Axonal sprouting and synaptogenesis in temporal lobe epilepsy: possible pathogenetic and therapeutic roles of neurite growth inhibitory factors.
Axonal sprouting and synaptic reorganization within the temporal lobe following neuronal injury have been implicated in the pathogenesis of temporal lobe epilepsy (TLE). The molecular species responsible for these structural changes have yet to be fully defined. The recent characterization of molecules whose normal function within the nervous system is to inhibit neurite outgrowth and synaptogenesis prompts the suggestion that a diminution or loss of such molecules might be of relevance to the pathogenesis of TLE. If so, the possibility of developing a novel therapeutic approach to TLE, distinct from currently available symptomatic therapies, to arrest the pathogenetic processes is also raised.
Larner
A J
AJ
University of Cambridge Department of Anatomy, UK.
D000544:Alzheimer Disease / Q000188:drug therapy / Q000503:physiopathology; D000818:Animals; D001369:Axons / Q000187:drug effects / Q000502:physiology; D001921:Brain / Q000187:drug effects / Q000503:physiopathology; D004833:Epilepsy, Temporal Lobe / Q000139:chemically induced / Q000188:drug therapy* / Q000503:physiopathology*; D006801:Humans; D007608:Kainic Acid / Q000009:adverse effects / Q000494:pharmacology; D009414:Nerve Growth Factors / Q000009:adverse effects / Q000494:pharmacology / Q000627:therapeutic use*; D009473:Neuronal Plasticity; D051381:Rats; D018079:Receptors, GABA / Q000187:drug effects; D016194:Receptors, N-Methyl-D-Aspartate / Q000187:drug effects; D013569:Synapses / Q000187:drug effects / Q000502:physiology
D009414:Nerve Growth Factors; D018079:Receptors, GABA; D016194:Receptors, N-Methyl-D-Aspartate; D007608:Kainic Acid