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)

Conjugate of horseradish peroxidase and wheat germ agglutinin (HRP-WGA conjugate) was injected into the midbrain central gray (MCG) of three adult rats. Frontal sections of the diencephalon were first treated with diaminobenzidine and hydrogen peroxide to detect the retrogradely transported conjugate. They were then stained immunohistochemically to detect pro-opiomelanocortin (POMC)-derived peptides (ACTH, beta-endorphin and alpha-MSH). The coexistence of the three POMC-derived peptides was confirmed by the immunohistochemistry of three consecutive sections stained with antiserum specific to each peptide. Some of the neuronal perikarya distributed in and around the arcuate nucleus were positive to the immunohistochemical stain for POMC-derived peptides, and, concomitantly, were labeled with HRP-WGA conjugate, which indicated that they projected to the MCG. They were mostly concentrated in the rostral three-fifths of the arcuate nucleus. The finding that some of the POMC neurons in the arcuate nucleus project to the midbrain central gray deserves interest, because the central gray is involved in analgesia induced by opioid peptides.
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PMID:Projection of pro-opiomelanocortin neurons from the rat arcuate nucleus to the midbrain central gray as demonstrated by double staining with retrograde labeling and immunohistochemistry. 245 87

The hypothesis that nitrous oxide stimulates the central pro-opiomelanocortin system in vivo was explored in this study. A concentration-dependent stimulation of central pro-opiomelanocortin neuropeptides was demonstrated after exposures to variable concentrations of nitrous oxide with oxygen. Rats exposed to 60% and 80% nitrous oxide with oxygen demonstrated an elevation of beta-endorphin concentration along the neuraxis involved with analgesia; no similar effect was observed in alpha-MSH concentration, neither duration of exposure nor acclimation to the enclosed environment altered this stimulation. The discontinuation of nitrous oxide exposure resulted in the diminution of beta-endorphin concentration to pre-exposure levels in 15-30 min. With an ACTH1-39 antisera, a semiquantitative increase in opiocortin immunoreactivity after exposures to nitrous oxide was demonstrated. In conclusion, the increase in beta-endorphin concentration and immunoreactive ACTH1-39 staining in the cells of origin, areas of fiber projection and terminal fields suggest that nitrous oxide stimulates the central pro-opiomelanocortin system in vivo in the rat.
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PMID:The effects of nitrous oxide on the central endogenous pro-opiomelanocortin system in the rat. 282 75

Certain neuropeptides previously linked to stress and implicated in CNS control of analgesia/algesia were tested using a recently developed analgesiometric model, the rabbit ear-withdrawal test. The latency to ear withdrawal increased in a dose-related manner after beta-endorphin was injected intracerebroventricularly (IVC). Intermediate doses (0.5 and 1.0 micrograms) of adrenocorticotropic hormone (ACTH) caused hyperalgesia as indicated by decreases in latency. Corticotropin-releasing factor (CRF, 0.5 and 1.0 micrograms) also caused significant hyperalgesia late in the testing period. alpha-Melanocyte stimulating hormone (alpha-MSH, 0.25-2.0 micrograms), a molecule that shares the first 13 amino acid sequence with ACTH, and somatostatin (0.25-2.0 micrograms), caused no significant change in latency. However, 1.0 microgram doses of each peptide antagonized the analgesic effect of beta-endorphin (1.0 microgram) in the following order of potency: ACTH = alpha-MSH greater than CRF greater than somatostatin. The results support the idea that CNS peptides that are released during stress can exert opposing actions on acute pain, even though they may cause little effect alone.
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PMID:Influence of centrally administered peptides on ear withdrawal from heat in the rabbit. 288 94

alpha-MSH (0.1, 1, 10 micrograms) was administered intracerebroventricularly and its action on pain sensitivity was investigated by the hot-plate method in mice. alpha-MSH produced dose-dependent analgesia and this analgesic effect was prevented by naloxone (1 mg/kg, s.c.). It is possible that alpha-MSH may play a role in the mechanism of pain through endogeneous opioid systems.
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PMID:Naloxone prevents the analgesic action of alpha-MSH in mice. 399 35

In two experiments the effects of the pituitary peptide alpha-MSH, the hypothalamic tripeptide MIF-I (P-L-G-NH2) and the pineal hormone melatonin were investigated on the attenuation of morphine analgesia measured by a tail flick test. In Experiment 1, alpha-MSH had minimal effect on morphine analgesia, whereas, MIF-I and melatonin clearly delayed the onset of morphine analgesia, and melatonin also shortened the duration of analgesia. Experiment 2 was designed to investigate the possible synergistic effect of MIF-I and melatonin. The combined treatment of MIF-I and melatonin significantly delayed the onset of morphine analgesia, and melatonin alone shortened the duration of analgesia. The relationships among the pituitary, hypothalamus and the pineal for the modulation of pain and response to morphine were discussed.
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PMID:Attenuation of morphine analgesia by alpha-MSH, MIF-I, melatonin and naloxone in the rat. 612 66

