TRP Channels in Neuronal and Glial Signal Transduction

Harteneck, Christian; Leuner, Kristina

doi:10.5772/58232

Cited by 7 publications

(6 citation statements)

References 154 publications

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“…As mentioned before, several members of the TRPC, TRPV, TRPM, and TRPA families are expressed in neurons and glial cells in the CNS and PNS (Figure 1; Riccio et al, 2002;Moran et al, 2004;Abel and Zukin, 2008;Harteneck and Leuner, 2014;Zhang and Liao, 2015;Echeverry et al, 2016;Belrose and Jackson, 2018). Evidence has shown that TRPs in the CNS have critical roles in modulating growth cone guidance, synaptogenesis, synaptic plasticity, and in the development of several neurodegenerative diseases (Nilius, 2012;Vennekens et al, 2012;Katz et al, 2017).…”

Section: Trps Structure and Expressionmentioning

confidence: 83%

“…Similarly, in PD, insufficient input from dopaminergic neurons to basal ganglia and motor and prefrontal cortices results in enhanced inhibitory inputs, which leads not only to body movement-related symptoms but also cognitive and emotional symptoms associated to altered pain perception (Chi et al, 2018). Figure 4 shows brain's structures involved in pain perception, which include the prefrontal cortex, hippocampus, amygdala, entorhinal cortex, anterior cingulate cortex, basal ganglia, thalamus, insula, and sensory cortex (Fenton et al, 2015;Mano and Seymour, 2015;Cao et al, 2019), and TRP channels expressed in each one of these structures (Kauer and Gibson, 2009;Harteneck and Leuner, 2014;Nilius and Szallasi, 2015;Frias and Merighi, 2016;Katz et al, 2017). As described before, TRP channels have an unique role in nociceptive, neuropathic, and inflammatory pain as diverse members of their families are involved in pain pathways (Hung and Tan, 2018).…”

Section: Trps Involvement In Pain Alzheimer's and Parkinson's Diseasesmentioning

confidence: 99%

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TRP Channels Role in Pain Associated With Neurodegenerative Diseases

et al. 2020

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Transient receptor potential (TRP) are cation channels expressed in both non-excitable and excitable cells from diverse tissues, including heart, lung, and brain. The TRP channel family includes 28 isoforms activated by physical and chemical stimuli, such as temperature, pH, osmotic pressure, and noxious stimuli. Recently, it has been shown that TRP channels are also directly or indirectly activated by reactive oxygen species. Oxidative stress plays an essential role in neurodegenerative disorders, such as Alzheimer's and Parkinson's diseases, and TRP channels are involved in the progression of those diseases by mechanisms involving changes in the crosstalk between Ca 2+ regulation, oxidative stress, and production of inflammatory mediators. TRP channels involved in nociception include members of the TRPV, TRPM, TRPA, and TRPC subfamilies that transduce physical and chemical noxious stimuli. It has also been reported that pain is a complex issue in patients with Alzheimer's and Parkinson's diseases, and adequate management of pain in those conditions is still in discussion. TRPV1 has a role in neuroinflammation, a critical mechanism involved in neurodegeneration. Therefore, some studies have considered TRPV1 as a target for both pain treatment and neurodegenerative disorders. Thus, this review aimed to describe the TRP-dependent mechanism that can mediate pain sensation in neurodegenerative diseases and the therapeutic approach available to palliate pain and neurodegenerative symptoms throughout the regulation of these channels.

