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J. Cell Biol.,
Volume 145, Number 5, May 31, 1999 1039-1048
* Department of Cellular Neurobiology, Deletion of the synapsin I genes, encoding
one of the major groups of proteins on synaptic vesicles,
in mice causes late onset epileptic seizures and enhanced experimental temporal lobe epilepsy. However,
mice lacking synapsin I maintain normal excitatory synaptic transmission and modulation but for an enhancement of paired-pulse facilitation. To elucidate the cellular basis for epilepsy in mutants, we examined whether
the inhibitory synapses in the hippocampus from mutant mice are intact by electrophysiological and morphological means. In the cultured hippocampal synapses from mutant mice, repeated application of a
hypertonic solution significantly suppressed the subsequent transmitter release, associated with an accelerated vesicle replenishing time at the inhibitory synapses, compared with the excitatory synapses. In the
mutants, morphologically identifiable synaptic vesicles
failed to accumulate after application of a hypertonic
solution at the inhibitory preterminals but not at the excitatory preterminals. In the CA3 pyramidal cells in hippocampal slices from mutant mice, inhibitory
postsynaptic currents evoked by direct electrical stimulation of the interneuron in the striatum oriens were
characterized by reduced quantal content compared
with those in wild type. We conclude that synapsin I contributes to the anchoring of synaptic vesicles,
thereby minimizing transmitter depletion at the inhibitory synapses. This may explain, at least in part, the epileptic seizures occurring in the synapsin I mutant mice.
Department of Cell Biology and Anatomy, and § Department of Neurophysiology,
University of Tokyo, Graduate School of Medicine, Tokyo 113-0033, Japan
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