Inhibition in Penicillin - Induced Epileptic

As an acute model o f focal epi lepsy, the penicil l in focus has been wide ly ut i l ized since the initial r epo r t by Walker and J o h n s o n (1945) . However , the cellular mechanisms responsible for the epi leptogenic e f fec t o f penlci lhn remain poo r ly u n d e r s t o o d . A characterist ic fea ture o f penici l l ininduced epilept ic foci is the pa roxysma l depolar iz ing shift (PDS), which m a y be observed in m a n y of the neurons in the focus (Mat sumoto and A j mone Marsan 1964). The PDS is well corre la ted t empora l l y wi th the inter ic ta l spike seen in the e lec t rocor t i cogram and appears to be a giant exc i t a to ry pos t synap t i c p o t e n t m l (EPSP) (Mat sumoto et al. 1969; Pr ince 1969) . A t t e m p t s to explain the basis fo r the PDS have led to invest igat ion of the e f fec t o f penicillin on inh ib i to ry processes in the cor tex . Curtis e t al. (1972) d e m o n s t r a t e d tha t penlcilhn Increased the firing rate o f un iden t i f i ed neurons in cat pos tc ruc ia te co r t ex and antagon ized the inh ib i to ry ac t ion o f gamma-aminobu ty r i c acid (GABA) on the discharge of those neurons . Still, the e f fec t o f penicil l in u p o n Inhibi to ry processes in m a m m a h a n co r t ex remains an open ques t ion . While inh ib i to ry pos t synapt ic potent ia l s (IPSPs) are still p resen t in epileptic foci (Dlchter and Spencer 1969; Matsum o t o et al. 1969; Pr ince 1969) , the i r func-