We studied the effects of arginine vasopressin (AVP) and somatostatin (SS) on glutamate release and characterized the receptors that mediate the effects of these two peptides from rat astrocytes.;Aginine vasopressin (AVP) acts through specific G protein-coupled receptors and not only induces [Ca2+]i' increase in astrocytes, but also has been shown to regulate astrocytic cell volume changes. Here we report a novel finding that AVP induces glutamate release from astrocytes isolated from the cerebral cortex and hippocampus. We also investigated the type of AVP receptors involved in the AVP-induced increase in glutamate release from astrocytes isolated from the hippocampus and cortex of neonatal rats. We showed that the AVP (0.1--1000 nM)-induced increase in glutamate release and [Ca2+]i is brought about by two distinct subtypes of AVP receptors (V1a & V1b). Our results suggested, that V1b receptors are predominantly expressed in astrocytes isolated from the hippocampus and V1a receptors are predominantly expressed in astrocytes isolated from the cortex of neonatal rats. In addition, the AVP-induced increase in glutamate did not contribute to an increase in [Ca2+]i, since blockade of metabotropic glutamate receptors did not alter the AVP-induced increase in [Ca2+ ]i. Also the administration of a phospholipase A2 (PLA2) inhibitor failed to alter AVP-induced [Ca 2+]i increase, suggesting the lack of involvement of PLA 2.;In the second part of the thesis, we investigated the effects of somatostatin (SS), a Gi/o-coupled receptor activating hormone on lowering of cAMP level, [Ca2+]i, and glutamate release from neonatal rat astrocyte cultures. Forskolin (10-7 to 10 -5 M) increased glutamate release, cAMP levels and [Ca2+] i. in a concentration-dependent manner; forskolin-induced increase in [Ca2+]i paralleled the increase in glutamate release, but the increase in cAMP levels did not. SS alone did not have any effect on basal glutamate release, cAMP levels or [Ca2+]i, but inhibited the forskolin-induced glutamate release and increase in cAMP level in a concentration-dependent manner. Somatostatin also inhibited forskolin induced increase in [Ca2+]i. These effects were mimicked by the selective SSTR4 agonist L-803,087, but not by the selective agonists for SSTR1, SSTR2, SSTR3 or SSTR5. Although the inhibitory effect of SS and L-803,087 (10-9 to 10-6 M) on forskolin-induced increase in cAMP levels and glutamate release was concentration-dependent, the inhibition of glutamate release, however, was not apparent at >10 -6 M of the agonists. This was probably due to the ability of SS and L-803,087 to increase [Ca2+]i at >10-6 M. Pretreatment with U-73122, a phospholipase C inhibitor, blocked 10 -6 M SS-induced increase in [Ca2+]i. Our findings suggest: In astrocytes, (1) SS inhibits forskolin-induced glutamate release by decreasing cAMP levels and at least partly by reducing [Ca 2+]i. (2) SSTR4 mediates SS-induced decrease in cAMP levels, [Ca2+]i and glutamate release. (3) SS at high concentrations (≥10-6 M) may increase glutamate release by activating phospholipase C pathway. SS or SSTR4 agonists could be used to reduce glutamate release from astrocytes.