Search

Experiments were performed on chronically prepared cats to determine the effect of cerebellar stimulation on generalized “centrencephalic” epilepsy produced by large intramuscular injections of penicillin. Diffuse epileptiform activity developed approximately 1 hr after penicillin injection. Recording of electrical activity from cerebellar structures indicated prominent paroxysmal activity to be present during cortical epileptiform activity. Cerebellar stimulation at 10 and 100 Hz resulted in prompt and significant decrease in the number and amplitude of paroxysmal events. Mesencephalic reticular formation stimulation also reduced the amount of abnormal activity, but, in contrast to cerebellar stimulation, this reduction did not outlast the stimulus period. Inhibition by cerebellar stimulation is attributed to activation of fastigial bulbar pathways.

Paired-pulse potentiation was studied in the CA1 region of rats exposed prenatally to alcohol. Pregnant rats were fed a liquid diet containing 35% ethanol-derived calories on days 3 to 21 of gestation. Control animals were fed liquid diets without ethanol. When the pups of both groups were 40 to 60 days old, hippocampal slices were prepared and maintained in vitro. Paired-pulse potentiation was examined at intervals from 5 to 400 ms. Recordings made from these slices showed that the response inhibition typically seen at short interpulse intervals was minimal or absent in the animals with prenatal exposure to alcohol. Potentiation of population spike amplitude was enhanced at intervals to 100 ms.

The cortex of an entire cerebral hemisphere in the cat was chronically isolated to allow assessment of the role of intrinsic association pathways in the regulation of focal epileptic activity induced by topical application of penicillin. EEG recordings indicated that interictal spike activity in the normal hemisphere was maximal at the focus and markedly reduced in amplitude at distances of 5 to 7 mm. Activity in the isolated hemisphere was similar in morphology to that of the normal cortex, but there were largeamplitude epileptiform discharges 10 to 15 mm from the focus. These distant penicillin spikes appeared early in the development of the focus and were not attributable to diffusion of penicillin. Intracellular recordings at the center of the focus and at remote sites showed the characteristic paroxysmal depolarizing shifts (PDSs) previously described for intact cortex, i.e., large-amplitude membrane depolarizations with superimposed high-frequency spike activity and subsequent spike inactivation. Hyperpolarizing potentials followed termination of PDSs in most cells and were occasionally seen as the sole accompaniment of the focal penicillin discharges. We suggest that the similarity of intracellular findings in normal and isolated cortices could have resulted from a direct effect of penicillin on neurons, whereas the spread of interictal spikes in the isolated hemisphere apparently involved abnormal utilization of existing intracortical association pathways.

Single-unit activity in the cerebellum of awake cats was recorded during generalized paroxysmal activity induced by intramuscular administration of penicillin. Cortical paroxysmal events could provoke changes in the gross electrical activity of the cerebellum that were associated with altered neuronal activity. Coincident with the cerebellar paroxysms, Purkinje cells showed one of two types of activity: an increase in simple spike discharges associated with the surface-negative phase of the paroxysm, or an excitatory-inhibitory sequence. Normal firing patterns resumed quickly after cessation of the paroxysmal discharges. The cerebellum thus appears to be markedly involved in this model of generalized epilepsy and may be involved in its physiopathogenesis.