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)

Effects of valproic acid administration on morphine analgesia and on morphine tolerance and dependence were investigated in mice. Valproate increased the reaction time to thermal stimulation in naive animals. This effect was additive with morphine when valproate was administered shortly before the analgesic. However, an antagonism was observed if a 4-hour period elapsed between valproate and morphine administration. When administered to mice receiving a sustained release preparation of morphine, valproate antagonized the development of tolerance to morphine. Valproate elicited a dual action on the abstinence signs observed after naloxone administration in morphine-treated mice. The effect consisted in a reduction of abstinence behavior if the anticonvulsant was administered a few minutes before naloxone; the same treatment increased the severity of the abstinence behavior when valproate was injected 1 h before the precipitating dose of naloxone. In this latter schedule, concomitant administration of gamma-vinyl-GABA failed to reduce the severity of the convulsions observed during the abstinence syndrome. These results suggest that valproate is metabolized to a compound responsible for decreased analgesia and intensified withdrawal signs.
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PMID:A dual action of valproic acid upon morphine analgesia and morphine withdrawal. 641 Apr 18

Muscimol, a structural analog of GABA, significantly potentiated pilocarpine-induced analgesia in rats, but failed to alter pilocarpine-induced catalepsy. It also failed to affect pilocarpine-elicited increase in homovanillic acid levels in the striatum. These findings suggest that the potentiation of pilocarpine-induced analgesia by muscimol is unrelated to an interaction of the GABAergic system with the striatal cholinergic or dopaminergic systems.
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PMID:Effect of muscimol, a central GABA receptor agonist, on the catalepsy, striatal homovanillic acid increase, and analgesia induced by pilocarpine in rats. 679 90

THIP (4,5,6,7-tetrahydroisoxazolo (5,4-c) pyridone-3-ol), a direct acting GABA receptor agonist, has been shown to have antinociceptive properties. To determine whether tolerance develops to the analgesic response, mice received multiple injections of THIP for up to 21 days after which analgesia was tested using both tail immersion and hot-plate methods. Both tests indicated a significant reduction in the antinociceptive response to THIP, as well as other GABA agonists, beginning between days 3 and 5 of chronic administration. Moreover, these animals demonstrated a decreased analgesic response to morphine, and morphine tolerant animals were also less responsive to THIP. These data indicate that opiates and GABA agonists induce analgesia by acting through separate but related pathways in the central nervous system.
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PMID:THIP analgesia: cross tolerance with morphine. 684 95

The analgesic effect of morphine in conditions of serotonin- and GABA-ergic activation was studied in experiments on male albino rats. The serotonin re-uptake blockers fluoxetin and citalopram (10 and 20 mg/kg) did not exert clear analgesic effect or did not potentiate morphine action in doses of 5 and 10 mg/kg. The GABA agonist muscimol (0.5--2 mg/kg) did not influence the pain reaction structure and did not enhance morphine-induced analgesia. The role of serotonin- and GABA-ergic processes in realization of the analgesic action of morphine is discussed.
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PMID:[Possibility of modulating morphine analgesia against a background of activation of serotonin- and GABA-ergic processes]. 697 90

In the mouse hot-plate test (50 degrees C), muscimol produced analgesia which was blocked by bicuculline but not by picrotoxin. Analgesia produced by baclofen was dose-dependent and stereoselective, but was not blocked by bicuculline, picrotoxin or naloxone. Morphine-induced analgesia was not altered by bicuculline. The inhibitors of GABA-transaminase, amino-oxyacetic acid, gamma-acetylenic GABA and gamma-vinyl GABA, produced analgesia which was much more prolonged than that observed with muscimol, baclofen or morphine. The analgesic action of these agents was not significantly altered by bicuculline. At a higher plate temperature (55 degrees C), GABA-transaminase inhibitors produced minimal analgesia but significantly enhanced the analgesic action of baclofen. gamma-Vinyl GABA markedly increased both the peak effect and the duration of analgesia but gamma-acetylenic GABA and amino-oxyacetic acid caused smaller increases. In the mouse hot-plate test, bicuculline-sensitive GABA receptors appear to mediate the analgesic action fo muscimol. Analgesia produced by baclofen, morphine and inhibitors of GABA-transaminase may involve another class of GABA receptors which are insensitive to bicuculline.
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PMID:On the involvement of GABA in the analgesia produced by baclofen, muscimol and morphine. 711 May 28

The present study was performed on 22 cats to explore whether r-aminobutyric acid (GABA), endogenous opioid peptide and substance P (SP) were involved in the regulation of presynaptic inhibition in acupuncture analgesia. The size of the antidromic compound C action potentials of the sural nerve evoked by the testing stimulation in spinal cord was measured as an indicator of C-afferent terminal excitability. It was found that the electro-acupuncture (EA) at "Huantiao" (GB30) and "Yang lingquan" (GB34) points induced significant enlargement of the antidromic C-waves, showing the depolarization of presynaptic terminals of primary C-afferents was enhanced. The depolarization effect of EA was significantly reduced by bicuculline, naloxone and the antiserum of SP locally applied to the surface of spinal cord respectively. It is supposed that GABA, endogenous opioid peptide and SP may be involved in the regulation of presynaptic inhibition in acupuncture analgesia.
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PMID:[Relationship between the presynaptic depolarization effect of acupuncture and r-aminobutyric acid, opioid peptide and substance P]. 752 93

