The role of spinal nitric oxide in the control of spontaneous pain following nociceptive input

Abstract

Publisher Summary This chapter discusses the role of spinal nitric oxide in the control of spontaneous pain following nociceptive input. The constitutive neuronal nitric oxide synthase (nNOS or NOS I) shows mark changes in expression during pathological alteration of peripheral tissues and, therefore, is assumed to be involved in lesion-induced central nervous changes. The chapter discusses the model that shows persistent myositis, the nociceptive input from the inflamed muscle causes a bidirectional change in both NADPH-dependent diaphorase (NDP) and nNOS-IR cells. This change is likely to be a major factor influencing the background activity of dorsal horn cells. During a longer lasting myositis, the spontaneous pain increases more and more, because the number of NO synthesising neurons declines which results in an increase in the background activity of nociceptive neurones. In patients an increased level of background activity in nociceptive dorsal horn neuron is assumed to cause spontaneous pain, a decrease in the spinal release of NO is probably followed by spontaneous pain.