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Diana M. Bautista

Researcher at University of California, Berkeley

Publications -  71
Citations -  16779

Diana M. Bautista is an academic researcher from University of California, Berkeley. The author has contributed to research in topics: Transient receptor potential channel & Mechanotransduction. The author has an hindex of 32, co-authored 69 publications receiving 14748 citations. Previous affiliations of Diana M. Bautista include University of California & Helen Wills Neuroscience Institute.

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Journal ArticleDOI

Cellular and Molecular Mechanisms of Pain

TL;DR: Genetic, electrophysiological, and pharmacological studies are elucidating the molecular mechanisms that underlie detection, coding, and modulation of noxious stimuli that generate pain.
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Mustard oils and cannabinoids excite sensory nerve fibres through the TRP channel ANKTM1

TL;DR: It is shown that mustard oil depolarizes a subpopulation of primary sensory neurons that are also activated by capsaicin, the pungent ingredient in chilli peppers, and by Δ9-tetrahydrocannabinol, the psychoactive component of marijuana.
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TRPA1 mediates the inflammatory actions of environmental irritants and proalgesic agents.

TL;DR: Using TRPA1-deficient mice, it is shown that this channel is the sole target through which mustard oil and garlic activate primary afferent nociceptors to produce inflammatory pain.
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The menthol receptor TRPM8 is the principal detector of environmental cold

TL;DR: It is shown that cultured sensory neurons and intact sensory nerve fibres from TRPM8-deficient mice exhibit profoundly diminished responses to cold, validating the hypothesis that TRP channels are the principal sensors of thermal stimuli in the peripheral nervous system.
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TRPA1 mediates formalin-induced pain

TL;DR: It is shown that TRPA1 is the principal site of formalin's pain-producing action in vivo, and that activation of this excitatory channel underlies the physiological and behavioral responses associated with this model of pain hypersensitivity.