Vol 6 n° 2 - Neuroplasticity
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tressful life events are among the most potent factors  that  trigger  or  induce  depressive  episodes  in humans. The brain responds to stress experiences in a complex manner related to the activation and inhibition of neurons that are involved in sensory, motor, auto- nomic,  cognitive,  and  emotional  processes.  Chronic stress, which is known to be accompanied by hyperac- tivity  in  central  nervous  neurotransmitter  systems, induces cellular changes that can be regarded as a form of plasticity.This causes mood alterations in the affected individual  and  has  the  potential  to  reverse  the  psy- chopathological processes, thus alleviating the symptoms of  depression.  Since  social  stress  in  animals  evokes symptoms  that  resemble  those  found  in  depressed patients, chronic social stress can serve as an experi- mental paradigm to investigate the neuronal processes that may also occur during depressive disease in humans. Research  over  past  years  has  led  to  considerable advances in the understanding of the neural causes of depression and the cellular mechanisms that underlie the beneficial effects of currently available antidepressants. More importantly, such research forms the basis for the future development of more effective antidepressant drugs. Stress changes the activity of noradrenergic and adrenergic neurons Stress is known to activate neurohormonal systems, such as the hypothalamo-pituitary-adrenal (HPA) axis, to release  the  central  nervous  “stress  peptide”  corti- cotropin-releasing factor,1 and to secrete glucocorticoids from the adrenal gland.2 These corticosteroids have been identified as prominent factors that modify metabolic processes in both the body and the brain during stress as well as depression.3 However, the other group of essen- tial  substances  in  basic  and  accelerated  metabolism includes the monoamines, noradrenaline, adrenaline, 1 7 1 P h a r m a c o l o g i c a l   a s p e c t s S Copyright © 2004 LLS SAS.  All rights reserved www.dialogues-cns.org Cellular consequences of stress and depression Eberhard Fuchs, PhD; Gabriele Flügge, PhD Stress is known to activate distinct neuronal circuits in the brain and induce multiple changes on the cellular level, including alterations in neuronal structures. On the basis of clinical observations that stress often precipitates a depressive disease, chronic psychosocial stress serves as an experimental model to evaluate the cellular and mol- ecular alterations associated with the consequences of major depression. Antidepressants are presently believed to exert their primary biochemical effects by readjusting aberrant intrasynaptic concentrations of neurotransmit- ters, such as serotonin or noradrenaline, suggesting that imbalances  within  the  monoaminergic  systems  con- tribute to the disorder (monoaminergic hypothesis of depression). Here, we review the results that comprise our understanding of stressful experience on cellular processes, with particular focus on the monoaminergic systems and structural changes within brain target areas of monoaminergic neurons.   © 2004, LLS SAS Dialogues Clin Neurosci. 2004;6:171-183. Keywords: noradrenaline; adrenaline; serotonin; dopamine; histamine; neuronal remodeling; 2-adrenoceptor; 5-HT1A receptor; dopamine transporter; tree shrew Author   affiliations:   Clinical   Neurobiology   Laboratory,   German   Primate Center, Göttingen, Germany Address  for  correspondence:  Eberhard  Fuchs,  PhD,  Clinical  Neurobiology Laboratory, German Primate Center, Kellnerweg 4, 37077 Göttingen, Germany
(e-mail: efuchs@gwdg.de)