Aberrant synapse formation has been implicated in development and prop
agation of epileptic potential. Litzinger et al. (1993a) showed that o
mega-GVIA conotoxin may be used as a marker for synapse formation in n
onepileptic mice. We conducted omega-GVIA binding in synaptosomal prep
arations from epileptic DBA/2J mice at different developmental ages. B
inding in DBA/2J mice was compared with omega-GVIA binding in synaptos
omal preparations from nonepileptic C57/B1, Swiss Webster, and AJ mice
. Striking differences between these strains of mice are evident in th
e developmental sequence and pattern of N-type voltage:sensitive calci
um channels (VSCC). In contrast to nonepileptic mice, the DBA/2J mice
show a slow increase in omega-GVIA binding between postnatal days 2 an
d 8. This increase corresponds to onset of susceptibility to seizure i
n this strain. In addition to the difference in developmental sequence
, DBA/2J mice have fewer binding sites for omega-GVIA throughout devel
opment, 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 pre
synaptic membranes responsible for neurotransmitter release may repres
ent a change in synaptic activity that plays a role in epileptogenesis
.