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5‐HT 1A Receptor Agonist Flesinoxan Enhances Fos Immunoreactivity in Rat Central Amygdala, Bed Nucleus of the Stria Terminalis and Hypothalamus
Author(s) -
Compaan J. C.,
Groenink L.,
Gugten J.,
Maes R. A. A.,
Olivier B.
Publication year - 1996
Publication title -
european journal of neuroscience
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.346
H-Index - 206
eISSN - 1460-9568
pISSN - 0953-816X
DOI - 10.1111/j.1460-9568.1996.tb01197.x
Subject(s) - stria terminalis , medicine , endocrinology , chemistry , hypothalamus , vasopressin , corticotropin releasing hormone , dorsal raphe nucleus , 5 ht1a receptor , central nucleus of the amygdala , agonist , 5 ht receptor , receptor , serotonin , biology , serotonergic
5‐Hydroxytryptamine‐1A (5‐HT 1A ) receptor agonists, including flesinoxan, reduce anxiety and activate the hypothalamus‐pituitary‐adrenal (HPA) axis under basal conditions. In order to investigate the underlying neural mechanisms we investigated immunoreactivity for the immediate early gene protein product Fos (Fos‐ir) in rat brains 1 h after flesinoxan treatment (0.0, 0.3 or 3.0 mg/kg p.0.). Typically, 5‐HT 1A receptor‐containing brain areas, such as the dorsal raphe nuclei, hippocampus, septum, diagonal band and the cortical and basomedial amygdala, do not show Fos‐ir. Apparently, binding of flesinoxan at the 5‐HT 1A receptor does not directly lead to activation of c‐fos in the cell, probably due to its negative coupling to adenylate cyclase. However, in typically non‐5HT lA receptor‐containing brain areas Fos‐ir is increased due to flesinoxan treatment, as in the paraventricular nucleus of the hypothalamus (PVN), the dorsolateral part of the bed nucleus of the stria terminalis (BNSTd1) and the central amygdala (CeA). Flesinoxan‐treated rats also exhibited higher plasma corticosterone levels than vehicle‐treated animals, which suggests the involvement of corticotropin‐releasing hormone (CRH) or vasopressin in the hypothalamus. After double immunolabelling (Fos/CRH or Fos/vasopressin), every CRH neuron detected in the PVN also contained Fos. Moreover, a significant correlation existed between the number of Fos‐ir neurons in the PVN and the plasma corticosterone level. Hardly any Fos/ vasopressin double labelling was visible in the PVN. Accordingly, flesinoxan exerts its activating effects on the HPA axis via CRH neurons in the PVN. These effects are transsynaptically mediated by other brain areas, such as the CeA and BNSTdl, which also show increased Fos‐ir.