Kindling: the first decade.
The kindling phenomenon is a progressive increase in the strength of epileptiform activity evoked by spaced (in time) and repeated electrical stimulation of certain brain structures. The work that has been done on the kindling phenomenon is reviewed, with an emphasis on those studies that deal with underlying mechanisms. Based on the work that has been done thus far, it is clear that the kindling effect is not due to any type of gross tissue damage. It is also clear that at least some of the effects are due to changes at the synapse and that these changes are widely distributed in the brain. The changes might be due to an increasing efficacy at excitatory synapses or a decreased effectiveness at inhibitory synapses, or both. The long term post-tetanic potentiation data and some preliminary electron microscopic studies support the former mechanism, whereas the depletions of catecholamines in kindled tissue support the latter. In addition to these transynaptic changes, there may be other changes that occur at the site of the stimulating electrode, and these changes may be based on a different mechanism. These ideas and the relevant data are discussed.
D000818:Animals; D000927:Anticonvulsants / Q000494:pharmacology; D001522:Behavior, Animal; D001921:Brain / Q000187:drug effects / Q000502:physiology*; D002415:Cats; D004195:Disease Models, Animal; D004285:Dogs; D004558:Electric Stimulation; D004594:Electrophysiology; D004827:Epilepsy / Q000209:etiology / Q000503:physiopathology*; D000882:Haplorhini; D006801:Humans; D009434:Neural Pathways; D011817:Rabbits; D051381:Rats; D013569:Synapses / Q000187:drug effects / Q000502:physiology*
D000927:Anticonvulsants