Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0030193 (pain)
 261,466 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The effects of GABA and 5-HT on the electric activities of neurons of nucleus parafascicularis thalami (Pf) were observed in anesthetized rats with multimicropipete and iontophoresis and technique. It was found that: (1) Pain discharges of the Pf neurons were inhibited by microiontophoretically applied (MIA) GABA, an effect that could be reversed by MIA picrotoxin. Picrotoxin alone could enhance the pain discharges. The results indicate that GABA may be an inhibitory neurotransmitter responsible for the electric activities of Pf neurons. (2) MIA 5-HT has both excitatory and inhibitory effects on the pain discharge of Pf neurons, while only the former could be blocked by MIA cyproheptadine. It was suggested that 5-HT may participate in the modulation of the electric activities of the Pf neurons with different subtypes of receptors.
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PMID:[Effects of microiontophoretically applied GABA and 5-HT on the electric activities of neurons in nucleus parafascicularis of thalamus in rats]. 797 8

To investigate whether progesterone metabolites' antinociceptive effects correlate with their previously established binding efficacies at the GABA receptor complex (GBR), seven progestin metabolites were administered to ovariectomized Long-Evans rats s.c. (Expt. 1), via i.c.v. implantation (Expt. 2) and then i.c.v. infusion (Expt. 3). Progestins, listed from most to least efficacious at the GBR, were THP [5 alpha-pregnan-3 alpha-ol-20-one], THDOC [5 alpha-pregnan-3 alpha,21-diol-20-one], P [4-pregnen-3,20-dione], DHP [5 alpha-pregnan-3,20-dione],17-OH-P [17-hydroxyprogesterone], DHEAS [5-androsten-3 beta-ol-17-one sulfate] and PS [5-pregnen-3 beta-ol-20-one sulfate]. Pain sensitivity was measured via the radiant heat tailflick method 0, 5, 20, 40, 60, 80, 100 and 120 min after weekly progestin administration. Peripheral administration of 0.0, 0.1, 0.4, 1.6, 3.2 or 6.4 mg/kg of potent to moderate agonists of the GBR (THP, THDOC, P and DHP) tended to elevate tailflick latencies above baseline, whereas administration of the non-5 alpha-reduced metabolite (17-OH-P) and GBR antagonists (DHEAS and PS) did not. Intracerebroventricular implantation and infusion (0.0, 0.5, 1.0, 2.0 micrograms/rat) of THP, THDOC, P and DHP all significantly increased tailflick latencies above baseline and vehicle control, consistent with their GBR efficacies. Central 17-OH-P, DHEAS and PS did not elevate tailflick latencies. These rapid differences were unlikely confounded by stress given that corticosterone levels were not elevated (Expt. 4). As pain sensitivity was attenuated rapidly (0-5 min post-i.c.v.) and consistent with GBR efficacies, this suggests that progestins' modulation of pain may occur via GBR action.
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PMID:Progesterone metabolites, effective at the GABAA receptor complex, attenuate pain sensitivity in rats. 803 14

After intraperitoneal injection of ACTH, the content of GABA in hippocampus and the pain threshold were increased. This effect could be decreased by cyclosporin. ACTH decreased SI of MSBT and production of IL-II, and this suppression could be reversed by GABA synthesis inhibitor isoniazid, or GABA receptor blocker picrotoxin. These results suggest that: the analgesic effect of ACTH is related with the increase of GABA content in hippocampus, and cell immunity could be involved the regulation of GABA content in the brain regions. ACTH inhibited the effect of cell immunity, and this effect related to GABA content. Above effect is at least partly mediated by GABA synthesis and GABA receptor.
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PMID:[Interaction between r-aminobutyric acid content of the brain regions and cell immunity in the analgesic effect of adrenocorticotropic hormone in rats]. 808 82

L-glutamic acid, bicuculline (a GABA receptor antagonist), lidocaine and GABA were injected into entopeduncular and habenular nuclei respectively in rats. Pain threshold was measured by the latency of avoidance response (tail-flick) elicited by radiant heat exposure before and after intracerebral injection. Microinjection of different concentration of L-glutamic acid (25 nmol/L.0.5 microliter-1, 50 nmol/L.0.5 microliter-1, 100 nmol/L.0.5 microliter-1) into bilateral entopeduncular nuclei resulted in increases of pain threshold in a dose-dependent manner. Similar increase of pain threshold could also be observed by microinjection of 200 nmol/L GABA.0.5 microliter-1 into bilateral habenular nuclei. Both the effect of GABA and that of glutamate, could be antagonized by 0.2% bicuculline. The results mentioned above indicate that GABAergic fibers are involved in the analgesic effect of entopeduncular-habenular complex.
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PMID:[The role on the analgesia of entopeduncular nucleus]. 810 14

The intrathecal (IT) injection of progesterone (PROG) or three of its ring A-reduced metabolites (5 beta,3 alpha-pregnanolone, 5 alpha,3 alpha-pregnanolone, or 5 beta,3 beta-pregnanolone) did not significantly alter any of two pain thresholds (vocalization threshold to tail shock, VTTS, or tail flick latency, TFL) in ovariectomized rats when tested in a wide range of doses (2.5-250 micrograms). When combined with a subanalgesic dose of muscimol (MUSC; 1 microgram IT), PROG and its two 3 alpha-hydroxy derivatives, but not the 3 beta, caused significant analgesia in the VTTS but not in the TFL test. No clear dose-response relationships were noted in the analgesic response to the combination of the progestins and MUSC. The present results indicate that PROG, either directly or through its ring A-reduction, can modulate nociceptive information by enhancing the action of GABA agonists on GABAA receptors.
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PMID:Perispinal progestins enhance the antinociceptive effects of muscimol in the rat. 811 19

