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 effect of periaqueductal gray (PAG) injection of neurotensin (NT), anti-NT serum (ANTS), and naloxone (Nx) on both the pain threshold and electroacupuncture (EA) analgesia in rat was investigated in this study. The potassium iontophoresis-induced tail-flick was used to measure the pain threshold. NT administration induced an increase in pain threshold and enhanced EA analgesia. Injection of ANTS reduced the pain threshold significantly and diminished the effect of EA analgesia. Furthermore, pre-injection of Nx into PAG could weaken analgesia effect of NT and NT-EA analgesia. These results indicate that NT in PAG is involved in pain modulation and plays a role in EA analgesia. The effect of NT may be partly conducted by endogenous opiate peptides.
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PMID:[The role of periaqueductal gray neurotensin in electroacupuncture analgesia]. 1007 78

During acute attacks of hepatic porphyria, levels of polypeptides, vasoactive intestinal peptides, neurotensin, substance P, pancreatic polypeptide, gastrin releasing polypeptide, gastrin, and motilin increased in the circulation while the clinical symptoms were evident. However, somatostatin decrease was not detected. Somatostatin belongs to a group of regulatory peptides that antagonize the action of endogenous steroid hormones, and decreasing their bioavailability decreases the rate of synthesis of delta-aminolevulinate synthase, alpha-aminolevunilic acid (ALA), and polypeptides. Plasma exchange was conducted in courses for 2 consecutive days every 28 days (total of 6 courses), removing more than 100% of the patient plasma each time. Between the 2 courses of plasmapheresis, subcutaneous injections of somatostatin (100-500 mcg) were administered. A lasting disappearance of pain and complete remission were obtained in all 7 patients treated. Plasmapheresis combined with somatostatin may be considered as a treatment of porphyria exacerbation.
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PMID:Plasmapheresis combined with somatostatin is a successful treatment of porphyrias. 1022 63

The possible physiological and pathophysiological role of monoamines-adrenergic transmitter (norepinephrine), serotonin; cholinergic transmitter (acetylcholine); inhibitory (gamma-aminobutyric acid) and excitatory (glutamate) amino acids; opioid and nonopioid peptides, enkephalins, beta-endorphin and substance P, neurokinin-A, neurokinin-B, neurotensin, cytokines, calcitonine gene-related peptide, galanin, neuropeptide Y, nerve growth factor, cholecystokinin; purines; nitric oxide; vanilloid receptor agonists (capasaicin); and nociceptin-in spinal transmission of pain is reviewed. The role of substance P, neurokinin-A and neurokinin-B in the dorsal horn has been identified. These were suggested to be primary afferent transmitters mediating or facilitating the expression of nociceptive inputs. Pronociceptive modulators will be discussed later. Recent findings showing that N-methyl-D-aspartate (NMDA) receptor activation generates nitric oxide and prostanoids that enhance pain transmission whereas adenosine release acts to control these NMDA-mediated events are also mentioned. The clinical importance of centrally acting alpha2-adrenoceptor agonists (clonidine and dexmedetomidine) is also discussed. Antinociceptive and morphine-potentiating drugs are ideal adjuvants for anesthesia; their application in spinal anesthesia is highlighted. The recent development in understanding the importance of noradrenergic transmission and subtypes of alpha2-adrenoceptors (alpha2A and alpha2B) for the first time is reviewed.
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PMID:Transmitters involved in antinociception in the spinal cord. 1023 Jul 4

Protein kinase C (PKC) is thought to have a role in sensitization of dorsal horn neurons in certain pain states, and a recent study has reported that mice which lack the gamma isoform (PKCgamma) show reduced neuropathic pain after peripheral nerve injury. Although PKCgamma is present at high levels in the ventral part of lamina II we have limited information concerning the types of neuron in which it is located. In this study we have used immunocytochemistry to characterise the neurons which contain PKCgamma. Immunoreactive neurons were concentrated in ventral lamina II, but were also present in lamina III. Some weakly-immunoreactive neurons were located in the dorsal part of lamina II and in lamina I. The great majority (92%) of cells with PKCgamma were not GABA-immunoreactive, and these cells are likely to be excitatory interneurons. Dual-immunofluorescence labelling showed that PKCgamma was not randomly distributed amongst non-GABAergic neurons, since it was present in 76% of cells with neurotensin and 45% of those with somatostatin, but only 5% of those with the mu-opioid receptor (MOR-1). Cells with the neurokinin 1 receptor are found in lamina I and lamina III, and PKCgamma was present in 22% and 37% of these populations, respectively. These results suggest that excitatory interneurons in laminae II and III which lack the micro-opioid receptor may have a significant role in generating neuropathic pain.
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PMID:The types of neuron which contain protein kinase C gamma in rat spinal cord. 1037 78

