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Forced swim stress activates rat hippocampal serotonergic neurotransmission involving a corticotropin-releasing hormone receptor-dependent mechanism

MPG-Autoren

Linthorst,  ACE
Max Planck Institute of Psychiatry, Max Planck Society;

Peñalva,  RG
Max Planck Institute of Psychiatry, Max Planck Society;

Flachskamm,  C
Max Planck Institute of Psychiatry, Max Planck Society;

Holsboer,  F
Max Planck Institute of Psychiatry, Max Planck Society;

Reul,  JMHM
Max Planck Institute of Psychiatry, Max Planck Society;

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Zitation

Linthorst, A., Peñalva, R., Flachskamm, C., Holsboer, F., & Reul, J. (2002). Forced swim stress activates rat hippocampal serotonergic neurotransmission involving a corticotropin-releasing hormone receptor-dependent mechanism. European Journal of Neuroscience, 16(12), 2441-2452.


Zitierlink: http://hdl.handle.net/11858/00-001M-0000-000E-9FFF-6
Zusammenfassung
Serotonin is important for adequate coping with stress. Aberrant serotonin function is implicated in the aetiology of major depression and anxiety disorders. Dysregulation of the hypothalamic-pituitary-adrenocortical axis, involving elevated corticotropin-releasing hormone (CRH) activity, also plays a role in these stress-related illnesses. Here we studied the effects of stress on hippocampal serotonin and the role of the CRH system using in vivo microdialysis. First, rats were subjected to a forced swim stress, resulting in a dramatic increase in hippocampal serotonin (1500% of baseline), which was associated with the occurrence of diving behaviour. The diving-associated increase in serotonin depended on activation of CRH receptors, as it was antagonized by intracerebroventricular pretreatment with D-Phe-CRH12-41. Secondly, the effects of intracerebroventricular administration of CRH and urocortin (0.03-1.0 mug) were studied. Both CRH and urocortin caused a dose-dependent rise in hippocampal serotonin (maximally 350% of baseline) and 5-hydroxyindoleacetic acid levels, suggesting the involvement of CRH receptor type 1. Because the effects of urocortin were prolonged, CRH receptor type 2 could play a role in a later phase of the neurotransmitter response. Experiments using adrenalectomized rats showed that CRH-induced serotonin changes were adrenally independent. These data suggest that the raphe-hippocampal serotonin system is able to mount, CRH receptor-dependent, responses to specific stressful situations that surpass the usually observed maximal increases of about 300% of baseline during stress and enhanced vigilanc