Experimental partial epileptogenesis.
Identification of the responsible mutant genes and of the functional consequences of the mutations in experimental preparations have begun to shed light on mechanisms underlying a rare form of partial epilepsy in humans, autosomal dominant nocturnal frontal lobe epilepsy. Likewise, study of the mechanisms of nongenetic models of a common form of human epilepsy, complex partial epilepsy of temporal lobe origin, has established the hippocampal dentate granule cells as a functional barrier to invasion of epileptiform activity into hippocampus in normal brain; this barrier is defective in an epileptic brain. Potential mechanisms by which the 'barrier function' might become flawed, such as mossy fiber sprouting, are discussed.
Bausch
S B
SB
Department of Medicine (Neurology), Duke University Medical Center, Durham, North Carolina 27710, USA.
McNamara
J O
JO
D000818:Animals; D004195:Disease Models, Animal; D004828:Epilepsies, Partial / Q000209:etiology / Q000503:physiopathology*; D017029:Epilepsy, Complex Partial / Q000503:physiopathology; D017034:Epilepsy, Frontal Lobe / Q000235:genetics / Q000503:physiopathology; D004833:Epilepsy, Temporal Lobe / Q000503:physiopathology; D006624:Hippocampus / Q000503:physiopathology*; D006801:Humans; D007696:Kindling, Neurologic / Q000502:physiology; D019599:Mossy Fibers, Hippocampal / Q000503:physiopathology; D009414:Nerve Growth Factors / Q000502:physiology; D009433:Neural Inhibition / Q000502:physiology; D011978:Receptors, Nicotinic / Q000235:genetics; D013702:Temporal Lobe / Q000503:physiopathology*
D009414:Nerve Growth Factors; D011978:Receptors, Nicotinic