Abstracts

Due to its major inhibitory output toward deep cerebellar nuclei and extracerebellar structures, the cerebellum has been postulated to inhibit epileptic activity. However, depending on the intensity and frequency of the seizures, such inhibitory capacity may be compromised by epilepsy. Epileptic activity generated in limbic structures could reach the cerebellum, via anatomically distant but interconnected areas, and may induce severe neuronal damage. This investigation is aimed at studying the physiological and structural properties of Purkinje neurons (PNs) in the model of temporal lobe epilepsy induced by pilocarpine in rodents. In the present study, using patch clamp recordings, we show differences in the pattern of spontaneous firing of PNs recorded in adult male mice with temporal lobe epilepsy (TLE). In addiction, the concentrations of main amino acids were quantified, in the cerebellum, trough HPLC technique. PN loss was also investigated. The cerebella of adult male Wistar rats were cut at 8-10 mm, stained in Nissl preparation and nucleated cells were counted during the silent and chronic phase of the model. Most PNs of this group did not fire spontaneously in the presence of 50[mu]M picrotoxin and 5mM kynurenic acid. In addition, mice with epilepsy did not show the same potenciation in spontaneous firing rate in response to the NO donor analog 8p-CPT-cGMP (50[micro]M).
The concentrations of all amino acids tested decreased significantly in the chronic phase of the pilocarpine model of temporal lobe epilepsy.
The [italic]status epilepticus[/italic] per se was sufficient to generate neuron loss, which was aggravated after the spontaneous recurrent seizures started. In addition, we quantified the dendrite spines in Purkinje neurons during the chronic phase of the model, but observed no alterations. Taken together, the results showed different levels of alterations and damage to the cerebellar circuitry. As PNs are the main output cells of the cerebellum our finding may represent a larger cascade of events in the whole cerebellum induced by temporal lobe epilepsy. (Supported by CAPES,CNPq and FAPESP.)