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- W2053251168 abstract "TRPV1 receptors have classically been defined as heat-sensitive, ligand-gated, nonselective cation channels that integrate nociceptive stimuli in sensory neurons. TRPV1 receptors have also been identified in the brain, but their physiological role is poorly understood. Here we report that TRPV1 channel activation is necessary and sufficient to trigger long-term synaptic depression (LTD). Excitatory synapses onto hippocampal interneurons were depressed by either capsaicin, a potent TRPV1 channel activator, or the endogenously released eicosanoid, 12-(S)-HPETE, whereas neighboring excitatory synapses onto CA1 pyramidal cells were unaffected. TRPV1 receptor antagonists also prevented interneuron LTD. In brain slices from TRPV1-/- mice, LTD was absent, and neither capsaicin nor 12-(S)-HPETE elicited synaptic depression. Our results suggest that, in the hippocampus, TRPV1 receptor activation selectively modifies synapses onto interneurons. Like other forms of hippocampal synaptic plasticity, TRPV1-mediated LTD may have a role in long-term changes in physiological and pathological circuit behavior during learning and epileptic activity." @default.
- W2053251168 created "2016-06-24" @default.
- W2053251168 creator A5027354717 @default.
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- W2053251168 creator A5043873239 @default.
- W2053251168 creator A5059663427 @default.
- W2053251168 creator A5085437683 @default.
- W2053251168 date "2008-03-01" @default.
- W2053251168 modified "2023-10-09" @default.
- W2053251168 title "TRPV1 Channels Mediate Long-Term Depression at Synapses on Hippocampal Interneurons" @default.
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- W2053251168 doi "https://doi.org/10.1016/j.neuron.2007.12.027" @default.
- W2053251168 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/2698707" @default.
- W2053251168 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/18341994" @default.
- W2053251168 hasPublicationYear "2008" @default.
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