Vanilloid receptor loss in rat sensory ganglia associated with long term desensitization to resiniferatoxin

  title={Vanilloid receptor loss in rat sensory ganglia associated with long term desensitization to resiniferatoxin},
  author={Arpad Szallasi and Peter M. Blumberg},
  journal={Neuroscience Letters},

analgesic effects of vanilloid receptor desensitization by capsaicin in the oral surgery model

Data indicate that 100μg capsaicin demonstrates analgesic activity in a clinical model predictive of analgesia for vanilloid receptor ablation in humans, and may be due to incomplete receptor inactivation due to dose-limiting discomfort initially produced by sub-mucosal administration of Capsaicin and the contribution of other nociceptive fibers over time not containing TRPV1 receptors.

Pharmacological characterization of the vanilloid receptor in the rat dorsal spinal cord

Results suggest that the antagonistic effects of capsazepine were agonist‐independent, and the pharmacology of the vanilloid receptor in the rat dorsal spinal cord is not identical to that previously found in other systems.

Vanilloid-Induced Conduction Analgesia: Selective, Dose-Dependent, Long-Lasting, with a Low Level of Potential Neurotoxicity

Data indicate possible clinical applicability of vanilloid-induced conduction analgesia, and the frequency of unmyelinated fiber degeneration was more than an order of magnitude lower than that with the therapeutic concentration of lidocaine.

Peripherally induced resiniferatoxin analgesia

[3H]resiniferatoxin binding by the vanilloid receptor: species-related differences, effects of temperature and sulfhydryl reagents

Preincubation with heavy metal cations and other sulfhydryl-reactive agents inhibited specific [3H]RTX binding indicating that the vanilloid receptor is a thiol-protein, and that free sulfHydryl groups play an essential role in agonist binding activity.



Effects of colchicine, vinblastine and vincristine on degeneration transmitter release after sympathetic denervation studied in the conscious rat.

It is proposed that the drugs postpone the degeneration transmitter release by slowing down the rate by which an “axotomy information” is transported distally along the neuron.

Direct evidence for neurogenic inflammation and its prevention by denervation and by pretreatment with capsaicin.

The question of the role played by the sensory nerves in the mechanism of the inflammatory response arose at the beginning of this century and was almost entirely neglected in modem research and experimental work has been confined mainly to the study of axon reflex flare in human skin.

Topical capsaicin in the treatment of cutaneous disorders

The utility of capsaicin appears to be limited at present primarily by its irritant properties and secondarily by less than optimal therapeutic response, perhaps resulting from insufficient drug delivery.