In vivo electrophysiology of dorsal-horn neurons.

The dorsal horn of the spinal cord is a key relay in the transmission of sensory information to the brain. Furthermore, this circuitry of spinal-cord neurons, and hence the spinal processing of sensory information, is subject to a great deal of plasticity, both pharmacological and physiological, in persistent pain states. This chapter describes in detail the procedure by which the activity and pharmacological modulation of these dorsal-horn neurons can be recorded in vivo in anesthetized rats, allowing a comprehensive study of spinal sensory processing in an intact and integrated system.

The effect of ABT-702, a novel adenosine kinase inhibitor, on the responses of spinal neurones following carrageenan inflammation and peripheral nerve injury.

1. Adenosine (ADO) receptor activation modulates sensory transmission in the dorsal horn. Little is known about the circumstances underlying release of the purine.

Electrophysiologic evidence for increased endogenous gabaergic but not glycinergic inhibitory tone in the rat spinal nerve ligation model of neuropathy.

Background: Changes in the inhibitory activity mediated by gamma-aminobutyric acid (GABA) and glycine, acting at spinal GABAA receptors and strychnine-sensitive glycine receptors, are of interest in the development of neuropathic pain. There is anatomic evidence for changes in these transmitter systems after nerve injuries, and blocking either GABAA or glycine receptors has been shown to produce allodynia-like behavior in awake normal animals.

Methods: In this study, the possible changes in GABAergic and glycinergic inhibitory activity in the spinal nerve ligation model of neuropathic pain were studied by comparing the effects of the GABAA-receptor antagonist bicuculline and the glycine-receptor antagonist strychnine in neuropathic rats to their effects in sham-operated and nonoperated control rats.

Warm-coding deficits and aberrant inflammatory pain in mice lacking P2X3 receptors.

ATP activates damage-sensing neurons (nociceptors) and can evoke a sensation of pain. The ATP receptor P2X3 is selectively expressed by nociceptors and is one of seven ATP-gated, cation-selective ion channels. Here we demonstrate that ablation of the P2X3 gene results in the loss of rapidly desensitizing ATP-gated cation currents in dorsal root ganglion neurons, and that the responses of nodose ganglion neurons to ATP show altered kinetics and pharmacology resulting from the loss of expression of P2X(2/3) heteromultimers.

Role of Ca2+-permeable non-NMDA glutamate receptors in spinal nociceptive transmission.

The functional role of Ca2+-permeable non-NMDA receptors in spinal nociceptive processing was investigated using joro spider toxin (JSTx), a selective blocker of these receptors. JSTx 0.25 and 1 microg administered spinally produced a significant facilitation of the C-fibre evoked response and post-discharge, but not the A-fibre response, of dorsal horn neurones recorded in adult rats.