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Abstract
Ca2+ entry is essential for regulating vital physiological functions in all neuronal cells. Although neurons are engaged in multiple modes of Ca2+ entry that regulates variety of neuronal functions, we will only discuss a subset of specialized Ca2+-permeable non-selective Transient Receptor Potential Canonical (TRPC) channels and summarize their physiological and pathological role in these excitable cells. Depletion of endoplasmic reticulum (ER) Ca2+ stores, due to G-protein coupled receptor activation, has been shown to activate TRPC channels in both excitable and non-excitable cells. While all seven members of TRPC channels are predominately expressed in neuronal cells, the ion channel properties, mode of activation, and their physiological responses are quite distinct. Moreover, many of these TRPC channels have also been suggested to be associated with neuronal development, proliferation and differentiation. In addition, TRPCs also regulate neurosecretion, long-term potentiation and synaptic plasticity. Similarly, perturbations in Ca2+ entry via the TRPC channels have been also suggested in a spectrum of neuropathological conditions. Hence, understanding the precise involvement of TRPCs in neuronal function and in neurodegenerative conditions would presumably unveil avenues for plausible therapeutic interventions for these devastating neuronal diseases.
Highlights
In neurons, Ca2+ is essential for a variety of physiological processes that regulate functions, such as gene transcription to neuronal growth, survival and even differentiation [1]
TRPC3 and TRPC6 expressions were decreased in neuronal stem cell (NSC) populations [55,56]. These results suggest that perhaps in NSC cells, TRPC1 could associate with TRPC4 rather than
Expression of a dominant-negative TRPC1-pore mutant (F561A) in cerebellar Purkinje neurons resulted in a 49% reduction of mGluR-evoked slow excitatory postsynaptic currents (EPSCs), whereas fast transmission mediated by AMPA-type glutamate receptors remained unaffected, indicating that mGluR1 receptor activation is essential for the gating of TRPC1
Summary
Ca2+ is essential for a variety of physiological processes that regulate functions, such as gene transcription to neuronal growth, survival and even differentiation [1]. Influx could be more directly controlled either by store-depletion per se (through SOCE), or by the activation of the G-protein coupled receptors, or by the alterations in the membrane potential (through the activation of the voltage-gated Ca2+ channels). SOCE mechanism is essential for the refilling of the ER Ca2+ stores, but is critical for maintaining [Ca2+]i that regulates neuronal functions, such as neurosecretion, sensation, long-term potentiation, synaptic plasticity, gene regulation, as well as neuronal growth and differentiation. SOCE channels maintain a prolonged increase in cytosolic Ca2+ upon stimulation that is essential for the refilling of the ER Ca2+ stores, but can activate many of the Ca2+-dependent processes that regulates neuronal functions. A number of biological functions have been assigned to these TRPC proteins and are presented in this review [6,7,8,9]
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