression, that can be precipitated or worsened by stress and that are often characterized by hypercortisolism. Electroconvulsive seizure therapy, as well as antidepressant drugs, increase the expression of brain derived neurotrophic factor and its receptor, trkB, in the brain, demon- strating that neurotrophins are a target of antidepressant treatments. These findings outline a role of neurotrophic factors in the etiology and treatment of certain psychiatric illnesses. The Neuroscientist 1:351-360, 1995 KEY WORDS Brain derived neurotrophic factor, Glutamate, Hippocampus, Electroconvulsive seizure, Cell survival, Atrophy Exposure to stress results in the activation of several stress and adrenal-glucocorticoids on neuronal sur- neurotransmitter pathways (e.g., norepinephrine, se- vival and function and the potential role of neuro- rotonin, dopamine, and glutamate) and neuroendocrine trophic factors in these actions. In addition, the influ- systems, most notably the hypothalamic-pituitary-ad- ence of neurotrophic factors on serotonin and renal axis, which are designed to prepare an animal for norepinephrine, two neurotransmitter systems in- fight or flight responses. However, severe, traumatic volved in the manifestation and treatment of depres- stress or repeated exposure to stress can result in long- sion and other affective illnesses, and the role of neu- term deleterious effects, including even cell atrophy rotrophic factors in the actions of antidepressant and death, which result in behavioral abnormalities. treatments will be discussed. For example, stress is thought to precipitate or exac- erbate several psychiatric illnesses, including depres- Influence of Stress and Glucocorticoids on Neuronal Survival and Growth sion, posttraumatic stress disorder, and schizophrenia. Advances in basic research demonstrate that many of The neurochemical and morphological effects of the deleterious effects of stress on neuronal systems stress and high levels of adrenal-glucocorticoids have may result from complex interactions between neuro- been best characterized in the subfields of the hip- transmitters, hormones, and neurotrophins at the cel- pocampus. In certain subfields, the neurons are vul- lular level. This review will discuss the influence of nerable to stress and excess glucocorticoids and cell survival may be decreased. In other subfields, the neurons are more resistant to stress and glucocorti- Dr. Duman’s research is supported by USPHS grants MH45481 coids and their survival is dependent on the presence and 2 PO1 MH25642 and by a Veterans Administration National Cen- of glucocorticoids. This work and the possible mech- ter Grant for PTSD, VA Hospital in West Haven, Connecticut. anisms the actions of stress and Address reprint requests to: Ronald S. Duman, Connecticut Men- underlying glucocor- tal Health Center, 34 Park Street, New Haven, CT 06508. ticoids are briefly reviewed ( 1-4). Volume 1, Number 6, 1995 351 Copyright @ 1995 by Williams & Wilkins ISSN 1073-8584 Downloaded from nro.sagepub.com at HOMI BHABHA CENT SCI EDUC on January 31, 2013 Stress-induced Atrophy and Survival of it is possible that similar effects occur on select popu- Hippocampal Neurons lations of neurons throughout the brain. The hippocampus, due to high levels of both type I and Although stress and high levels of adrenal-glucocor- II glucocorticoid receptors, is one of the primary targets ticoids lead to neuronal atrophy of CA3 neurons, the of stress and adrenal steroids in the brain. The effects survival and the function of other neurons in the hip- of stress and adrenal-glucocorticoid treatments are not pocampus are dependent on the presence of glucocor- uniform across the different pyramidal fields and den- ticoids. This effect is most prominent in the dentate gy- tate gyrus (Fig. 1). Severe chronic stress or prolonged rus, where removal of adrenal-glucocorticoids (i.e., exposure to glucocorticoids has been shown to cause adrenalectomy) leads to degeneration and death of gran- cell loss and atrophy of the pyramidal neurons in the ule cells (Fig. 1) (10-13). Long-term adrenalectomy is CA fields, prominently in the CA3 region, whereas the also reported to cause degeneration of CA4 pyramidal granule cells of the dentate gyrus are relatively resistant neurons. Although the exact mechanisms by which glu- to damage by these treatments (5, 6). Dendritic atrophy cocorticoids influence cell survival in the hippocampus of CA3 pyramidal neurons, characterized by the de- are not known, the regulation of cell cycling may be creased number and length of apical dendrites, occurs involved. Granule cells of the dentate gyrus continue to in response to repeated restraint stress or glucocorticoid undergo cell birth and death and thereby maintain a treatment (7, 8). In addition, stress or glucocorticoid relatively static number of cells in the presence of nor- treatments can exacerbate the loss of hippocampal neu- mal physiological levels of glucocorticoids (11, 12). rons in response to other insults, such as excitotoxins, The absence of glucocorticoids enhances cell birth and hypoxia-ischemia, and hypoglycemia (1, 2, 9). The in- death, but cell death proceeds at a faster rate and even- fluence of stress and glucocorticoids on the survival of tually leads to fewer healthy cells. This process can be neurons in other brain regions has not been studied, but reversed by glucocorticoid replacement ( 10-12). These Fig. 1. Schematic diagram of the hippocampus and the influence of stress on the growth and sur- vival of individual populations of neurons. The CA pyramidal neurons, including CA1 and CA3, and the dentate gyrus granule cells comprise the pri- mary cell groups in the hippocampus. Afferent pathways from the granule cells to CA3 (mossy fi- ber pathway) and from CA3 to CA1 (Schaffer col- lateral) provide connections within the hippocam- pus. Exposure to stressful stimuli leads to several effects that may contribute to the atrophy and death of CA3 pyramidal neurons. This includes decreased expression of BDNF in CA3 and CA1 neurons, which would reduce the autocrine and target derived sources of this neurotrophin, re- spectively. CA3 neurons also lack Ca2+ binding proteins. These characteristics may contribute to increased sensitivity of CA3 neurons to the dele- terious effects of stress and glucocorticoids (GCs), including enhanced vulnerability to gluta- mate neurotoxicity and atrophy of apical den- drites. In contrast, the dentate gyrus granule cells express Ca2+ binding proteins (calbindin-D28 and parvalbumin) and the protective protein, bcl-2, that may make these neurons more resistant to the damaging effects of stress and other neuronal insults. In addition, although stress decreases lev- els of BDNF in granule cells, chronic, but not acute, stress increases levels of NT-3, which may also contribute to the resistance of these neurons. 352 Downloaded from nro.sagepub.com at HOMI BHABHA CENT SCI EDUC on January 31, 2013 findings indicate that neuronal survival and function is These findings suggest that the maintenance of neuronal dependent on the appropriate balance of glucocorticoid growth and survival may be dependent, in part, on the levels. presence of serotonin. Cellular and Neurochemical Mechanisms of Alterations of Hippocampal Function and Volume
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