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)

Antisera against two mammalian peptides related to the molluscan cardioexcitatory peptide Phe-Met-Arg-Phe-NH2 were used to locate immunoreactive neurons in the rat brain, nerve fibres and terminals in the spinal cord, sympathetic ganglion cells and adrenal chromaffin cells. Immunoreactivity for the newly characterised octa- and octadecapeptide was detected in nerve cell bodies in the hypothalamic area, including parts of the dorsomedial, periventricular and paraventricular nuclei, and in the nucleus tractus solitarii. Nerve terminals in the superficial laminae of the spinal cord were also immunoreactive for these peptides, while the sensory ganglia were nonreactive. Some principal ganglion cells in the superior cervical ganglia exhibited bright immunofluorescence for the peptides, and a few adrenal medullary cells were immunoreactive. The presence of these peptides in the substantia gelatinosa of the spinal cord suggests that they may be involved in sensory neurotransmission, especially in the mechanisms mediating pain. In the hypothalamo-hypophysial system these peptides may be involved in the regulation of hormonal systems. They may also act as co-transmitters in the sympathetic nervous system.
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PMID:Neuroanatomy of morphine-modulating peptides. 365 12

Rats were taught to self-administer Leu-E (10, 25 and 100 micrograms/microliters) or Met-E (0.5, 10 and 100 micrograms/microliters) through a cannula implanted in the lateral cerebral ventricle (i.c.v.). Their self-injection behaviour was studied before, during and after nociceptive stimulation. In the course of the control period of the experiment, the rats rapidly learned lever pressing for self-injection of enkephalin but they did not increase their self-administration of Leu-E or Met-E during the nociceptive electrical stimulation period. Also studied were the acute effect of i.c.v. enkephalin and morphine on tail-flick latency (sec) and electrical threshold vocalization (mA). The analgesic effect of Leu-E and Met-E was of short duration (less than 2-6 min). The mean rise (i.e., analgesia) of the tail-flick threshold showed a significant difference after i.c.v. Met-E only. The acute i.c.v. effect of 20 or 30 micrograms of morphine induced a long-lasting analgesia, greater than 40 min. These results show that Leu-E and Met-E are not rewarding during a nociceptive stimulus. This may be due to the short and inconstant analgesic action of i.c.v. enkephalins.
Pain 1985 May
PMID:A study of intracerebroventricular self-administration of leucine or methionine enkephalin by rats in response to intermittent electric shocks. 401 Dec 83

The finding of a number of peptides in the central nervous system and the discovery of the endogenous opiates represent major recent advances in the understanding of neural transmission. A number of these neuropeptides are found in the dorsal root entry zone and may play a role in pain. An analysis of changes in distribution of substance P, methionine-enkephalin, and somatostatin after simulated nerve root avulsion injury suggested a possible mechanism for deafferentation pain. A review of the localizations and actions of these peptides in the dorsal root entry zone is included.
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PMID:Neuropharmacology of the dorsal root entry zone. 608 4

Substance P (Arg-Pro-Lys-Pro-Gln-Gln-Phe-Phe-Gly-Leu-Met-NH2) may be used as a neurotransmitter by certain primary afferent neurones, particularly those carrying pain impulses. Substance P-like immunoreactivity has been localised to the cell bodies of one population of dorsal root ganglion neurones by immunocytochemistry. It is contained in vesicles in the central terminals of these neurones, and has also been demonstrated in the peripheral terminals. As axons and terminals have very little capacity for peptide biosynthesis, it is possible that substance P is synthesised and packaged in the perikaryon and transported to the terminals by an axoplasmic transport process. Consistent with this is the finding that substance P accumulates proximal to a ligature placed on the dorsal root. There has, however, been no direct demonstration of the biosynthesis of substance P in the nervous system. We report here that rat dorsal root ganglia incorporate 35S-methionine into substance P, characterised as authentic by immunoprecipitation followed by HPLC. There is a delay of 1-2 h between addition of label and its incorporation into substance P. Synthesis is blocked by cycloheximde suggesting that, in dorsal root ganglia, substance P is synthesised by a conventional ribosomal process. Synthesis of substance P is reduced by some 90% in ganglia from rats treated neonatally with capsaicin, a drug which is thought to destroy a population of primary afferent neurones.
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PMID:Cycloheximide-sensitive synthesis of substance P by isolated dorsal root ganglia. 615 59

The effect of various opioid or putative neurotransmitter peptides on histamine-induced itch and flare responses was studied in humans after intradermal injection. Significant enhancement of the histamine responses was induced by the stable methionine-enkephalin analogue FK 33-824, beta-endorphin and morphine. The putative neurotransmitters substance P and vasoactive intestinal polypeptide (VIP)--which moreover are potent histamine liberators--had no enhancing effect. The potentiation induced by FK 33-824 was induced neither by local pretreatment with Compound 48/80 to deplete the local stores of mast-cell-bound histamine, nor by oral pretreatment with indomethacin to inhibit prostaglandin formation in the skin. Thus, the enhancement did not seem to be due to histamine release or to prostaglandin formation and the mechanism of the effect remains to be shown. The specific morphine antagonist naloxone did not inhibit the potentiation by FK 33-824, which might indicate that ordinary opiate receptors were not involved. The results support the idea that pain and itch are qualitatively separate processes and suggest possible mechanisms of morphine-induced pruritus. The findings are of particular interest in view of recent reports on the presence of methionine-enkephalin in Merkel cells.
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PMID:Potentiation of histamine-induced itch and flare responses in human skin by the enkephalin analogue FK-33-824, beta-endorphin and morphine. 618 98