Aversive behavior is produced by stimulating some brain structures, such as the dorsal periaqueductal gray and the medial hypothalamus. We have used c-fos immunoreactivity to map brain areas which are influenced by stimulation of these two structures. Stimulation was produced in freely moving rats by electrical stimulation or by microinjections of either excitatory amino acids or GABA blocking drugs. Behavior was monitored to detect emotional changes. The effects on labeling induced by the stimulation of either structure were then compared. Structures labeled include the amygdala, the stria terminalis, the supramamillary area, the hypothalamus, the periaqueductal gray, the superior colliculus, the nucleus cuneiformis, and the locus coeruleus. Regardless whether chemical or electrical stimulation was used or the structure stimulated, there was a large overlap among the brain areas labeled. We then compared our results with data from the literature where other methods of inducing aversion have been used, including pain and stress. There was remarkable similarity in the patterning of labeling irrespective of the type of stimulation (central-peripheral, chemical-electrical). There was, however, one interesting difference produced by central vs. peripheral stimulation. Labeling was unilateral in the former case and bilateral in the latter case. Our results suggest that there is a neural substrate that mediates aversive behavior, no matter how it is produced. Nevertheless, that peripheral stimulation produces mainly bilateral activation of this substrate whereas central stimulation produces mainly unilateral activation suggests that natural peripheral stimuli are also integrated at a higher functional level. Future work could be directed toward explicit comparisons of central versus peripheral stimulation to identify the structures involved in higher level integration of aversive behavior.
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PMID:What brain structures are active during emotions? Effects of brain stimulation elicited aversion on c-fos immunoreactivity and behavior. 813 52

The intrathecal application of the GABA-B agonist baclofen has become more and more popular for severe spinal spasticity. Since it was first introduced in 1984 more than 1000 patients worldwide have been treated by this method, using an implantable drug administration device. Clinical data from 48 patients are presented, as well as further experience from a multicentre trial conducted in Europe, in conjunction with a literature overview. The method is now generally accepted as a powerful treatment for spasticity due to spinal lesions of whatever aetiology; improvement in mobility and function as well as relief of spastic pain are the most obvious benefits for the patient. Bladder function is improved in terms of increased bladder volume and lowered residual volume. In patients with supraspinal lesions causing muscle hypertension, where several mechanisms usually contribute besides hyper-reflexia (spasticity), the response has been less pronounced, but intrathecal baclofen still seems to have clinical effects that are superior to those of any oral drug treatment. The initial technical and methodical problems have been solved and today the procedure is generally assessed as safe.
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PMID:Intrathecal baclofen. 814 75

A model of acute spinal and phantom pain syndromes caused by the formation of an abnormally increased excitation generator (AIEG) in the system of dorsal horns of the spine was used to study the effects of sodium valproate when used chronically in the phantom pain syndrome, when given in a single dose in the acute pain syndrome and when applied to the spine with disinhibitors inducing the pain syndrome. It was shown that during chronic administration sodium valproate produced a stress-preventive action, but failed to affect pain sensation and to prevent the development of the pain syndrome. When used in the acute pain syndrome, sodium valproate had a marked analgesic effect, and when applied to the spine it substantially reduced the manifestations of the pain syndrome. The action of sodium valproate on the AIEG can be accounted for by the higher GABA level that results in the hyperpolarization of neurons which are a part of AIEG. When the latter is formed and operates in acute and chronic pain syndromes there are differences in the functional activity of the neurochemical structures responsible for the realization of pain reaction components. This is suggested by varying effects of sodium valproate on pain sensation during acute and chronic experiments.
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PMID:[The action of sodium valproate in central pain syndromes]. 820 57

Previous studies have shown that CCK-8 has distinct antiopioid effect in the central sites related with pain control and blood pressure control. The aim of this study was to explore the receptor mechanism by which CCK-8 antagonized the depressor effect of u- and k-opioid agonists, and to observe whether CCK-8 could antagonize the depressor effect induced by muscimol, a nonopioid substance. The results showed that (i) The antagonistic effect of CCK-8 on opioid-induced hypotension could be blocked by intrathecal (i. t.) administration of CCK-B antagonist L-365, 260 at nanogram doses, or by CCK-A antagonist devazepide at doses 20-40 times higher than L-365, 260, indicating that it was the CCK-B receptor which mediates the antiopioid effect. (ii) The depressor effect induced by intrathecal muscimol, a GABA agonist, was blocked neither by naloxone nor by CCK-8, supporting the notion that CCK-8 is an endogenous opioid antagonist rather than a universal anti-hypotension agent.
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PMID:The antagonistic effect of cholecystokinin octapeptide (CCK-8) on opioid effects in cardiovascular activities was mediated by CCK-B receptor. 821 42

The present study was designed to characterise the analgesia produced by the GABA B agonist baclofen in tonic pain in monkeys. The effect of various doses of baclofen was studied on formalin induced pain. Baclofen was injected intraperitoneally 30 min prior to formalin injection in five doses of 2, 4, 6, 8, and 10 mg/kg and the pain was quantified for a period of one hour. Baclofen produced dose related analgesia, 6 mg/kg having maximal effect. The antinociceptive effect of baclofen could be attributed to the effect of baclofen on GABA B receptors producing presynaptic inhibition of primary nociceptive afferents in the dorsal horn of the spinal cord.
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PMID:GABA B mediated analgesia in tonic pain in monkeys. 827 93


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