Excitotoxic lesions of the parabrachial nuclei prevent conditioned taste aversions and sodium appetite in rats.

Abstract

Electrolytic lesions of the parabrachial nuclei (PBN) disrupt conditioned taste aversion (CTA) in the rat, but it is not known whether this effect is due to damaging axons of passage or to destruction of intrinsic neurons. We tested 10 rats with electrophysiologically guided, ibotenic acid lesions of the PBN (PBNx) to determine whether they could acquire a LiCl-induced CTA to l-alanine (0.3 M) or demonstrate a sodium appetite following furosemide treatment and overnight access to sodium deficient chow. Vehicle-treated and nonsurgical controls were included in the design. PBNx rats failed to develop a CTA, even after 3 conditioning trials. Moreover, more than 8 months later, a subset of the PBNx rats were again unable to learn a CTA using NaCl as the conditional stimulus (CS). After the furosemide treatment, the control rats drank an average of 20.3 ml of strong salt in 24 hr. The PBNx rats drank virtually no NaCl during the first 2 hr and averaged only 4.0 ml in 24 hr. In the PBN, damage to neuronal somata is more critical than interrupting fibers of passage for producing deficits in taste-guided behaviors.