The occurrence of methionine enkephalin (379 pg/g tissue), beta-endorphin (448 pg/g tissue) and Substance P (2.4 pg/g tissue) in human placental villus were demonstrated by sensitive and specific radioimmunoassays. Conditions for the bioassay of placental extracts for enkephalin-like activities using the rat vas deferens were described. Substance P did not interfere in this bioassay. Comparison of the enkephalin-like activities determined by bioassay and the content of beta-endorphin and methionine enkephalin determined by radioimmunoassays indicated that placental villus extracts contain other unidentified potent opioid-like peptides or substances. It is suggested that methionine enkephalin and/or beta-endorphin and Substance P regulate release of acetylcholine or hormones from placental villus. Alternatively, these peptides may regulate sensory transmission (pain impulses) locally from the distended uterus during pregnancy or from the vaginal tract during childbirth.
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PMID:Peptides from human placenta: methionine enkephalin and substance P. 619 22

The relationship between neuropeptides and serotonergic neurones was investigated in rat spinal cord, in vivo, using a subarachnoidal perfusion technique. The 5-hydroxytryptamine (5-HT) release from the spinal cord could be evoked by substance P and peripheral pain stimulation (tail pinch), but not by methionine-enkephalin (met-EK). The substance P-evoked 5-HT release was slightly potentiated by met-EK. The tail pinch-evoked 5-HT release was inhibited by met-EK and baclofen, but potentiated by naloxone. These findings may infer a possible mechanism by which neuroactive peptides regulate 5-HT release from serotonergic neurones in the spinal cord.
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PMID:Further evidence for the possible relationship between neuropeptides and serotonergic neurones in rat spinal cord. 620 98

beta-Endorphin and methionine(met)-enkephalin in cerebrospinal fluid (CSF) were measured before and after removal of an adrenocorticotropic hormone-(ACTH)-secreting adenoma in Cushing's disease by a sensitive radioimmunoassay and a radio-receptor assay, respectively. After tumor resection, the level of ACTH in plasma markedly decreased from 82.6 +/- 22.7 pg/ml to 16.7 +/- 4.1 pg/ml (mean +/- S.E., n = 4). It was found that the level of beta-endorphin in CSF significantly increases from 32.0 +/- 4.5 pg/ml to 61.8 +/- 10.7 pg/ml (P less than 0.05) after tumor resection, while the level of metenkephalin in CSF remained unaltered. This result suggests that hypophysectomy induces an increase of beta-endorphin in CSF.
Pain 1981 Aug
PMID:Increase of beta-endorphin in cerebrospinal fluid after removal of ACTH-secreting pituitary adenoma. 627 76

Met5-enkephalin, tyr-gly-phe-met, is an endogenous pentapeptide, with morphine agonist activity. In this study, we demonstrated that met5-enkephalin was degraded with the release of tyrosine by resting human PMN, whereas it was degraded as well as oxidized to its sulfoxide derivative, met5-(O)-enkephalin, by phagocytosing PMN. PMN also degraded met5-(O)-enkephalin but to a lesser extent. Bacitracin at 1 gm/L inhibited the degradation and oxidation of met5-enkephalin without affecting the production of superoxide and viability of PMN. The oxidation of met5-enkephalin by phagocytosing PMN was inhibited by catalase or NaN3 but not by SOD. This suggests that the oxidation of met5-enkephalin by phagocytosing PMN was, at least in part, dependent on the MPO system (MPO-H2O2-halide). Using purified canine MPO, we further demonstrated that MPO-H2O2-CI- oxidized met5-enkephalin to met5-(O)-enkephalin. The MPO-mediated oxidation of met5-enkephalin was inhibited by methionine but not by methionine sulfoxide, tyrosine, glycine, or phenylalanine, confirming that it was the methionine moiety of met5-enkephalin which was oxidized. Since both the sulfoxide derivative and the degradation products met5-enkephalin have reduced opiate agonist activity, oxidation and degradation of met5-enkephalin by PMN may contribute to the pain at the site of inflammation. (J Lab Clin Med 99:418, 1982.)
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PMID:Degradation and oxidation of methionine enkephalin by human neutrophils. 627 80

Properties of the opiate receptor, such as its discrimination of agonists and antagonists, and the relationship between receptor localization and central sites of pain perception suggested that this receptor might interact with a normally occurring opiate-like substance. Such opioid peptides have now been described in at least two systems of distinct neurons which occur in areas particularly associated with pain and emotion. Understanding the relationship between the multiple opiate receptors described pharmacologically and those distinguished by binding studies in methionine- or leucine-enkephalin-containing neurons might be useful for the development of new drugs that suppress pain or alter emotion without producing tolerance or withdrawal effects.
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PMID:A multiplicity of opiate receptors and enkephalin neuronal systems. 628 18


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