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Animals decrease intake of an indispensable amino acid (AA)-deficient or devoid diet, due in part to decreased dietary limiting AA (DLAA) concentrations within the anterior piriform cortex (APC), and to a recognition process that occurs as early as 20 min following exposure to AA deficiencies. Glutamate levels within the APC change in response to AA deficiencies. The APC projects to the lateral hypothalamus (LH), where glutamate acts to stimulate food intake. We hypothesize that the APC, through glutamatergic projections to the LH, inhibits the LH, which signals to reject the AA-deficient or devoid diet, and trigger aversions to the AA-deficient or devoid diet via an ascending pathway to the APC. We examined the effects of (1) bilateral APC and LH blockade of glutamate's NMDA receptors with the antagonist, D-AP5, (2) APC blockade of AMPA receptors with the antagonist, NBQX, to block glutamate transmission from the APC, and (3) direct injection of the agonist, NMDA, into the LH on intake of the AA-deficient, devoid, or corrected diet. Administration of D-AP5 into the APC increased intake of AA-deficient diet by 6 h, but D-AP5 in the LH decreased AA-devoid diet preferentially over AA corrected intake sooner. NBQX in the APC increased AA-deficient diet intake, also at 6 h. NMDA injection into the LH-stimulated intake of the AA corrected diet by 3 h, but did not affect AA-devoid diet intake. Thus, the glutamate receptors in the APC and LH are involved in the feeding responses to AA-deficient diet, albeit with regional differences. We suggest that glutamate mediates the anorectic responses to AA-deficient diets through recognition of AA-devoid diet with the glutamatergic output cells of the APC sending glutamate-based signals for changes in food intake within the LH and through learned avoidance of AA-deficient diet within the APC, as indicated through the more immediate and prolonged periods of activation within the LH and APC, respectively.

The effects of GABA(A) and GABA(B) receptors in the anterior piriform cortex (APC) on intake of an amino acid imbalanced diet and a basal diet were evaluated in rats. Administration of muscimol (GABA(A) receptor agonist) to the APC immediately suppressed ingestion of both amino acid imbalanced and basal diets. Central administration of bicuculline (a GABA(A) receptor antagonist) stimulated feeding of the amino acid imbalanced diet but had no effect on intake of the basal diet. The GABA(B) receptor antagonist phaclofen decreased consumption of the basal diet but did not affect consumption of the amino acid imbalanced diet. These findings demonstrate that manipulation of GABA-sensitive cells in the APC can have a pronounced effect on feeding behavior that is not selective to aminoprivic feeding. However, these data suggest that GABA(A) and GABA(B) receptors may function as regulators that are activated by monoaminergic systems and neuropeptides in response to amino acid imbalanced diet intake. Inhibitory effects of GABA(A) and GABA(B) receptors may modulate the pyramidal cells, contributing to the reduced feeding response to the amino acid imbalanced diet. Also, transcription of mRNA for both GABA receptors and the GABA reuptake transporter was affected by a threonine deficient but not a corrected diet, compared to the basal diet. Taken together, these results support the involvement of GABA receptors in the APC in feeding in general and the responses to amino acid deprivation in vivo.