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Potential Corticotropin‐Releasing Factor Pathways in the Rat Brain as Determined by Bilateral Electrolytic Lesions of the Central Amygdaloid Nucleus and the Paraventricular Nucleus of the Hypothalamus
Author(s) -
KoeglerMuly Susan M.,
Owens Michael J.,
Ervin Gregory N.,
Kilts Clinton D.,
Nemeroff Charles B.
Publication year - 1993
Publication title -
journal of neuroendocrinology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.062
H-Index - 116
eISSN - 1365-2826
pISSN - 0953-8194
DOI - 10.1111/j.1365-2826.1993.tb00367.x
Subject(s) - endocrinology , medicine , hypothalamus , median eminence , amygdala , nucleus , chemistry , central nucleus of the amygdala , radioimmunoassay , hippocampal formation , locus ceruleus , central nervous system , locus coeruleus , biology , neuroscience , dopamine , dopaminergic , substantia nigra
The projection fields of corticotropin‐releasing factor (CRF)‐containing perikarya in the rat central nervous system were studied using a combination of electrolytic lesions, microdissection and radioimmunoassay. The effects of bilateral electrolytic lesions of the central nucleus of the amygdala (Ce) or the paraventricular nucleus (PVN) of the hypothalamus were measured by a sensitive and specific radioimmunoassay. Following lesions of the Ce, CRF concentrations in the locus ceruleus (LC) were significantly decreased. Following lesions of the PVN, CRF concentrations in the median eminence were markedly decreased (>85%), with smaller but consistent reductions of CRF in the hippocampus as well. In contrast to the Ce lesions, PVN lesions resulted in increases in CRF concentratixhtmlons in the LC. These results further confirm the projection of CRF‐containing cells from the PVN to the median eminence, provide evidence for a PVN‐hippocampal CRF pathway, and suggest that the PVN modulates CRF neurons innervating the LC. Moreover, the existence of a CRF‐containing pathway from the Ce to the LC appears likely, and such a circuit may play a role in the behavioral and physiological responses to stress.