Neuropeptide Y input to the rat basolateral amygdala complex and modulation by conditioned fear.

Randy J Leitermann, Amanda B Rostkowski, Janice H Urban,

The Journal of comparative neurology, January 18, 2016

Within the basolateral amygdaloid complex (BLA), Neuropeptide Y (NPY) buffers against protracted anxiety and fear. While the importance of NPY’s actions in the BLA is well-documented, little is known about the source(s) of NPY fibers to this region. These current studies identified sources of NPY projections to the BLA using a combination of anatomical and neurochemical approaches. NPY innervation of the BLA was assessed in rats by examining the degree of NPY co-expression within interneurons or catecholaminergic fibers using somatostatin and tyrosine hydroxylase (TH) or dopamine β-hydroxylase (DβH), respectively. Numerous NPY+/somatostatin+ and NPY+/somatostatin- fibers were observed suggesting at least two populations of NPY fibers within the BLA. No co-localization was noted between NPY and TH or DβH immunoreactivities. Additionally, Fluorogold retrograde tracing with immunohistochemistry was used to identify the precise origin of NPY projections to the BLA. FG+/NPY+ cells were identified within the amygdalostriatal transition area (AStr), stria terminalis and scattered throughout the bed nucleus of the stria terminalis (BNST). The subpopulation of NPY neurons in the AStr also co-expressed somatostatin. Subjecting animals to a conditioned fear paradigm increased NPY gene expression within the AStr, whereas no changes were observed within the BLA or stria terminalis. Overall, these studies identified limbic regions associated with stress circuits providing NPY input to the BLA and demonstrated a unique NPY projection from the AStr may participate in the regulation of conditioned fear. This article is protected by copyright. All rights reserved.

© 2016 Wiley Periodicals, Inc.

Pubmed Link: 26779765

DOI: 10.1002/cne.23960