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Section: Trps Structure and Expressionmentioning

confidence: 83%

Section: Trps Involvement In Pain Alzheimer's and Parkinson's Diseasesmentioning

confidence: 99%

TRP Channels Role in Pain Associated With Neurodegenerative Diseases

et al. 2020

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“…We then narrowed down which TRPC(s) in the skin initiate UVB‐induced [Ca 2+ ] i elevation via the phospholipase C pathway. IP 3 activates TRPC1, TRPC4, and TRPC5 channels, whereas diacylglycerol activates TRPC6 and TRPC7 channels (Harteneck & Leuner, ). No difference was observed in uncaged IP 3 –mediated Ca 2+ influx in keratinocytes in the presence or absence of UVB pre‐exposure (Figure a,b).…”

Section: Resultsmentioning

confidence: 99%

Nociceptive transient receptor potential canonical 7 (TRPC7) mediates aging‐associated tumorigenesis induced by ultraviolet B

Hsu

Tsai

et al. 2019

Aging Cell

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Aging, cancer, and longevity have been linked to intracellular Ca2+ signaling and nociceptive transient receptor potential (TRP) channels. We found that TRP canonical 7 (TRPC7) is a nociceptive mechanoreceptor and that TRPC7 channels specifically mediate the initiation of ultraviolet B (UVB)‐induced skin aging and tumor development due to p53 gene family mutations. Within 30 min after UVB irradiation, TRPC7 mediated UVB‐induced Ca2+ influx and the subsequent production of reactive oxygen species in skin cells. Notably, this function was unique to TRPC7 and was not observed for other TRP channels. In TRPC7 knockout mice, we did not observe the significant UVB‐associated pathology seen in wild‐type mice, including epidermal thickening, abnormal keratinocyte differentiation, and DNA damage response activation. TRPC7 knockout mice also had significantly fewer UVB‐induced cancerous tumors than did wild‐type mice, and UVB‐induced p53 gene family mutations were prevented in TRPC7 knockout mice. These results indicate that TRPC7 activity is pivotal in the initiation of UVB‐induced skin aging and tumorigenesis and that the reduction in TRPC7 activity suppresses the UVB‐induced aging process and tumor development. Our findings support that TRPC7 is a potential tumor initiator gene and that it causes cell aging and genomic instability, followed by a change in the activity of proto‐oncogenes and tumor suppressor genes to promote tumorigenesis.

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“…Channels of the TRPC family which are known to be expressed in the brain are TRPC1, TRPC4, TRPC5 [91], TRPC3 and TRPC6 [92]. While TRPC1, TRPC4 and TRPC5 are activated via IP3, TRPC2, TRPC3, TRPC6 and TRPC7 are activated via diacylglycerol (DAG) [93]. TRPC1 expression has been described on OPC, where it mediates OPC differentiation [94].…”

Section: Trp Channelsmentioning

confidence: 99%

Strategies for Neuroprotection in Multiple Sclerosis and the Role of Calcium

Enders

Heider

Ludwig

et al. 2020

IJMS

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Calcium ions are vital for maintaining the physiological and biochemical processes inside cells. The central nervous system (CNS) is particularly dependent on calcium homeostasis and its dysregulation has been associated with several neurodegenerative disorders including Parkinson's disease (PD), Alzheimer's disease (AD) and Huntington's disease (HD), as well as with multiple sclerosis (MS). Hence, the modulation of calcium influx into the cells and the targeting of calcium-mediated signaling pathways may present a promising therapeutic approach for these diseases. This review provides an overview on calcium channels in neurons and glial cells. Special emphasis is put on MS, a chronic autoimmune disease of the CNS. While the initial relapsing-remitting stage of MS can be treated effectively with immune modulatory and immunosuppressive drugs, the subsequent progressive stage has remained largely untreatable. Here we summarize several approaches that have been and are currently being tested for their neuroprotective capacities in MS and we discuss which role calcium could play in this regard.

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TRP Channels in Neuronal and Glial Signal Transduction

Cited by 7 publications

References 154 publications

TRP Channels Role in Pain Associated With Neurodegenerative Diseases

TRP Channels Role in Pain Associated With Neurodegenerative Diseases

Nociceptive transient receptor potential canonical 7 (TRPC7) mediates aging‐associated tumorigenesis induced by ultraviolet B

Strategies for Neuroprotection in Multiple Sclerosis and the Role of Calcium

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