Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0344307 (analgesia)
 28,200 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In barbiturate anaesthetized cats, tonic inhibition of the excitation of lumbar dorsal horn neurones by impulses in unmyelinated primary afferents was measured by reversibly cooling the spinal cord at the thoraco-lumbar junction. Tonic inhibition was reduced by microinjection of the GABA analogue, piperidine-4-sulphonic acid (2.5 nM in 0.5 microliter) mainly at AP -7, L 2-5 and V -8 to -10. This area in the ventrolateral medulla is just ventral to the facial nucleus and has been shown to be important in cardiovascular control, particularly in relation to fear-defence reactions. It is proposed that tonic inhibition of the nociceptive responses of spinal neurones is part of such a reaction in response to the trauma of surgery. Since previous experiments had shown that the ventrolateral medulla was important in spinal inhibition produced by PAG stimulation, these experiments support the proposal that analgesia does not occur in isolation but is part of a complex behavioural response of an animal in a potentially injurious environment.
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PMID:Brain-stem areas tonically inhibiting dorsal horn neurones: studies with microinjection of the GABA analogue piperidine-4-sulphonic acid. 380 42

Cocaine hydrochloride (50 mg) pellets implanted subcutaneously in male Wistar rats potentiated the analgesia of morphine, levorphanol, methadone and buprenorphine as measured by the tail-withdrawal test. Potentiated opiate analgesia was abolished by naloxone and further enhanced by desipramine and phenoxybenzamine. Yohimbine, alpha-methyl p-tyrosine, haloperidol, zimelidine, methysergide, p-chlorophenylalanine produced no significant effect on potentiated opiate analgesia. Pseudo-cocaine (dextro-cocaine), which is several-fold less potent than cocaine as an inhibitor of noradrenaline and dopamine reuptake in the CNS, had no significant effect on opiate analgesia. Analgesia produced by low doses of baclofen, a GABA agonist, was also not potentiated by cocaine. This study suggests a predominant role for noradrenaline in the stereospecific potentiation of opiate analgesia by cocaine.
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PMID:Stereospecific potentiation of opiate analgesia by cocaine: predominant role of noradrenaline. 382 92

Pretreatment with baclofen prolonged the duration of fentanyl-induced analgesia from 18 to 30 min in patients undergoing neurosurgical anaesthesia (fentanyl plus nitrous oxide in oxygen). This observation is consistent with a potentiating effect of GABA on opioid analgesia.
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PMID:Baclofen prolongs the analgesic effect of fentanyl in man. 404 21

It has been shown in experiments on rats exposed to a gradually increasing nociceptive action that subarachnoidal injection of GABA and its agonists (CHBA) isoguvacin, phenibut) in a dose of 0.6 mg causes an elevation of the thresholds of motor and, to a less degree, of emotional behavioral component of the painful reaction. Analgesia is potentiated by simultaneous subarachnoidal injection of inactive doses of chlorodiazepoxide. The GABA uptake inhibitor guvacin potentiates the effect of isoguvacin. The GABA-and phenibut-induced analgesia is not abolished by nalozone (0.04 mg subarachnoidally).
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PMID:[Nonopiate subarachnoid analgesia induced by GABA-positive substances]. 404 65

Ethylenediamine, a GABA receptor agonist induced a small hyperalgesic state in mice, but increased morphine analgesia. The interaction with this morphine effect was not dose-dependent. Ethylenediamine significantly antagonized tolerance development at relatively low doses (5-10 mg/kg). The GABA mimetic agent increased the frequency of abstinence signs in the naloxone-precipitated morphine withdrawal in mice. The effect of ethylenediamine on morphine withdrawal was suppressed by the irreversible GABA transaminase inhibitor, gamma-vinyl GABA.
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PMID:Effects of ethylenediamine on morphine analgesia and tolerance-dependence in mice. 405 78

Unilateral microinjections of the GABA agonists muscimol and baclofen into the lateral preoptic area (LPOA) of the rat brain resulted in a significant increase in the latency to respond to a hotplate stimulus on the side contralateral to the injection. Muscimol injected 1.5 mm dorsal to the LPOA site was significantly less effective in changing the hotplate reaction time. The LPOA therefore represents a site from which GABA receptor-mediated analgesia can be elicited.
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PMID:GABA agonist induced analgesia elicited from the lateral preoptic area in the rat. 609 83

