TRPV1 activity and substance P release are required for corneal cold nociception
As a protective mechanism, the cornea is sensitive to noxious stimuli. Here, we show that in
mice, a high proportion of corneal TRPM8+ cold-sensing fibers express the heat-sensitive
TRPV1 channel. Despite its insensitivity to cold, TRPV1 enhances membrane potential
changes and electrical firing of TRPM8+ neurons in response to cold stimulation. This
elevated neuronal excitability leads to augmented ocular cold nociception in mice. In a
model of dry eye disease, the expression of TRPV1 in TRPM8+ cold-sensing fibers is …
mice, a high proportion of corneal TRPM8+ cold-sensing fibers express the heat-sensitive
TRPV1 channel. Despite its insensitivity to cold, TRPV1 enhances membrane potential
changes and electrical firing of TRPM8+ neurons in response to cold stimulation. This
elevated neuronal excitability leads to augmented ocular cold nociception in mice. In a
model of dry eye disease, the expression of TRPV1 in TRPM8+ cold-sensing fibers is …
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