| Article ID | Journal | Published Year | Pages | File Type |
|---|---|---|---|---|
| 3050809 | Epilepsy & Behavior | 2009 | 9 Pages |
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.
