Protein kinase C in the parabrachial nucleus of rats during conditioned taste aversion induced by amphetamine.

D-Amphetamine (AM) is a potent inducer of conditioned taste aversion (CTA) the mechanism of which differs from that induced by lithium. The aim of the present communication is to see whether AM-induced CTA will produce shift in the protein kinase (PKC) activity in the parabrachial nucleus (PBN). Activity of PKC was measured in PBN of rats during AM-induced CTA. In the control experiments a single intraperitoneal (i.p.) injection of AM (3 mg/kg) alone (not paired with saccharin drinking) resulted in rise of particulate bound PKC by 77% and a tendency to decrease its activity in cytosol 60 min but not 24 and 48 h after AM administration. The results suggest translocation of the enzyme from cytosol to membrane. Cytosolic PKC increased by 17 and 50%, 24 and 48 h, respectively, after acquisition of CTA (15 min after the retrieval test), when the direct effect of AM on PKC had already disappeared. Particulate PKC did not change at either of the two time intervals. Thus the total PKC activity was increased. Since we have previously observed the same PKC shifts using LiCl or CuSO4 as CTA unconditioned stimuli, we assume that any CTA inducer will elicit the same alteration of PKC in PBN.