Physiological events involved in nociception and pain perception are examined. Substance P could be a primary afferent transmitter of certain nociceptive information. Transmission of this information can be modulated within the spinal cord by intrinsic and descending mechanisms. The intrinsic mechanism involves inhibitory opiate effects within substantia gelatinosa. Centres for descending systems are located in medulla and periaqueductal gray matter. They are activated by exogenous narcotic agonists, and by regional connections. Descending inhibitory pathways are serotonergic and noradrenergic. GABA and glycine are also possibly involved in antinociception. Narcotics have been shown to produce analgesia when administered to the intrathecal or epidural spaces of humans. These routes are still experimental. The place of clinical modification of transmitter system is discussed, but no conclusions or recommendations can be made at this early stage.
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PMID:Pharmacology of pain and analgesia. 615 88

The possible involvement of bulbospinal serotonergic systems in the mediation of analgesia has created a need for a better understanding of the influence this system has on neuronal mechanisms in the spinal cord. Therefore, these studies were designed to examine the effects of caudal raphe stimulation on primary afferent depolarization and to determine the role of serotonin (5-HT) and GABA in the mediation of these stimulation-produced effects. Stimulation of the raphe evoked two electrotonically conducted dorsal root potentials (DRP-1 and DRP-2) and two compound action potentials (VRP-1 and VRP-2) which were recorded from the dorsal and ventral roots, respectively. Length constant measurements indicated that DRP-1 was generated in group II and DRP-2 in group I primary afferent fibers. Histological determination of stimulation sites revealed that short-latency potentials (DRP-1 and VRP-1) were evoked from many sites within the caudal brain stem, while the long-latency potentials (DRP-2 and VRP-2) were evoked primarily from sites within the caudal raphe nuclei. The role of serotonin in mediating these evoked potentials was assessed by administering various antagonists of serotonin (cinanserin, methysergide and D-lysergic acid diethylamide). These agents consistently attenuated the long-latency potentials (DRP-2 and VRP-2) but increased the magnitude of DRP-1. The possibility of a GABAergic neuron in the descending systems projecting to primary afferent terminals was studied. Depletion of GABA by semicarbazide blocked DRP-1, but had only a modest effect of DRP-2. However, the putative GABA antagonist, bicuculline, inhibited both DRP-1, and DRP-2. These results suggest that a GABA interneuron is not involved in the bulbospinal serotonergic depolarization of primary afferent terminals. This system appears to constitute a presynaptic filter of afferent input, with the capacity to inhibit different fiber groups.
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PMID:The role of GABA and serotonin in the mediation of raphe-evoked spinal cord dorsal root potentials. 624 39

A variety of behavioral tests were used to characterize the cataleptic state induced by various treatments. Besides catalepsy, posture, locomotion, rigidity and the presence of reflexive responses were assessed. Measures of analgesia and body temperature were taken. The behavioral profiles of beta-endorphin, morphine, etonitazene, haloperidol, arecoline and GABA were compared at the time maximal catalepsy scores were obtained. Results indicated that, for an equivalent degree of catalepsy, the profile of beta-endorphin was similar to that of opiates, except for changes in body temperature; beta-endorphin's profile differed markedly from that of haloperidol, arecoline and GABA. Catalepsy was less pronounced with the latter two drugs. There were similarities in the behavioral profile of haloperidol and arecoline.
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PMID:Similarities of the cataleptic state induced by beta-endorphin and morphine. 629 79

In decerebrate, cerebellectomized cats, a comparison was made between the effects of electrical stimulation in nucleus raphe magnus (NRM) and iontophoretic application of GABA, glycine, met-enkephalin and beta-endorphin on the responses of neurones in the medial brain stem reticular formation to tooth pulp stimulation. NRM stimulation, GABA, glycine and enkephalin produced a short lasting inhibition of tooth pulp evoked responses whilst the time course of the inhibition produced by beta-endorphin was much slower, often lasting up to 1 h following a 3-7 min ejection period. The effects of GABA and glycine could be antagonised by iontophoresis of bicuculline and strychnine respectively whilst intravenous injection of naloxone antagonised the inhibition induced by the opioid peptides. In most neurones tested, inhibition of tooth pulp evoked responses by NRM stimulation was blocked by iontophoretic application of bicuculline but not by strychnine or naloxone (i.v.). We conclude that GABA may act as a transmitter which mediates the inhibitory effects of NRM on the responses of reticular neurones to tooth pulp stimulation. Thus GABA may be involved in stimulation produced analgesia.
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PMID:Actions of GABA, glycine, methionine-enkephalin and beta-endorphin compared with electrical stimulation of nucleus raphe magnus on responses evoked by tooth pulp stimulation in the medial reticular formation in the cat. 630 24


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