Feline generalized penicillin epilepsy: changes of glutamic acid and taurine parallel the progressive increase in excitability of the cortex.

Abstract

A coinciding temporal sequence of electrophysiological and biochemical correlates of developing generalized penicillin epilepsy in cats may indicate a "cause and effect" relationship between the two phenomena. After intramuscular injection of penicillin, in the pre-epileptic state prior to the onset of spike-and-wave discharge, the cortical content of glutamic acid decreases. This change occurs when an increased amplitude of visual evoked potentials in association cortex heralds the approach of spike-and-wave activity. The decrease of glutamic acid and that of aspartic acid occur in parallel with an almost stoichiometric increase of glutamine, gamma-aminobutyric acid (GABA), or both, while taurine levels in the pre-epileptic state remain near normal. As the pre-epileptic progresses to the epileptic state, characterized by generalized 4-5 cycles/s spike-and-wave discharges, a failure of the glial capture mechanisms for taurine and glutamate appears to occur, since both amino acids are lost from the tissue and glutamine levels fall while GABA levels are maintained or become elevated but increasingly at the expense of aspartic acid. A presumed increase in interstitial glutamic acid concentration possibly in combination with subsequent failure of GABA inhibition appears the most plausible explanation for the increasing hyperexcitability during the development of feline generalized penicillin epilepsy.