Infusions of norepinephrine (NE), the gamma-aminobutyric acid agonist, musc
imol (MUS), or neuropeptide Y (NPY) into the paraventricular nucleus (PVN)
of the hypothalamus all increase food intake. Such feeding may be due to di
rect activation of behavioral processes driving ingestion and/or to alterat
ions in nutrient metabolism that feeding serves to normalize. To examine th
ese possibilities, male Sprague-Dawley rats received PVN infusions of vehic
le, 20 nmol NE, 1 nmol MUS or 100 pmol NPY at dark onset, then food intake
was measured under three feeding conditions: (1) I and 2 h immediately afte
r injections, (2) I h after a I h delay between injections and access to fo
od, and (3) 1 h after a 1 h feeding delay, bur with injections occurring ju
st before presenting food. Measures of energy expenditure (EE) and respirat
ory quotients (RQs) in the absence of food were made over 2 h in parallel e
xperiments. Results confirmed that NE, MUS and NPY all increased dark-onset
feeding, but only NPY increased intake above control levels after a 1 h fe
eding delay. No neurochemically-induced changes in EE were observed, nor we
re there changes in RQs after NE or MUS. However, NPY reliably enhanced RQs
from 30 to 120 min of testing. Our findings imply that NE and MUS initiate
relatively immediate, short-term feeding that is not associated with chang
es in nutrient metabolism and does not summate with cues stimulated by dela
yed access to food. NPY initiates more protracted feeding temporally linked
to enhanced carbohydrate metabolism This may indicate that part of NPY's f
eeding stimulatory effects are secondary to physiological processes driving
ingestion. (C) 2000 Elsevier Science B.V. All rights reserved.