Somatostatin augments the spread of limbic seizures from the hippocampus.
The role of the neuropeptide somatostatin in limbic seizures was studied using electrical stimulation of the hippocampus in kindled rats. Cysteamine, an agent which selectively and reversibly depletes brain somatostatin stores, had a biphasic action. An early proconvulsant effect was seen within a few hours, consisting of prolonged electrographic seizures in the hippocampus and more severe behavioral convulsions. A later anticonvulsant effect, maximal at 1 to 2 days and dissipating within a week, was manifested by less intense behavioral convulsions without change in the duration of electrical seizure activity. Both effects were dose-dependent. No change in afterdischarge thresholds was detected at any time after the administration of cysteamine. Intraventricular administration of somatostatin to animals with behavioral seizures attenuated by cysteamine treatment restored the responses to precysteamine levels. We conclude that somatostatin facilitates the spread of seizures over limbic circuits from a region of focal seizure initiation.
D000818:Animals; D003543:Cysteamine / Q000494:pharmacology; D004569:Electroencephalography; D004827:Epilepsy / Q000503:physiopathology*; D005071:Evoked Potentials / Q000187:drug effects; D006624:Hippocampus / Q000503:physiopathology*; D007276:Injections, Intraventricular; D007696:Kindling, Neurologic; D008032:Limbic System / Q000503:physiopathology*; D008297:Male; D051381:Rats; D013004:Somatostatin / Q000502:physiology*
D013004:Somatostatin; D003543:Cysteamine