Subcutaneous formalin and intraplantar carrageenan increase nitric oxide release as measured by in vivo voltammetry in the spinal cord.

The paper describes in vivo voltammetric detection of nitric oxide with carbon fibre microelectrodes at the lumbar spinal dorsal horn level of decerebrated-spinalized rats during peripheral noxious inflammatory processes. At the lumbar (L3-L4) dorsal horn level, a nitric oxide dependent peak of oxidation current (650 mV), remaining stable for up to 4h ((92 +/- 5)% of control) could be detected indicating that significant amounts of nitric oxide are produced continuously. Following subcutaneous injection in the hindpaw of 50 microl of 0.

Increased nitric oxide release by transient peripheral noxious inputs to the spinal cord of rats: an in vivo voltammetric approach.

Using in vivo voltammetric detection of nitric oxide (NO) a previous study demonstrated an increased NO release at the lumbar dorsal horn level of the spinal cord by peripheral inflammatory processes in decerebrated-spinalized rats. This study concerns the effects of acute peripheral stimulations. Gentle non-noxious or isolated nociceptive stimulation did not modify the oxidation current due to NO.

Nitric oxide (NO) release by glutamate and NMDA in the dorsal horn of the spinal cord: an in vivo electrochemical approach in the rat.

Glutamate acts as a neurotransmitter of primary afferent messages in the spinal cord. Through glutamatergic mechanisms nitric oxide (NO) is also a potential intermediary in the transmission of sensory messages, particularly nociceptive, at the spinal level. The aim of the present study was, by using electrochemical monitoring of NO, to determine if the activation of glutamatergic transmission, particularly through NMDA receptors, could increase NO production within the dorsal horn of the lumbar spinal cord in the rat.

Cholinergic modulation of the picrotoxin-induced electrocorticographical events and behavioral "pain-like" symptoms at somatomotor cortical level in the rat.

In this study, we examined the modulation by acetylcholine of electrocorticographical (ECoG) ictal events and spontaneous pain-like behaviors following cortical application of the GABA(A) antagonist picrotoxin in the awake rat. Distilled water as vehicle, the cholinomimetic substance eserine, and the general muscarinic antagonist atropine were microinjected 10 min before the second microinjection of 2 microg picrotoxin into the hind paw region of the somatomotor cortex (SmI). Under these conditions, we observed that eserine (physostigmine, 1 microg, 10 microg, and 20 microg) did not consistently modify the number of the picrotoxin-induced ECoG spikes and bursts, but instead produced a massive enhancement of the number of hind paw licks compared with vehicle at 10 microg and, to a lesser extent, the number of the stereotyped "turn-in" and "neglected" paws following picrotoxin.

Picrotoxin produces a "central" pain-like syndrome when microinjected into the somato-motor cortex of the rat.

In this study, we report the possibility of producing marked electrocorticographic changes and "pain-like" reactions, when the GABAA antagonist picrotoxin is microinjected unilateraly into the rat somato-motor Sml cortex in the region of the hind paw. After the microinjection, we observed continuous seizure isolated spikes, spikes-and-waves, bursts, and pain-like reactions, almost exclusively confined to the hind paw. These reactions considered of lifting off the floor, licking of the paw palm or digits, biting, paw tremors, and a peculiar paw position that we called "turn-in" paw.