The pain message originates peripherally from a great variety of substances either released from preformed stores or extemporaneously synthetized. They stimulate or sensitize nociceptors which are associated with the peripheral endings of sensitive protoneurones. Their central endings release many types of transmitters in the dorsal horn of medulla (substance P, NO, CGRP.). At this level their release, triggered by the firing rate, is modulated by the stimulation of various presynaptic receptors operated by transmitters produced by either interneurones (enkephalins) or medullar descending neurons (dopamine, norepinephrine, serotonine). These modulations correspond to the so-called gate control. The sensitive consecutive neurones which climb towards various brain areas are submitted to contradictory influences. Several of them enhance the pain perception (nociceptin, cholecystokinin, neuropeptide FF.) whereas several other reduce it (endorphines, neurotensin, neuromedin N, anandamide.).
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PMID:[Pain and its main transmitters]. 1079 Jun

Exposure to stressful or fear-inducing environmental stimuli activates descending antinociceptive systems resulting in a decreased pain response to peripheral noxious stimuli. Stimulating mu opioid receptors in the basolateral nucleus of the amygdala (BLA) in anesthetized rats produces antinociception that is similar to environmentally induced antinociception in awake rats. Recent evidence suggests that both forms of antinociception are mediated via projections from the amygdala to the ventral periaqueductal gray (PAG). In the present study, we examined the types of neurochemicals released in the ventral PAG that may be important in the expression of antinociception produced by amygdala stimulation in anesthetized rats. Microinjection of a mu opioid receptor agonist into the BLA resulted in a time dependent increase in tail flick latency that was attenuated by preadministration of a mu opioid receptor or a neurotensin receptor antagonist into the ventral PAG. Microinjection of a delta(2) opioid receptor antagonist or an NMDA receptor antagonist into the ventral PAG was ineffective. These findings suggest that amygdala stimulation produces antinociception that is mediated in part by opioid and neurotensin release within the ventral PAG.
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PMID:Antinociception produced by mu opioid receptor activation in the amygdala is partly dependent on activation of mu opioid and neurotensin receptors in the ventral periaqueductal gray. 1081 29

Our objective was to determine the least invasive surgical procedure; to do this we compared postoperative pain, duration of ileus, and level of neurohormonal stress response after laparoscopic cholecystectomy (LC) and open cholecystectomy (OC). Postoperative recovery of patients was faster after LC than OC but comparison of the neurohormonal stress response after laparoscopic and open surgical procedures revealed conflicting results. Forty-one consecutive patients with noncomplicated gallstones were randomized for LC (N = 25) and OC (N = 16). The stress level was evaluated in patients before surgery by the Hamilton anxiety scale. Postoperative pain was assessed by a visual analogic scale (VAS) pain score and by the amount of analgesic drugs (propacetamol) administered, while the duration of ileus was determined by the delay between surgery and the time to first passage of flatus as well by the colonic transit time (CTT) measured by radiopaque markers. Plasma concentrations of anti-diuretic hormone (ADH), adrenocorticotropic hormone (ACTH), beta-endorphin (BE), neurotensin (NT), and aldosterone (Ald) were measured before and during surgery as well as 2 and 5 hr after the surgery (D0) and on the day following surgery (D1). Urinary cortisol (uCOR) and urinary catecholamine metabolites were assessed before surgery, during D0, and on D1. Patient characteristics, the duration of surgery, and the doses of anesthetic drugs were not different in LC and OC. In LC patients the VAS pain score and the doses of postoperative antalgics were lower (P < 0.05), the time to first passage of flatus was shorter (P < 0.001), and the CTT tended to be shorter (54 +/- 12 hr vs 81 +/- 17) compared to OC patients. Patients who required the highest doses of postoperative antalgics had the longest delay to first passage of flatus (P < 0.01). During surgery, all neurohormonal parameters increased compared to the preoperative period (P < 0.05), and only plasma NT concentrations were lower during LC than OC (P < 0.05). During the postoperative period, ACTH, BE, Aid, catecholamines, and uCOR concentrations were lower in LC than in OC (P < 0.05). Concentrations of hormonal parameters were higher when the duration of surgery increased (P < 0.05). A greater need for propacetamol to relieve pain was associated with a greater increase in BE, ACTH, and urinary catecholamine levels (P < 0.05-P < 0.005). When the time to first passage of flatus was delayed, levels of BE, ACTH, and catecholamines and NT concentrations were increased (P < 0.05-P < 0.005). In conclusion, LC is less invasive because this surgical procedure induces a shorter neurohormonal stress response than OC, even if the peroperative response is not different. Postoperative pain levels and the duration of ileus are associated with BE, ACTH, and catecholamine levels and NT concentrations, suggesting the importance of hormones in postoperative functional recovery.
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PMID:Operative stress response is reduced after laparoscopic compared to open cholecystectomy: the relationship with postoperative pain and ileus. 1105 8

