The rewarding properties of neuropeptide Y in perifornical hypothalamus vs, nucleus accumbens

Citation
Cm. Brown et al., The rewarding properties of neuropeptide Y in perifornical hypothalamus vs, nucleus accumbens, PEPTIDES, 21(8), 2000, pp. 1279-1287
Citations number
28
Categorie Soggetti
Biochemistry & Biophysics
Journal title
PEPTIDES
ISSN journal
01969781 → ACNP
Volume
21
Issue
8
Year of publication
2000
Pages
1279 - 1287
Database
ISI
SICI code
0196-9781(200008)21:8<1279:TRPONY>2.0.ZU;2-M
Abstract
There is a high coexistence of substance abuse in humans with eating disord ers. One theory offered to account for this fact is that a common biochemic al substrate may exist that mediates both processes. Brain neuropeptide Y ( NPY) is one neurochemical system that might contribute to these separate, y et related, problems. To clarify the role of NPY in mediating reward proces ses and the possible interaction between reward and feeding, the present st udy examined the effects of injecting NPY bilaterally into the perifornical hypothalamus (PFH) vs. the nucleus accumbens (NAC) on intake of preferred vs. non-preferred food types, as well as on conditioned place preference (C PP) learning. NPY (24, 78, 156 and 235 pmol/side) stimulated intake of both regular powdered chow and sucrose when injected into the PFH, but not the NAG. A CPP that was negatively col related with food intake occurred with t he low (24 pmol/side) dose of NPY in the PFH, while a CPP that was not corr elated with food intake was produced with the same dose in the NAG. The ext ent of the CPPs produced by NPY injection in both brain sites mirrored that produced by peripheral injection of amphetamine (2.5 mg/kg). These results indicate that NPY elicits reward-related behavior, but not feeding, from t he NAG, and both behaviors from the PFH. However, the feeding effect derive d from the PFH appears to overshadow a rewarding effect derived from this s ite. Considered together, these findings suggest that altered NPY functioni ng in both brain regions may contribute to some of the pathophysiological p rocesses observed in eating disordered patients who have additional procliv ities for substance abuse. (C) 2000 Elsevier Science Inc. All rights reserv ed.