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Modulation of defensive behavior by Transient Receptor Potential Vanilloid Type-1 (TRPV1) Channels
2014, Neuroscience and Biobehavioral ReviewsCitation Excerpt :This subset of bipolar neurons is involved in the development of chronic pain. Their cellular bodies are located in the dorsal root (DRG), nodose and trigeminal ganglion, from where they send terminals that make synapses with second-order neurons in the central nervous system (CNS; Chad et al., 1983; Holzer, 1991; Szallasi, 1995; Williams and Zieglgansberger, 1982). It was later found that capsaicin effects were antagonized in a competitive way by a drug named capsazepine (Walpole et al., 1994).
Chapter 4 TRPV1: A Polymodal Sensor in the Nociceptor Terminal
2006, Current Topics in MembranesCitation Excerpt :The subsequent development of an antagonist of vanilloid action, capsazepine (Fig. 1), by Bevan and colleagues allowed the “vanilloid receptor” to be further defined as a distinct pharmacological site (Bevan et al., 1992). Data derived from the application of electrophysiological and fluorescent calcium imaging methods to cultured sensory neurons or explanted ganglia provided further evidence that vanilloid receptor binding could lead to the activation of nociceptive neurons by triggering the activation of a nonselective cation channel, leading to Na+ and Ca2+ influx (Williams and Zieglgansberger, 1982; Baccaglini and Hogan, 1983; Heyman and Rang, 1985; Marsh et al., 1987; Winter, 1987; Bleakman et al., 1990; Bevan and Docherty, 1993; Oh et al., 1996). These events have two consequences.
Nasal receptors responding to noxious chemical irritants
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