Cooling lesions of the lateral parabrachial nucleus during LiCl activation block acquisition of conditioned taste avoidance in male rats

Abstract

Lesions of the lateral parabrachial nucleus (lPBN) disrupt acquisition of LiCl-induced conditioned taste avoidance. Animals with lesions in this area also fail to exhibit taste neophobia. This raises the possibility that an inability of rats to recognize the taste solution as novel contributes to the deficit in taste avoidance learning. If this is the case, then one would expect conditioned taste avoidance not to be disrupted if the lPBN is functional during taste processing but not during LiCl processing. The first three experiments demonstrated that cooling was a viable method by which to temporarily inactivate the lPBN. Measurement of neural temperature during cooling indicated that the lPBN was cooled to temperatures that have been shown to block synaptic transmission but not axonal transmission. Cooling the lPBN itself induced a conditioned avoidance to a sucrose solution but this avoidance was abolished by exposure to daily cooling for 1 week prior to acquisition. In experiment 4, all animals were preexposed to lPBN cooling for 1 week. Those rats that received cooling lesions during a period that started immediately after sucrose solution consumption and extended through the peak effectiveness of LiCl failed to acquire a taste avoidance. These results fail to support the hypothesis that the deficit in taste avoidance learning after permanent lesions of the lPBN is due to an inability of lesioned animals to recognize the taste as novel. They are consistent with the hypothesis that this neural area processes ascending information about LiCl.