S Mense1, U Hoheisel. 1. Institut für Anatomie und Zellbiologie III, Universität Heidelberg.
Abstract
AIM OF THE STUDY: The role of nitric oxide (NO) in the processing of nociceptive information is controversely discussed. The present review aims at answering the questions how a spinal lack of NO influences the discharge behaviour of dorsal horn neurones, and if the NO-synthesising neurones exhibit a change in histologically visualised cell numbers under the influence of a nociceptive input from the body periphery. METHODS: The data were obtained from anaesthetised rats. The impulse activity of single sensory dorsal horn neurones was recorded with glass microelectrodes. In the spinal segments studied, the NO synthase (NOS) was blocked with L-NAME. The NO-synthesising cells were visualized histochemically with the diaphorase reaction or immunohistochemically with antibodies to the NOS. RESULTS: The inhibition of the NO synthesis by L-NAME was followed by a marked increase in the background activity almost exclusively in nociceptive neurones. In the histological evaluation, the NO-synthesising neurones reacted to a nociceptive input with an initial increase in cell number which was followed by a decrease. CONCLUSIONS: Normally, a tonic release of NO in the spinal cord appears to exist which inhibits the discharges of nociceptive dorsal horn neurones. Accordingly, a local lack of NO synthesis leads to an increase in the electrical activity in these neurones. Under chronic painful conditions there is a decrease in the number of NO-synthesising cells which is associated with a lack of NO in the dorsal horn. If such changes occur also in patients they are likely to cause spontaneous pain. Thus, NO could be an important factor for spontaneous pain in patients with chronic painful lesions in the body periphery.
AIM OF THE STUDY: The role of nitric oxide (NO) in the processing of nociceptive information is controversely discussed. The present review aims at answering the questions how a spinal lack of NO influences the discharge behaviour of dorsal horn neurones, and if the NO-synthesising neurones exhibit a change in histologically visualised cell numbers under the influence of a nociceptive input from the body periphery. METHODS: The data were obtained from anaesthetised rats. The impulse activity of single sensory dorsal horn neurones was recorded with glass microelectrodes. In the spinal segments studied, the NO synthase (NOS) was blocked with L-NAME. The NO-synthesising cells were visualized histochemically with the diaphorase reaction or immunohistochemically with antibodies to the NOS. RESULTS: The inhibition of the NO synthesis by L-NAME was followed by a marked increase in the background activity almost exclusively in nociceptive neurones. In the histological evaluation, the NO-synthesising neurones reacted to a nociceptive input with an initial increase in cell number which was followed by a decrease. CONCLUSIONS: Normally, a tonic release of NO in the spinal cord appears to exist which inhibits the discharges of nociceptive dorsal horn neurones. Accordingly, a local lack of NO synthesis leads to an increase in the electrical activity in these neurones. Under chronic painful conditions there is a decrease in the number of NO-synthesising cells which is associated with a lack of NO in the dorsal horn. If such changes occur also in patients they are likely to cause spontaneous pain. Thus, NO could be an important factor for spontaneous pain in patients with chronic painful lesions in the body periphery.