ArticleChannels (Austin, Tex.)
Further evidence for the role of IP 3R 1 in regulating subsynaptic gene expression and neuromuscular transmission.
Article in Channels (Austin, Tex.). The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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2 authors at 1 institution in 1 country.
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Abstract
The inositol 1,4,5-triphosphate IP 3R channel is highly expressed on specialized ER membrane, where it initiates a slow wave of Ca ( 2+) release from internal stores, allowing subcellular compartmentalization of Ca ( 2+) signals. In skeletal muscle, IP 3R 1 is also highly concentrated at some myonuclei, particularly near the NMJ. We have reported that in fully developed adult muscle, IP 3R 1 knockdown by siRNA increases synaptic strength at both pre- and post-synaptic sites of neuromuscular transmission, increasing both the amplitude and frequency of spontaneous quantal events and quantal content, as well as expression of AChR subunits and other NMJ-specific genes. Here, we demonstrate that reducing IP 3R 1 activity in mouse TA muscle by promoting hydrolysis locally of IP 3R 1 also amplifies expression of subsynaptic genes and transcription factors. Furthermore, using a retrograde tracer, cholera toxin B subunit, we find that siRNA-mediated silencing of IP 3R 1 in TA muscle increases vesicle trafficking. These studies suggest that postsynaptic IP 3R 1 activity regulates synaptic gene expression and neuromuscular transmission.
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