Abstract
The role of glutamate in conditioned taste aversion was investigated. Both, in the amygdala (AMYG) and in the lateral hypothalamus (LH) extracellular levels of glutamate were assessed by microdialysis and capillary electrophoresis with laser induced fluorescence detection. Rats were conditioned by pairing a novel flavor (strawberry flavor) with an intraperitoneal injection of lithium chloride. When the conditioned stimulus (strawberry flavored solution) was injected into the mouth of conditioned rats, there was an increase of glutamate release in the AMYG, and a decrease in glutamate release in the LH. These results predicted that glutamate release in the AMYG and the LH was involved in CTA. This possibility was tested by MK-801 (glutamate antagonist) and glutamate microinjections. MK-801 injections in AMYG attenuated the rejection of the novel flavor, and in the LH did not cause any effect on CTA. Glutamate microinjections in the AMYG caused CTA. These results suggest that glutamatergic activity in the AMYG might be a relevant neurochemical correlate and cause of conditioned taste aversion.
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