AJP - Regulatory, Integrative and Comparative Physiology, Vol 268, Issue 3 676-R682, Copyright © 1995 by American Physiological Society
Parabrachial nucleus lesions impair feeding response elicited by 2,5-anhydro-D-mannitol
H. J. Grill, M. I. Friedman, R. Norgren, G. Scalera and R. Seeley
Graduate Group of Psychology, University of Pennsylvania, Philadelphia 19104.
Systemic injection of the fructose analogue 2,5-anhydro-D-mannitol (2,5-AM)
elicits a feeding response and induces c-fos activity in the parabrachial
nuclei (PBN). We used bilateral ibotenic acid lesions of PBN to determine
whether the activation inferred from c-fos activity was causally related to
the feeding response. The relationship between the PBN lesion and feeding
behavior was also examined with the glucose analogue 2-deoxy-D-glucose
(2-DG). The PBN lesions interfered with the feeding response to 2,5-AM but
spared the feeding response to 2-DG. Rats were also tested in a conditioned
taste-aversion paradigm. Differences were observed in the relationship
between lesion extent and behavioral deficit for feeding responses to
2,5-AM and taste-guided intake after taste-aversion conditioning. These
data provide the first demonstration that central lesions can disrupt
feeding responses to peripherally acting 2,5-AM. The results suggest that
the neural substrate for this response differs from that mediating
taste-aversion conditioning and from that involved in the feeding response
to 2-DG.
