Effect of ammonium acetate on the somatostatinergic system in the rat frontoparietal cortex

Short (90 min)-, mid (5 days)-, and long-term (15 days) ammonium acetate (5 mmol/kg IP) administration decreased the number of specific [125I][Tyr11]somatostatin receptors in synaptosomes from the frontoparietal cortex without changing the affinity constant. Administration of ammonium acetate did no affect the levels of somatostatin-like immunoreactivity in the frontoparietal cortex. The administration of a single dose of N-carbamyl-L-glutamate (1 mmol/kg) plus L-arginine (1 mmol/kg) 1 h before the last administration of ammonium acetate totally blocked the inhibitory effects of the latter on somatostatin receptor number in the frontoparietal cortex synaptosomes. N-Carbamyl-L-glutamate plus L-arginine alone had no observable effect on the somatostatinergic system. The decrease in the number of somatostatin receptors induced by ammonium acetate might reflect decreased target cell sensitivity to somatostatin, a phenomenon that could contribute to the depressed neuronal excitability induced by ammonia in the rat frontoparietal cortex.