Abstract
It has been known that systemically administered local anesthetic agents such as procaine and lidocaine manifest depressant effects similar to barbiturates on the central nervous system. They abolished the tonic extensor phase of the maximal electroshock seizure in experimental animals (1-4), inhibited the reticular activating system (5), and blocked the amygdaloid (6) as well as hippocampal after-discharges (7).
On the other hand, some discrepancies were observed between the actions of local anesthetics and of barbiturates in behavioral and electrical manifestations of convulsion. Procaine and lidocaine in larger doses induced clonic convulsions. They did not modify or even enhanced the clonic phase of electrically induced seizure (8), whereas barbiturates could suppress it. Moreover, the local anesthetics tended to enhance the spike and wave complex in EEG elicited by bemegride in rabbits, whereas barbiturates definitely inhibited it (9). These inconsistencies may be due to different mechanisms of depressant actions of local anesthetics and barbiturates on neurons of central nervous system. In fact, Galindo (10, 11 ) showed different patterns of synaptic inhibition by procaine and pentobarbital in cuneate neurons of the oblongate medulla in cats.
We intend to search the difference in the mechanisms of inhibitory action of lidocaine and pentobarbital on the activities of reticular neurons, since the reticular formation is regarded as a site to play an important role in the manifestation of tonic convulsion (12, 13) and the activities of its neurons are closely related to cortical spikes induced by pentetrazol (14).
The present study is concerned with the midbrain reticular neurons of which activities are influenced by stimulation of the thalamic reticular nucleus.
