Seizure elements and seizure element transitions during tonic-clonic seizure activity in the synapsin I/II double knockout mouse: a neuroethological description.
Inactivation of genes for the synaptic terminal proteins synapsin I and synapsin II leads to development of epileptic seizures in mice (Syn-DKO mice) in which no other behavioral abnormalities or any gross anatomical brain deformities have been reported. In humans, mutated synapsin I is associated with epilepsy. Thus, the Syn-DKO mouse might model human seizure development. Here we describe a neuroethological analysis of behavioral elements and relationships between these elements during seizures in Syn-DKO mice. The seizure elements belong to one of three clusters each characterized by specific patterns of activity: truncus-dominated elements, myoclonic elements, and running-fit activity. The first two clusters, constituting the majority of seizural activity, evolve quite differently during ongoing seizure activity. Whereas truncus-dominated elements unfold in a strict sequence, the myoclonic elements wax and wane more independently, once myoclonic activity has started. These differences may point to neurobiological mechanisms relevant to both rodent and human epilepsies.
Etholm
Lars
L
Department of Physiology, Institute of Basic Medical Sciences, University of Oslo, Blindern, Oslo, Norway. lars.etholm@medisin.uio.no
Heggelund
Paul
P
D000818:Animals; D001522:Behavior, Animal; D004195:Disease Models, Animal; D004569:Electroencephalography; D005260:Female; D008297:Male; D051379:Mice; D018345:Mice, Knockout; D012640:Seizures / Q000235:genetics* / Q000503:physiopathology*; D016704:Synapsins / Q000172:deficiency*; D014743:Videotape Recording
D016704:Synapsins