ABSTRACT
The development of new analogues of excitatory amino acids has led to the detection of three subclasses of excitatory receptor in the brain and spinal cord. These receptor subtypes, categorized by the electrophysiological potency of certain agonists, have become known as n-methyl-d-aspartate, quisqualate, and kainate receptors, abbreviated A1, A2, and A3, respectively. Glutamate given systemically can cause tissue lesions in the circumventricular organs of the brain where there is effectively no blood-brain barrier due to the presence of fenestrated capillaries. Kainate injected into the striatum usually causes hippocampal neurodegeneration as well. The necrotic lesions produced can become chronically epileptogenic and may produce spontaneous recurrent seizures in rats. Massive spillover of glutamate to the extracellular space could be expected to occur during brain damage due to head trauma or even following brain surgery, both of which can result in epilepsy. Kindling is an animal model which is increasingly used for studying the biochemistry and pharmacology of epilepsy.
