Changes in GABA-immunoreactive cell density during motor focal epilepsy induced by cobalt in the rat.

The distribution of GABA-immunoreactive cell bodies and terminals was studied using an anti-GABA serum during the development of chronic focal epilepsy induced by cobalt deposits onto the motor cortex of the rat. Cell counts of GABA-positive neurons were carried out in the epileptogenic area and correlated with the electrophysiological activity of the cobalt focus. In normal control rats, we identified GABA-immunoreactive somata and processes in the motor agranular cortex; they were multipolar or bipolar but never pyramidal and were present in all layers, especially in layer II. GABA-immunoreactive terminals were widely scattered in the neuropil and surrounded the unlabelled cell bodies. In the cobalt-treated animals, changes in the GABAergic innervation were observed during the development of the epileptic focus: decreases in the GABA-positive cell density and in the number of GABA-positive terminals were present before the onset of epileptic discharges and became more marked during the period of maximal spiking activity; a progressive return to normal values of GABA-positive cell density (except in the deep layers) as well as the reappearance of GABA positive terminals were associated with the extinction of the epileptic syndrome. Our observations suggest that the impaired inhibitory neurotransmission mediated by GABA plays a role in the development of the cobalt-induced epilepsy; moreover the recovery of GABAergic function which occurs during the extinction of the epileptic syndrome might imply a capacity for axonal regeneration of the GABAergic neurons.