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• W3174694564 abstract "In cerebellar circuitry the Purkinje cells (PCs) are the most prominent neuronal element and are characterized by thick and highly branched dendritic tree. The signaling molecule PKCγ is critically linked to Purkinje cell function and has a strong negative impact on the dendritic growth and development of PCs. Recent evidence links enhanced PKCγ to long-term alteration in calcium equilibrium in PCs. Observations also show that blocking the voltage gated calcium channels could partially or completely protect Purkinje cell dendrites from stunted growth thought to be associated with enhanced PKCγ activity. Additional evidence from moon walker mutant mice also link the increased calcium influx through TRPC3 channels to dampened dendritic morphology. In this study we investigate that how the calcium influx and homoeostasis is regulated in PCs? Here, we propose an integrated model of calcium equilibrium in PCs, by converging the mGluR1 induced membrane generation of DAG and calcium influx through TRPC3 channels into an integrated signaling cascade. The model proposed here link the DAG generation after membrane depolarization to PKCγ activation as well as the activation of TRPC3 through direct binding of DAG. This proposed signaling cascade suggests that DAG signaling in Purkinje cells is tightly regulated through a double-negative feed-back loop. The results show that DAG- PKCγ-DGKγ axis forms the first negative feedback loop whereas, the DAG-TRPC3-PKCγ-DGKγ axis forms the second negative feedback loop where, both PKCγ and DGKγ molecules in second negative feedback loop are contributing due to Ca+2 influx through TRPC3 channel, which in turn, stimulates the cytosol-to-membrane translocation of these molecules in PCs. Our results suggest that for wild-type case the double negative feedback on DAG and subsequently on TRPC3 channel is exquisite and specific enough to maintain the calcium homeostasis in PCs, thus ensuring their viability. However, for PKCγ with enhanced activity the second double negative feedback loop is not able to tightly regulate the gating characteristics of TRPC3 channels thus disrupting the calcium homeostasis and leading to degeneration and dysfunction of PCs. Support or Funding Information Private Funding This abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal." @default.
• W3174694564 created "2021-07-05" @default.
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• W3174694564 date "2019-04-01" @default.
• W3174694564 modified "2023-09-23" @default.
• W3174694564 title "How the calcium influx and homeostasis might be disrupted in the Purkinje cell degeneration and cerebellar dysfunction?" @default.
• W3174694564 doi "https://doi.org/10.1096/fasebj.2019.33.1_supplement.802.47" @default.
• W3174694564 hasPublicationYear "2019" @default.
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