Responses of spinal cord dorsal horn neurones to non-noxious and noxious cutaneous temperature changes in the spinal rat.

(1) Lumbar dorsal horn units characterized by their mechanical cutaneous sensitivities were tested for their responses to temperature changes of the skin in the decerebrate spinal rats. (a) Class 1 units (i.e. driven by non-noxious mechanical stimuli) were rarely thermally sensitive. (b) Nearly all class 2 units (i.e. driven by both non-noxious and noxious mechanical stimuli) and 4 of the 5 class 3 units (i.e. driven by noxious mechanical stimuli) were sensitive to temperature changes. (2) According to their thermal response threshold and their response range, these units were divided into 3 groups. (a) Warming units whose response threshold and maximum response were below 42.5 degrees C. Such units were rarely encountered. (b) Warming/noxious heat units whose response threshold was below 42.5 degrees C but with a maximum response above this temperature. They represented approximatively one-third of the radiant heat-sensitive units. (c) Noxious heat units whose response threshold was above 42.5 degrees C and maximum discharge several degrees above it. Approximately 50% of units activated by radiant heat belonged to this group. (3) Responses to radiant heat stimulation were frequently affected by a first noxious heat application. It consisted: --in a threshold decrease and/or an increase of their cellular discharge for a same temperature range. Only observed for warming/noxious heat units and noxious heat units, this sensitization phenomenon predminantly affected noxious heat units. --in a decrease of cellular discharge for a same temperature range. This desensitization phenomenon was observed for the 3 groups of units driven by radiant heat but mainly for warming units. (4) Supramaximal transcutaneous electrical stimulation revealed that nearly all the thermally sensitive units received A delta and/or C inputs. These units were largely distributed throughout the dorsal horn (laminae I, IV and V). Ten of the 12 lamina I units responded to noxious thermal stimuli. (5) These data indicate that an increase in skin temperature is coded at the level of the rat spinal cord dorsal horn by both an increase in discharge of low threshold temperature sensitive units and a progressive recruitment of high threshold units.

Pressure-induced hydrogen bonding: structure of D2S phase I'

The full structure of the high-pressure cubic phase I' of hydrogen sulfide has been solved using neutron diffraction data. The molecules are partially rotationally disordered about the <111> axes, as in phase II at ambient pressure but with markedly greater nonuniformity of the toroidal D distribution. The changes in structure at the II-->I' transition signal the onset of significant pressure-induced hydrogen bonding.

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 0.5% formalin the oxidation current rapidly increased ((115 +/- 5)% of control at 25 min) and reached (120 +/- 6)% of control 1h later. Subsequently the voltammograms stabilized for up to 90 min and decreased ((107 +/- 4)% at 124 min). After an injection in the hindpaw of 150 microl of 4% carrageenan, the voltammograms remained at control level for 1h and then the oxidation current increased continuously for up to 4h ((145 +/- 16)% of control at 240 min); such an increase was reversed by ketamine. In these two models of inflammation, the delay in onset and the duration of the increases in NO release within the dorsal horn relate, to some extent, to the time course of the peripheral inflammatory processes, since they are shorter after formalin than after carrageenan. The results provide a direct in vivo demonstration that the intercellular messenger nitric oxide participates in the transmission of noxious afferent messages within the dorsal horn of the spinal cord following peripheral inflammation.