PubMed1980
Cefazolin, a semisynthetic cephalosporin, reported to reproduce in several animal species an experimental model of epilepsy, was microinjected into the head of the caudate nucleus in rats. The effects on behavior, electrocortical activity and the antagonism by GABA receptor agonists and GABA-transaminase activity inhibitors were studied. Cefazolin given into the III cerbral ventricle produced an intense pattern of behavioral and locomotor stimulation culminating into several episodes of wild-running crisis, myoclonic jerks of the limbs and in some occasions generalized clonic seizures, these effects lasting over 2 h. At the same time bursts of electrocortical high-voltage spikes followed bu intermittent high-voltage single spikes were recorded. Similarly cefazolin, given into the caudate nucleus produced contralateral circling, an increase locomotor activity, myoclonic jerks of contralateral limbs, intense stereotyped behavior and occasionally generalized clonic convulsions. In addition postural changes consisting in tonic contralateral head-neck deviation were observed. This picture was accompanied by epileptic electrocortical changes, i.e. high-voltage spikes, spike-waves complexes, recruiting polyspikes. The subsequent intraventricular or intrastriatal infusion of GABA, GABOB, muscimol or of GABA-transaminase inhibitors, ethanolamine-o-sulphate and GABA-vinyl-GABA was able to antagonize clinical and electrocortical changes evoked by cefazolin. In conclusion, the present results suggest that cefazolin motor and electrocortical effects are due to an impairment of GABA-ergic transmission.