Abstract
Recent evidence suggests that SNARE fusion machinery play critical roles in postsynaptic neurotransmitter receptor trafficking, which is essential for synaptic plasticity. However, the key SNAREs involved remain highly controversial; syntaxin-3 and syntaxin-4 are leading candidates for the syntaxin isoform underlying postsynaptic plasticity. In a previous study, we showed that pyramidal-neuron specific conditional knockout (cKO) of syntaxin-4 significantly reduces basal transmission, synaptic plasticity and impairs postsynaptic receptor trafficking. However, this does not exclude a role for syntaxin-3 in such processes. Here, we generated and analyzed syntaxin-3 cKO mice. Extracellular field recordings in hippocampal slices showed that syntaxin-3 cKO did not exhibit significant changes in CA1 basal neurotransmission or in paired-pulse ratios. Importantly, there were no observed differences during LTP in comparison to control mice. Syntaxin-3 cKO mice performed similarly as the controls in spatial and contextual learning tasks. Consistent with the minimal effects of syntaxin-3 cKO, syntaxin-3 mRNA level was very low in hippocampal and cortex pyramidal neurons, but strongly expressed in the corpus callosum and caudate axon fibers. Together, our data suggest that syntaxin-3 is dispensable for hippocampal basal neurotransmission and synaptic plasticity, and further supports the notion that syntaxin-4 is the major isoform mediating these processes.
Highlights
Recent evidence suggests that soluble NSF-attachment protein receptor (SNARE) fusion machinery play critical roles in postsynaptic neurotransmitter receptor trafficking, which is essential for synaptic plasticity
We examined the role of the t-SNARE syntaxin-3 in synaptic transmission and synaptic plasticity in vivo using syntaxin-3 conditional knockout (cKO) mice (Figs. 1 and 2)
We observed no significant differences between syntaxin-3 cKO mice and control mice with respect to basal CA1 neurotransmission, long-term potentiation (LTP), learning and memory (Figs. 3–6)
Summary
Recent evidence suggests that SNARE fusion machinery play critical roles in postsynaptic neurotransmitter receptor trafficking, which is essential for synaptic plasticity. We showed that pyramidalneuron specific conditional knockout (cKO) of syntaxin-4 significantly reduces basal transmission, synaptic plasticity and impairs postsynaptic receptor trafficking. This does not exclude a role for syntaxin-3 in such processes. Syntaxin-4 cKO caused a drastic decrease in NMDA current which could impair NMDA- and Ca2+-dependent LTP induction[17,18] These data do not directly indicate a functional role of syntaxin-4 in AMPAR delivery during LTP and implicate a possible role of another syntaxin isoform, potentially syntaxin-3 in such processes[11]. We generated syntaxin-3 cKO mice and performed electrophysiological and behavioral analyses to further examine the role of syntaxin-3 in postsynaptic basal neurotransmission, synaptic plasticity, learning and memory
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