Biomedical subjects
Publications and source records attributed to Y F Xie.
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The effects of intrathecally administered naloxone or aminophylline on the antinociception produced by intrathecal NE, 5-HT, morphine or adenosine receptor agonist, 5'-N-ethylcarboxamidoadenosine (NECA) were observed in rats using the tail-flick test. The results show that: (1) the antinociception produced by NE with doses of 0.5 or 1.0 nmol could be completely blocked by both naloxone (240 nmol) and aminophylline (120 nmol); (2) neither naloxone (240 nmol) nor aminophylline (120 nmol) could alter the antinociception produced by 5-HT with doses of 60 or 120 nmol; and (3) the antinociception produced by morphine (0.5 nmol) could be blocked by both naloxone (240 nmol) and aminophylline (120 nmol), while the antinociception by NECA (0.5 nmol) could be blocked only by aminophylline (120 nmol), but not by naloxone (240 nmol). The results suggest that opiate-like substances (OLS) and adenosine are involved in the mediation of the NE-produced antinociception, but not in 5-HT-produced antinociception. Results also suggest that NE, OLS and adenosine may act in a sequential order in the performance of NE-induced antinociception at the spinal level.
The interactions between different doses of serotonin (5-HT) and norepinephrine (NE) in in vivo experiments on rat spinal cord dorsal horn cells was investigated using the integrated electromyography (EMG) measurement of the nociceptive hindlimb flexor reflex (FR). The results indicate that (1) intrathecal (IT) administration of low doses of 5-HT (60 nmol) or NE (1.5 nmol) suppresses the nociceptive FR by 40% for 20 min, respectively; (2) administration of higher doses of 5-HT (240 nmol, IT) multiplies the suppression of the nociceptive FR by 80% for 40 min, and NE (15 nmol, IT) produces similar suppression of the nociceptive FR for 80 min; (3) concomitant administration of low doses of 5-HT (60 nmol, IT) and NE (1.5 nmol, IT) produces a summation of the nociceptive FR suppression both in amplitude and duration; (4) concomitant administration of the higher doses of 5-HT (240 nmol IT) with NE (15 nmol, IT) produces similar effect obtained as 5-HT given separately, and no summation was obtained as observed following the lower dosages; (5) serotonin (240 nmol, IT) given 40 min before NE (15 nmol, IT) attenuates the duration of the suppression induced by NE; (6) pretreatment with a selective 5-HT2 receptor antagonist ketanserin (60 nmol, IT) failed to abolish the 5-HT effects; (7) pretreatment with ketanserin prior to concomitant administration of the higher doses of 5-HT and NE prolongs the time duration of the nociceptive FR suppression.(ABSTRACT TRUNCATED AT 250 WORDS)
The purpose of this study was to examine whether adenosine or serotonin is involved in mediation of the antinociception produced by norepinephrine at the spinal cord level. Aminophylline, an adenosine receptor antagonist and naloxone given intrathecally (i.t.) were used to test the antinociception produced by i.t. norepinephrine, serotonin, morphine or the adenosine receptor agonist 5'-N-ethylcarboxamidoadenosine (NECA) by using the tail-flick assay in rats. It was observed that (1) aminophylline blocked the antinociception produced by norepinephrine, but exhibited no effect on the antinociception produced by serotonin, (2) aminophylline blocked the antinociception produced by morphine similarly to naloxone, (3) aminophylline blocked the antinociception produced by NECA and (4) naloxone failed to block the antinociception produced by NECA and serotonin. The results suggest that adenosine is involved in mediation of the norepinephrine-produced antinociception at the spinal level and that norepinephrine and adenosine may act in a sequential manner in norepinephrine-induced antinociception.
