| Abstract No.: | 102 |
| Country: | Canada |
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| Title: | REGULATION OF SYNAPTIC STRUCTURE BY NEURONAL ACTIVITY |
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| Authors/Affiliations: | Mei Zhen, Ph.D, Senior Principal Investigator, Samuel Lunenfeld Research Institute, Canada Research Chair, Toronto, ON, Canada |
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| Content: | Ion channels regulate neuron excitability through selective ion flux. Typically, voltage-gated sodium channels generate action potentials along axons, whereas voltage-gated calcium channels induce Ca2+ transients at cell bodies and synapses that lead to neuron excitation and synaptic transmission. We identified a gain-of-function allele of NCA-1/UNC-77, a novel conserved C. elegans protein with partial homology to ?1 subunits of voltage-gated sodium/calcium channels. nca-1 gain-of-function mutants display abnormal active zone development patterns, increased synaptic Ca2+ transient amplitude and hyperactive locomotion. Loss of NCA activities leads to Ca2+ transient silencing at synapses and frequent halting in locomotion, but does not affect Ca2+ transients at cell bodies. NCA-1 localizes along axons but is excluded from synapses. Its localization and function are inter-dependent on UNC-79 and UNC-80, two novel but evolutionarily conserved proteins that are also localized at non-synaptic regions. We propose that NCA-1, UNC-79 and UNC-80 are components of a new channel family that regulates synaptic activity and morphology by propagating or modulating depolarization signals from cell bodies to synapses.
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