Ibotenic acid lesion of the anterior piriform cortex does not increase high‐protein diet intake in rats

Abstract

INTRODUCTION High protein- or imbalanced amino acid diets are known to reduce food intake. The brain areas involved in this regulation are unknown. We hypothesized that the anterior piriform cortex (APC) plays this role. METHODS 34 male rats were included in either a control (n=8), sham (n=4) or a lesioned group (n=22). APC was lesioned bilaterally using ibotenic acid (6 μg) injected at one of two different sites: A-P 2.4 mm; L ± 4.0mm; D −6.5 mm (n=13) and A-P 3.0 mm; L ± 3.1 mm; D −6.3 mm (n=9) relative to bregma. Rats were then submitted to a P14 diet for at least 10 days, followed by a threonine devoid diet (Thr-Dev) for 5 days, then by a Thr-Dev corrected for threonine (Cor-diet) for 3 days and finally by a P55 diet for 3 days. Each period was preceded by 2 days of P14 diet in order to determine the basal level of energy intake. APC lesions were verified post-mortem using conventional histological methods. RESULTS Neither transition from P14 to Thr-Dev nor transition from P14 to Cor nor transition from P14 to P55 was altered by APC lesion. Moreover, relative to non-lesioned rats, APC lesioned rats did not increase food intake when given Thr-Dev or P55. Lesions were correctly placed. CONCLUSION The ibotenic acid sensitive neurons in the APC are not critical for the detection of high protein- or imbalanced amino acid diets.