SummaryRats were kindled by intraperitoneal injection of pentylenetetrazol (PTZ) (30 mg/Kg) every 48 h. Once kindled, some of the animals received a single injection of cysteamine (200 mg/Kg). Somatostatin-like immunoreactivity (SLI) and 125 I-Tyr II -somatostatin binding were measured in the frontoparietal cortex and hippocampus of the two experimental groups and the control rats. After PTZ kindling the following was observed: i) SLI content was increased in the two areas; 2) Somatostatin receptor affinity decreased in the frontoparietal cortex and was unaltered in the hippocampus;3) The number of somatostatin receptors decreased in the hippocampus and was unaltered in the frontoparietal cortex. Cysteamine, an agent which depletes brain somatostatin and suppresses kindled seizures in PTZ-treated rats, reversed the altered SLI levels and binding in these rats."Kindling" refers to an experimental model of epilepsy in which repeated administration of a subconvulsive dose of a drug (pentylenetetrazol, cocaine, carbachol and lidocaine) or electrical current induces a progressive intensification of seizure activity, that culminates with a generalized seizure (1-6). Although the phenomenon of kindling has been extensively investigated, the basic biochemical mechanism underlyng the development and maintenance of this effect is still unclear.It has been suggested that the peptide somatostatin, a possible neurotransmitter or neuromodulator in the central nervous system (7), may play a role in kindling processes (8-11). It was recently reported that the levels of somatostatin-like immunoreactivity (SLI) are decreased in the rat brain, particularly in the striatum, by the injection of a single convulsant dose of pentylenetetrazol (PTZ) (12). Moreover, Assouline et al.(ll) have demonstrated that seizures in pentylenetetrazol-kindled rats are suppressed following systemic administration of cysteamine ( B -mercaptoethylamine), an agent which causes depletion of brain and gastrointestinal SLI (13). These results suggest that changes in endogenous brain SLI and/or receptors may be critically involved in the kindled state. To test this hypothesis, we used two approaches. First, we determined the effect of the repeated administration of subconvulsant doses of pentylenetetrazol on somatostatin levels and receptor number in rat frontoparietal cortex and hippocampus. Secound, the effect of cysteamine on the same parameters in rats which had been subjected to repetitive systemic administration of subconvulsive doses of pentylenetetrazol.