Evidence that TRPC1 is involved in hippocampal glutamate-induced cell death

Narayanan, Kishore; Irmady, Krithi; Subramaniam, Srinivasa; Unsicker, Klaus; Halbach, Oliver von Bohlen und

doi:10.1016/j.neulet.2008.09.034

Cited by 32 publications

(25 citation statements)

References 19 publications

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“…A previous study suggested that TRPC1 plays a critical role in glutamate-induced excitotoxicity in the hippocampus in slice cultures [77]. However, we failed to detect any significant reduction in pilocarpine-induced neuronal cell death in the hippocampus in TRPC1KO mice.…”

Section: The Role Of Trpc1 4 5 In Seizure and Excitotoxicity In contrasting

confidence: 89%

The Role of Canonical Transient Receptor Potential Channels in Seizure and Excitotoxicity

Zheng

Phelan

2014

Cells

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Canonical transient receptor potential (TRPC) channels are a family of polymodal cation channels with some degree of Ca2+ permeability. Although initially thought to be channels mediating store-operated Ca2+ influx, TRPC channels can be activated by stimulation of Gq-coupled G-protein coupled receptors, or by an increase in intracellular free Ca2+ concentration. Thus, activation of TRPC channels could be a common downstream event of many signaling pathways that contribute to seizure and excitotoxicity, such as N-methyl-D-aspartate (NMDA) receptor-mediated Ca2+ influx, or metabotropic glutamate receptor activation. Recent studies with genetic ablation of various TRPC family members have demonstrated that TRPC channels, in particular heteromeric TRPC1/4 channels and homomeric TRPC5 channels, play a critical role in both pilocarpine-induced acute seizures and neuronal cell death. However, exact underlying mechanisms remain to be fully elucidated, and selective TRPC modulators and antibodies with better specificity are urgently needed for future research.

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Section: The Role Of Trpc1 4 5 In Seizure and Excitotoxicity In contrasting

confidence: 89%

The Role of Canonical Transient Receptor Potential Channels in Seizure and Excitotoxicity

Zheng

Phelan

2014

Cells

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“…Indeed, TRPC1 is a key channel mediating the depolarizing effects of leptins in hypothalamic proopiomelanocortin neurons (Qiu et al, 2010). TRPC1 also mediates glutamate-induced neuronal death and may represent a promising target for pharmacological intervention to prevent or at least reduce glutamateinduced neuronal damage (Narayanan et al, 2008).…”

Section: A Canonical Transient Receptor Potential Subfamilymentioning

confidence: 99%

Transient Receptor Potential Channels as Drug Targets: From the Science of Basic Research to the Art of Medicine

2014

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“…Accumulating evidence suggest that glutamate, an excitatory neurotransmitter intimately involved in learning and memory, is also involved in neurodegeneration [47,48]. Recently, Narayanan et al reported that glutamate activates cell death by massive increases in [Ca 2+ ] i via the TRPC1 channel [49]. TRPC1 expression was increased after glutamate treatment and 2APB, a blocker of TRPC channels, significantly reduces cell death in hippocampal organotypic slice cultures.…”

Section: Diverse Function Of Trpc In Neuronsmentioning

confidence: 99%

TRPC Channels and their Implications for Neurological Diseases

Selvaraj

Sun

Singh

2010

CNSNDDT

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Calcium is an essential intracellular messenger and serves critical cellular functions in both excitable and non-excitable cells. Most of the physiological functions in these cells are uniquely regulated by changes in cytosolic Ca2+ levels ([Ca2+]i), which are achieved via various mechanisms. One of these mechanism(s) is activated by the release of Ca2+ from the endoplasmic reticulum (ER), followed by Ca2+ influx across the plasma membrane (PM). Activation of PM Ca2+ channels is essential for not only refilling of the ER Ca2+ stores, but is also critical for maintaining [Ca2+]i that regulates biological functions, such as neurosecretion, sensation, long term potentiation, synaptic plasticity, gene regulation, as well as cellular growth and differentiation. Alterations in Ca2+ homeostasis have been suggested in the onset/progression of neurological diseases, such as Parkinson's, Alzheimer's, bipolar disorder, and Huntington's diseases. Available data on transient receptor potential conical (TRPC) protein indicate that these proteins initiate Ca2+ entry pathways and are essential in maintaining cytosolic, ER, and mitochondrial Ca2+ levels. A number of biological functions have been assigned to these TRPC proteins. Silencing of TRPC1 and TRPC3 has been shown to inhibit neuronal proliferation and loss of TRPC1 is implicated in neurodegeneration. Thus, TRPC channels not only contribute towards normal physiological processes, but are also implicated in several human pathological conditions. Overall, it is suggested that these channels could be used as potential therapeutic targets for many of these neurological diseases. Thus, in this review we have focused on the functional implication of TRPC channels in neuronal cells along with the elucidation of their role in neurodegeneration.

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Evidence that TRPC1 is involved in hippocampal glutamate-induced cell death

Cited by 32 publications

References 19 publications

The Role of Canonical Transient Receptor Potential Channels in Seizure and Excitotoxicity

The Role of Canonical Transient Receptor Potential Channels in Seizure and Excitotoxicity

Transient Receptor Potential Channels as Drug Targets: From the Science of Basic Research to the Art of Medicine

TRPC Channels and their Implications for Neurological Diseases

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