Light microscopic immunocytochemistry was employed to investigate possible sites of interaction between the endogenous opioid peptides and monoamines in the rat central nervous system. The opioid and related peptides examined included beta-endorphin (beta-END), alpha-MSH (alpha-MSH) and leucine-enkephalin (Leu-ENK). The monoamines were examined using antisera generated against tyrosine hydroxylase, dopamine-beta-hydroxylase as well as serotonin. Due to the long-tract nature of the central monoamine projections as well as beta-END/alpha-MSH fiber systems, serial section analyses were performed utilizing parasagittal brain sections. Many areas rich in both the monoamines as well as opioid peptides were investigated. These included several thalamic and hypothalamic nuclei, several limbic structures, mesencephalic periaqueductal gray, brain stem noradrenergic cell groups and their rostral projections, the dopaminergic nigrostriatal system, and the serotonergic raphe nuclei and their projections. The results suggest a more intimate linkage between the monoamines and the opioid peptides than previously realized. Some of the intricacies of monoamine-opioid peptide interaction, in particular those pertaining to their possible role in pain and analgesia, catalepsy, and neuroendocrine effects are also discussed.
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PMID:Some perspectives on monoamine-opioid peptide interaction in rat central nervous system. 612 45

Opioid analgesics influence the function of a number of neurotransmitter systems including classical neurotransmitters, neuropeptides and endogenous opioids. The role of these interactions in analgesia, tolerance and dependence is reviewed. Opioids inhibit the release of substance P from high threshold primary afferents, depress the activity of dorsal horn neurons and increase activity in serotonergic and noradrenergic neurons projecting from brainstem to spinal regions. Chronic administration of opioids modifies the dynamics of classical transmitters and those of endogenous opioid peptides in the brain, spinal cord and the pituitary gland. However, the effects observed are very variable. Several neuropeptides (vasopressin, MIF, alpha-MSH, CCK and dynorphin) have been reported to modify acute and chronic effects of opioids. Tolerance and dependence seen after opiate administration may involve changes in the function of these peptides.
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PMID:Opioid-neurotransmitter interactions: significance in analgesia, tolerance and dependence. 615 40

Dose-dependent analgesia was produced by microinjection of ORG 2766 into the periaqueductal gray (PAG). This analgesia was found to be potent and long-lasting and occurred at doses which were equimolar to those necessary for morphine analgesia. The same doses failed to produce analgesia by the cerebroventricular route, suggesting that the PAG was the site of action of this effect. Naloxone failed to reduce the analgesia and morphine tolerant did not diminish the effect significantly. Additionally, ORG 2766 at concentrations up to 10 micrometer failed to inhibit binding of [3H]naloxone to brain opiate receptors in vitro. These results suggest a non-opiate mechanism of action and are discussed in terms of a proposed alpha-MSH or ACTH receptor.
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PMID:Induction of analgesia by central administration of ORG 2766, an analog of ACTH4--9. 625 42

In a completely crossed, double blind designed study, six rats received intraventricular injections of 0.1, 1.0 and 10 micrograms of alpha-MSH and a placebo. The rats were tested for response to painful thermal stimuli with the tail-flick test. All of the doses of alpha-MSH produced hyperalgesia during the first 20 min of testing. Only the 1.0 microgram dose of alpha-MSH produced hyperalgesia throughout the 80 min course of the experiment. This study, coupled with previous reports that MSH/ACTH fragments may attenuate morphine-induced analgesia, suggest that MSH can have opposite actions from those of the endorphins. It is possible that alpha-MSH and related peptides may be endogenous anti-opiates.
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PMID:Intraventricular administration of MSH induces hyperalgesia in rats. 729 Oct 44

The effects of microinjections of recombinant human interleukin-1 beta (rhIL-1 beta) into the hypothalamus and neighboring basal forebrain on nociceptive behavior were studied using a hot-plate test in rats. The microinjection of rhIL-1 beta at doses between 5 pg/kg and 50 pg/kg into the medial part of the preoptic area (MPO) reduced the paw-withdrawal latency. The maximal reduction was obtained 30 min after the injection of rhIL-1 beta at 20 pg/kg. RhIL-1 beta (20 pg/kg)-induced hyperalgesia was completely blocked by the simultaneous injection of IL-1 receptor antagonist (IL-1ra, 20 ng/kg), Na salicylate (200 ng/kg) or alpha-melanocyte-stimulating hormone alpha-MSH, 20 ng/kg). The intra-MPO injection of rhIL-1 beta at doses of less than 5 pg/kg or more than 50 pg/kg (up to 2 ng/kg) into the paraventricular nucleus, the lateral hypothalamic area and the septal nucleus had no effect on nociception. The microinjection rhIL-1 beta (20 pg/kg-50 pg/kg) into the ventromedial hypothalamus produced a prolongation of the paw-withdrawal latency. A maximal prolongation was obtained 10 min after the injection of rhIL-1 beta at 50 pg/kg. This reaction was also blocked by the simultaneous injection of IL-1ra (50 ng/kg) and Na salicylate (500 ng/kg). These findings indicate that IL-1 beta in the MPO and the VMH produces hyperalgesia and analgesia, respectively, while, in addition, both effects are mediated by IL-1 receptors and the synthesis of prostaglandins.
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PMID:The opposing effects of interleukin -1 beta microinjected into the preoptic hypothalamus and the ventromedial hypothalamus on nociceptive behavior in rats. 862 21


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