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Neuropeptide Y localization in the rat amygdaloid complex
Author(s) -
Gustafson Eric L.,
Card J. Patrick,
Moore Robert Y.
Publication year - 1986
Publication title -
journal of comparative neurology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.855
H-Index - 209
eISSN - 1096-9861
pISSN - 0021-9967
DOI - 10.1002/cne.902510306
Subject(s) - stria terminalis , amygdala , neuropeptide y receptor , locus coeruleus , biology , central nucleus of the amygdala , nucleus , neuropeptide , brainstem , endocrinology , medicine , extended amygdala , neuroscience , anatomy , receptor , biochemistry
Neuropeptide Y (NPY)‐, avian pancreatic polypetide (APP)‐, and molluscan cardioexcitatory peptide (FMRF)‐like immunoreactivity in the amygdaloid complex of the rat was investigated immunohistochemically. The distribution of each of these peptides within the amygdala is identical and cross‐blocking studies indicate that all three antisera recognize the NPY antigen. Morphologically distinct populations of NPY immunoreactive neurons are differentially distributed in the medial amygdaloid nucleus and at the base of the stria terminalis. Dense plexuses of immunoreactive axons are present in the medial third of the central nucleus and in the dorsal half of the medial nucleus, with light to moderate fiber plexuses present in the lateral and basolateral nuclei and scattered axons present throughout the remainder of the amygdala. The distribution and appearance of NPY immunoreactive plexuses in the amygdala is similar to that described previously for noradrenergic axons arising from brainstem cell groups (Fallon, Koziell, and moore: J. Comp. Neurol. 180 :509–532, '78). However, injections of the noradrenergic neurotoxin 6‐hydroxydopamine into the amygdala result in a complete loss of dopamine‐beta‐hydroxylase (DBH) immunoreactivity in the amygdala and surrounding cortex but leave much of the NPY immunoreactive plexus intact. Similarly, lesions of the locus coeruleus deplete DBH immunoreactivity, leaving NPY‐like immunoreactivity in the amygdala unaffected. These results indicate that much of the NPY immunoreactive plexus observed in the amygdala does not arise from brainstem sources in which NPY and noradrenaline are colocalized. Lesions of the stria terminalis of medial nucleus have no observable effect on the density or distributiion of NPY immunoreactive terminal fields in the basal forebrain and hypothalamus, suggesting that immunoreactive neurons in the amygdaloid complex do not contribute significantly to this innervation.