Abstract:
:Aberrant synapse formation has been implicated in development and propagation of epileptic potential. Litzinger et al. (1993a) showed that omega-GVIA conotoxin may be used as a marker for synapse formation in nonepileptic mice. We conducted omega-GVIA binding in synaptosomal preparations from epileptic DBA/2J mice at different developmental ages. Binding in DBA/2J mice was compared with omega-GVIA binding in synaptosomal preparations from nonepileptic C57/B1, Swiss Webster, and AJ mice. Striking differences between these strains of mice are evident in the developmental sequence and pattern of N-type voltage-sensitive calcium channels (VSCC). In contrast to nonepileptic mice, the DBA/2J mice show a slow increase in omega-GVIA binding between postnatal days 2 and 8. This increase corresponds to onset of susceptibility to seizure in this strain. In addition to the difference in developmental sequence, DBA/2J mice have fewer binding sites for omega-GVIA throughout development, suggesting changes in channel structure or number. These data show that in DBA/2J mice development of the VSCC in brain is different from that in nonepileptic mice. This difference in development in presynaptic membranes responsible for neurotransmitter release may represent a change in synaptic activity that plays a role in epileptogenesis.
journal_name
Epilepsiajournal_title
Epilepsiaauthors
Esplin MS,Abbott JR,Smart ML,Burroughs AF,Frandsen TC,Litzinger MJdoi
10.1111/j.1528-1157.1994.tb02533.xsubject
Has Abstractpub_date
1994-09-01 00:00:00pages
911-4issue
5eissn
0013-9580issn
1528-1167journal_volume
35pub_type
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