ABSTRACT
Fluoride-resistant acid phosphatase (FRAP) has been suggested as an enzymatic marker for nociceptive primary afferent terminals in the spinal dorsal horn, however there has not been demonstrated a direct functional relation between FRAP activity and an increased nociceptive transmission. For this purpose, we quantitated FRAP activity in the spinal dorsal horn of the rat in a heat-induced cutaneous inflammatory model. Male Sprague-Dawley rats anaesthetised with thiopental were separated in two groups where the left hindpaw was submerged during 60 s either in water at room temperature (control group) or in water at 60 degrees C (inflammation group) which induce in this group a progressive hindpaw inflammation. After 8 h, the lumbar enlargement of the spinal cord was extracted, cut in slices and 1 mm micropunch fragments were obtained from the right and left dorsal horn. The activity of FRAP was determined using the Gomori colorimetric method and corrected by the protein concentrations. FRAP activity in the left dorsal horn was statistically higher than right dorsal horn in the inflammation group (3.05+/-0.54 versus 1.91+/-0.23 u/g per l; P<0.05). Also, FRAP activity from the left dorsal horn of the control and inflammation groups show a significant increase in the last group (3.05+/-0.54 versus 2.17+/-0.23 u/g per l; P<0.05). This results demonstrate that FRAP is not only an enzymatic marker for neuronal and fibre integrity of nociceptive primary afferents but also it is associated to the nociceptive afferent activation.
Subject(s)
Acid Phosphatase/metabolism , Fluorides/pharmacology , Neurons, Afferent/enzymology , Posterior Horn Cells/enzymology , Spinal Cord/cytology , Acid Phosphatase/drug effects , Animals , Functional Laterality , Hot Temperature/adverse effects , Inflammation/enzymology , Inflammation/pathology , Male , Physical Stimulation , Rats , Rats, Sprague-DawleyABSTRACT
A previous study has shown that lumbar spontaneous cord dorsum potentials (CDPs) are produced by background activity of a neuronal ensemble located in the dorsal horn. Here, the effects produced by intravenous application of the nitric oxide synthase inhibitor L-N(G)-nitro arginine (L-NOARG, 100 microg/kg) and of the nitric oxide donor 3-morpholinosydnonimine hydrochloride (SIN-1, 500 microg/kg) on spontaneous CDPs were examined. Experiments were performed on pentobarbitally anesthetized, paralyzed and spinalized cats. The amplitude of spontaneous CDPs increased after L-NOARG, however, decreased after SIN-1. These observations suggest that electrical activity of dorsal horn neurones generating spontaneous CDPs is dependent on nitric oxide production.