Thanks largely to the study of the brainstem nuclei that mediate stimulation analgesia, the involvement of the monoamines in the descending control of pain is now well established. The periaqueductal grey, the raphe nuclei (NRM and DRN) and the locus coeruleus are all key brainstem sites for the control of nociceptive transmission in the spinal cord. Although the initial emphasis was on 5-HT as the transmitter mediating this control at spinal levels, it is clear from more recent work that NA has an equally important part to play. How (or even if) the two amines differ in their roles and actions in analgesia is, however, still an open question. The small size and complexity of the brainstem areas from which analgesia may be elicited by electrical stimulation complicates the interpretation of the data. Stimulating currents may spread to surrounding regions mediating opposite effects to that of the main region stimulated. Opiates and GABA are clearly involved in descending control at both brainstem and spinal levels, although the relative roles of the different types of amino-acid and opiate receptors is still hotly debated. Despite the fact that the first report on stimulation analgesia appeared more than a quarter of a century ago in 1969, the precise connections and cord synaptology are still the basis of ongoing research. It is perhaps ironic, in an issue dedicated to new molecules and mechanisms, that those transmitters most involved in descending inhibition should be such old and familiar friends.
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PMID:Descending control of pain. 757 56

The nucleus paragigantocellularis lateralis (PGi) in the rostral ventral medulla is implicated in several functions including cardiovascular control, respiration, pain and analgesia. More recent studies implicate this region in alertness and attention as well, by virtue of its prominent projections to the nucleus locus coeruleus (LC). To investigate information that is integrated in the PGi, we used tract tracing to examine brain and spinal projections to this region. Afferents to PGi were found to be functionally diverse and topographically organized. Projections to the retrofacial PGi are primarily autonomic in nature. A wider range of inputs were found to target the rostral (juxtafacial) aspect of the PGi, including brain nuclei involved in the processing of somatosensory and auditory stimuli, as well as autonomic areas. Efferent projections to the LC were also examined in detail. Neuropharmacology experiments revealed that the PGi provides a potent excitatory amino acid input to the LC and an inhibitory input acting at alpha 2 receptors on LC neurons. PGi neurons projecting to the LC stained for markers of adrenaline, enkephalin, GABA and corticotropin releasing factor. Finally, some PGi neurons collateralize to innervate both the LC and the spinal cord. These results suggest that the LC may function in parallel to peripheral autonomic systems providing a cognitive complement to sympathetic function, and that the PGi may integrate a wide range of inputs to facilitate adaptive responses to urgent environmental events.
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PMID:Integration in the ventral medulla and coordination of sympathetic, pain and arousal functions. 773 66

Copulation in the male rat provoked an abrupt and significant rise in the threshold to induce vocalization by electrical shock to the tail (copulatory analgesia, CA). The possible effect on CA of the intrathecal (IT) administration of receptor antagonists to neurotransmitters participating in nociception was ascertained in this study. CA was significantly reduced, though not abolished, by IT injections of either naloxone, picrotoxin, or methysergide, but not by strychnine or yohimbine. This analgesic effect was achieved without significantly altering copulatory behavior. Results suggest that both brain and spinal systems participate in the development of CA. Brain effects would be mediated by descending serotonergic fibers, although intrinsic spinal systems would involve both opiate and GABA interneurons.
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PMID:Participation of opiatergic, GABAergic, and serotonergic systems in the expression of copulatory analgesia in male rats. 782 42

Effects of electrical stimulation of the somatosensory area II (S II) of the cerebral cortex and electroacupuncture (EA) on contents of r-aminobutyric acid (GABA), glutamic acid (Glu), aspartic acid (Asp) and alanine (Ala) in the precruciate cortex (PreCtx) were investigated in order to probe if the free amino acids in the preCtx are involved in the S II descending modulation and acupuncture analgesia. Adult cats were randomly divided into four groups: control, EA, electrical stimulation of S II and stimulation of S II plus EA. EA was applied at right Huantiao and Yanglingquan acupoints for 30 min and electrical stimulation was given on the S II surface. Amino acids were separated by paper chromatography and determined with spectrophotometry. Results showed that the stimulation of S II or/and EA had no significant effects on the contents of GABA, Glu, Asp and Ala in the PreCtx, indicating that the four amino acids are probably not involved in regulatory effects of EA and the stimulation of S II on the PreCtx.
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PMID:[Effects of electrical stimulation of S II and electroacupuncture on contents of some free amino acids in the precruciate cortex]. 783 61


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