RGD Reference Report - TRPV1 stimulation triggers apoptotic cell death of rat cortical neurons. - Rat Genome Database

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TRPV1 stimulation triggers apoptotic cell death of rat cortical neurons.

Authors: Shirakawa, H  Yamaoka, T  Sanpei, K  Sasaoka, H  Nakagawa, T  Kaneko, S 
Citation: Shirakawa H, etal., Biochem Biophys Res Commun. 2008 Dec 26;377(4):1211-5. Epub 2008 Nov 6.
RGD ID: 2317100
Pubmed: PMID:18996081   (View Abstract at PubMed)
DOI: DOI:10.1016/j.bbrc.2008.10.152   (Journal Full-text)

Transient receptor potential vanilloid 1 (TRPV1) functions as a polymodal nociceptor and is activated by several vanilloids, including capsaicin, protons and heat. Although TRPV1 channels are widely distributed in the brain, their roles remain unclear. Here, we investigated the roles of TRPV1 in cytotoxic processes using TRPV1-expressing cultured rat cortical neurons. Capsaicin induced severe neuronal death with apoptotic features, which was completely inhibited by the TRPV1 antagonist capsazepine and was dependent on extracellular Ca(2+) influx. Interestingly, nifedipine, a specific L-type Ca(2+) channel blocker, attenuated capsaicin cytotoxicity, even when applied 2-4 h after the capsaicin. ERK inhibitor PD98059 and several antioxidants, but not the JNK and p38 inhibitors, attenuated capsaicin cytotoxicity. Together, these data indicate that TRPV1 activation triggers apoptotic cell death of rat cortical cultures via L-type Ca(2+) channel opening, Ca(2+) influx, ERK phosphorylation, and reactive oxygen species production.

Gene Ontology Annotations    Click to see Annotation Detail View

Biological Process
TermQualifierEvidenceWithReferenceNotesSourceOriginal Reference(s)
positive regulation of apoptotic process  IMP 2317100 RGD 

Objects Annotated

Genes (Rattus norvegicus)
Trpv1  (transient receptor potential cation channel, subfamily V, member 1)


Additional Information