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Clonidine, but not Ritanserin, Suppresses Kainic Acid-induced Automatisms in Developing Rats

Publikace na 1. lékařská fakulta, 3. lékařská fakulta |
1994

Tento text není v aktuálním jazyce dostupný. Zobrazuje se verze "en".Abstrakt

In young rats, systemic or local administration of kainic acid (KA) elicits scratching as the prevailing automatism whereas in adult rats, wet dog shakes (WDS) are usually recorded. We tested the effects of the alpha(2)-adrenergic agonist clonidine (0.25 mg/kg, IP; also acting, however, on imidazoline receptors), which has been reported to block KA-induced WDS in adult rats and the 5-HT2 antagonist ritanserin (20 mg/kg, IP) in rats aged 7, 12, 18, 25, and 90 days treated IP with doses of KA that induce maximum number of automatisms with minimal early lethal effects (i.e., 4, 6, 8, 10, and 14 mg/kg, respectively).

Both WDS and scratching were frequently recorded together in one animal. Neither ritanserin nor its solvent had significant effects on the total number of automatisms or on their distribution between WDS and scratching.

In contrast, clonidine suppressed automatisms throughout the development studied. In 90-day-old (adult) rats clonidine decreased the incidence of both WDS and scratching, whereas it usually attenuated scratching at younger ages.

Kainic acid-induced seizures were also recorded because of reported incompatibility between tonic-clonic seizures and WDS in adult rats. In 18-90-day-old rats, tonic-clonic seizures and WDS were found incompatible.

In 7-18-day-old pups, scratching and KA-induced tonic-clonic seizures occurred together. Moreover, in 7-day-old rats, clonidine was anticonvulsant.

We have demonstrated that KA-induced automatisms develop from scratching in pups to prevailing WDS in adult rats, whereas the incidence of scratching rather decreases during development. As indicated by the presence of both automatisms in the same animal, we suggest that there are probably different neuronal circuits responsible for the induction of automatisms, however, both modulated by the alpha(2)-adrenergic or imidazoline receptor system.