BEHAVIORAL AND ELECTROCORTICAL EFFECTS AFTER INTRASTRIATAL CEFAZOLIN IN RATS ARE ANTAGONIZED BY DRUGS ENHANCING GABA-ERGIC TRANSMISSION

  • 1 January 1980
    • journal article
    • research article
    • Vol. 29  (3) , 445-458
Abstract
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 cerebral 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 time bursts of electrocortical high-voltage spikes followed by intermittent high-voltage single spikes were recorded. Cefazolin, given into the caudate nucleus produced contralateral circling, an increased 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 and recruiting polyspikes. The subsequent intraventricular or intrastriatal infusion of GABA, GABOB [.gamma.-amino-.beta.-hydroxybutyric acid], muscimol or of GABA-transaminase inhibitors, ethanolamine-O-sulfate and GABA-vinyl-GABA was able to antagonize clinical and electrocortical changes evoked by cefazolin. Cefazolin motor and electrocortical effects are due to an impairment of GABA-ergic transmission.