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Somatostatin binding reduced by ammonium acetate in the rat hippocampus can be reversed by treatment with N‐carbamyl‐L‐glutamate plus L‐arginine
Author(s) -
Del Carmen Boyano Maria,
Bodega Guillermo,
Alvaro Itziar,
Arilla Eduardo
Publication year - 1992
Publication title -
synapse
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.809
H-Index - 106
eISSN - 1098-2396
pISSN - 0887-4476
DOI - 10.1002/syn.890120107
Subject(s) - somatostatin , medicine , chemistry , glutamate receptor , endocrinology , hippocampus , receptor , arginine , ammonium acetate , ammonium , neurotransmitter , biochemistry , biology , amino acid , chromatography , high performance liquid chromatography , organic chemistry
The effects of short‐term (90 min), mid‐term (5 days), and long‐term (15 days) administration of ammonium acetate (5 mmol/Kg day i. p.) on the somatostatinergic neurotransmitter system of the rat hippocampus have been studied. Scatchard analysis of the binding of 125 I‐Tyr 11 ‐somatostatin to hippocampal dissociated cells indicated that administration of ammonium acetate at the times studied were associated with a decrease in the number of somatostatin receptors in this brain area, whereas the affinity of the same receptors remained unchanged. Administration of ammonium acetate did not affect the levels of somatostatin‐like immunoreactivity in the hippocampus. Treatment with N‐carbamyl‐L‐glutamate (1 mmol/Kg, i. p.) plus L‐arginine (1 mmol/Kg), which lead to the conversion of ammonia into urea, prevented the ammonium acetate‐induced changes in somatostatin binding in this brain area. 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 a decreased sensitivity of the target cells to somatostatin, a phenomenon that could contribute to the depressed neuronal excitability induced by ammonia in the rat hippocampus. © 1992 Wiley‐Liss, Inc.