The effects of intrathecally (IT) administered naloxone (Nal) on the antinociception produced by IT norepinephrine (NE), serotonin (5-HT), or morphine (Mor) were observed and compared in rats using the tail-flick (TF) assay. The results show that: a) NE, 5-HT, and Mor in doses of 1 nmol, 240 nmol, and 0.5 nmol, respectively, produce similar increases in amplitude and time in TF latency (TFL); b) Nal treatment of 240 and 360 nmol has no effects on TFL; c) the antinociception produced by NE (1 nmol) can be blocked by Nal (240 nmol); d) antinociception produced by Mor (0.5 nmol) can also be blocked by Nal (240 nmol); e) 240 nmol of Nal does not affect the 5-HT (120 nmol)-produced antinociception, while 360 nmol of Nal show a delayed blockade to the 5-HT (120 nmol)-produced antinociception. The results suggest that endogenous opiate-like substances may be involved in both NE- or 5-HT-produced antinociception at the spinal level, and these effects may be mediated through different types of opiate receptors.
Immunocytochemical technique was used to compare the content of substance P (SP), Met-enkephalin (Met-Enk) and neurotensin (NT) on two sides of the lumbar dorsal horn of rats in which the unilateral dorsolateral funiculus was transected while formalin (0.2 ml, 5%) was injected equally into two hindpaws. The results showed that the SP-like immunoreactivity (SP-LI) and Met-Enk-LI were significantly higher and the NT-LI was significantly lower in the superficial laminae of dorsal horn on the side ipsilateral to the intact DLF than that on the opposite side, implying that peripheral noxious inputs can activate the supraspinal descending inhibitory systems which in turn modulate the transmission of noxious message at the spinal level by changing the activities of related peptidergic neurons.
Immunocytochemical staining for serotonin (5-HT), tyrosine hydroxylase (TH) and galanin (GAL) was combined with horseradish peroxidase (HRP) retrograde tract-tracing technique to analyze the localizations of 5-HT-, catecholamine (CA)- and GAL-containing neurons in the brainstem which project to the nucleus parafascicularis (PF) in rats. It is demonstrated that most of the retrogradely HRP-labeled neurons (70%) in bilateral periaqueductal gray (PAG) and raphe nuclei are positively immunostained by antiserum to 5-HT, and that most of the retrogradely HRP-labeled neurons (over 80%) in bilateral locus coeruleus (LC) are positively immunostained by antisera to both TH and GAL. The possible functions of these PF-petal serotonergic, catecholaminergic (actually noradrenergic) and galaninergic projections are discussed.
An electrophysiological model has been developed to explore the transmitters and their relationships in the descending control of spinal transmission of noxious inputs. Nociceptive discharges were recorded extracellularly in parafascicular (Pf) neurons, and the caudal stump of longitudinally isolated dorsal half of the lower thoracic spinal cord was stimulated to simulate the descending volleys coming from the supraspinal structures. Nociceptive discharges in 34 Pf cells were markedly suppressed (83.2 +/- 13.9%) by the preceding spinal stimulation. Phentolamine, methysergide and naloxone were separately administered with random sequence in each of 25 cells by an intrathecal route to observe if the descending inhibition could be blocked by these drugs. The results suggested that in the dorsal spinal cord there exist at least two neurochemically different descending inhibitory fiber systems which comprise either the long descending adrenergic or serotonergic fibers and, most of the adrenergic fibers are succeeded by a propriospinal opioidergic neuron while a few of the serotonergic fibers have such a succession.
Effects of stimulation of the superior colliculus (SC) on the spontaneous and nociceptive discharges of parafascicular (PF) neurons were investigated in 43 urethane-anesthetized rats. Two groups of PF cells were sampled according to their responses to noxious stimuli: 59 of them were 'nociceptive-on' and 12 'nociceptive-off'. Following stimulation of the intermediate and deep layers of SC, the firing rate of nociceptive discharge of 'nociceptive-on' cells was inhibited significantly (-76 +/- 5%, P less than 0.01) in 75% cases tested, while the nociceptive response of 'nociceptive-off' cells was disinhibited markedly (79 +/- 9%, P less than 0.01) in 67% cases by the same stimulation. In 30 animals of this series the latency of hind limb withdrawal reflex elicited by noxious skin heating was compared before and after SC stimulation. In 24 cases in which the stimulating electrodes were positioned exactly in intermediate-deep layers of SC, SC stimulation lengthened the latency by 62 +/- 8% (P less than 0.01), while in 6 cases in which the electrodes drifted from these areas, the latency was not changed following the same stimulation.
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