Excitatory amino acids modulate epileptogenesis in the brain stem.

Activation of cholinergic mechanisms in the pontine reticular formation by local microinjections of carbachol was shown to induce pontine electrographic seizures and clonic convulsions. In this study we found that glutamate microinjections into the pons induced similar electrographic seizures and clonic convulsions. Microinjections into the PRF of glutamate in subconvulsive doses prior to carbachol potentiated the epileptogenic effect of carbachol. The duration of the seizure activity increased and the convulsions became more severe. The NMDA receptor antagonist MK-801 and the non-NMDA receptor antagonists DNQX significantly reduced the potentiating effect of glutamate. These results indicate a possible role of EAA receptors in the generation of epilepsy in the pons. They also suggest the importance of studying the role of synergistic interactions between EAA mechanisms and cholinergic mechanisms in the various pontine functions.