Stress-induced analgesia is a well-documented phenomenon that occurs in all mammalian species. Forced cold water swim produces a type of stress-induced analgesia that is independent of mu opioid receptors. The neuropeptide neurotensin (NT) has been implicated in mu opioid-independent analgesia (MOIA), but the circuitry of this system is largely unknown. The medial preoptic area (MPO) and lateral hypothalamus (LH) are two regions that are known to modulate pain processing. These two regions also contain neurotensinergic projections to the periaqueductal gray, a region that has been shown to produce MOIA upon injection of NT. The goal of this study was to determine if cold water swim (CWS) stress, which produces MOIA, activates the NT-ergic systems in these two regions. In situ hybridization results indicate that CWS increases the level of NT mRNA within neurons in the MPO and LH, suggesting that these two regions are activated during this process.
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PMID:Cold water swim stress increases the expression of neurotensin mRNA in the lateral hypothalamus and medial preoptic regions of the rat brain. 1116 81

With the use of potassium iontophoresis induced tail-flick for measuring the pain threshold, the effects of injecting neurotensin (NT), naloxone (NX), anti-metenkephalin serum (AMEKS), anti-beta-endorphin serum (AEPS) and anti-dynorphin A1-13 serum (ADYNS) into periaqueductal gray (PAG) on electroacupuncture (EA) analgesia in rats were investigated. NT administration enhanced EA analgesia remarkably. Pre-injection of NX, AMEKS and AEPS into PAG could significantly attenuate the enhancement of EA analgesia induced by NT, but not by administration of ADYNS. The results indicate that NT in PAG is responsible for the enhancement of EA analgesia. The effect of NT may be partly mediated by met-enkephalin and beta-endorphin.
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PMID:[Effect of anti-opioid peptide sera on the enhancement of electroacupuncture analgesia induced by neurotensin in PAG of rats]. 1149 20

Estradiol, progesterone and some of their metabolites modulate the activity of neurotransmitters and neuropeptides in the CNS. The distribution and concentrations of sex steroids in the various CNS regions is partly dependent on the serum levels, but also on the local synthesis of the steroids. In general, estradiol and testosterone exert a stimulatory, progesterone an inhibitory effect on neuronal activities which are mediated by excitatory (e.g. glutamate, aspartate), and inhibitory amino acids (e.g. GABA) and neuropeptides (e.g. beta-endorphin), respectively. Gonadotropin release is primarily governed by the rhythm of pulsatile secretion of GnRH in the hypothalamus which is controlled by estradiol and progesterone by means of inhibitory or stimulatory modulation of the amplitude and frequency of GnRH pulses. The discharges of GnRH neurons triggered by excitatory amino acids are modulated by estradiol, while the inhibitory effect of progesterone is mediated by GABA and beta-endorphin which cause hyperpolarization of the GnRH neurons and consequently a reduced pulse frequency. The pulse amplitudes are primarily influenced by estradiol, but neuropeptide Y, neurotensin and noradrenaline contribute to their preovulatory enhancement. The postovulatory rise in core temperature is caused by the increasing level of progesterone and its metabolite 3 alpha-pregnanolone, respectively. Despite of this, up to 20% of ovulatory cycles do not show any rise in body temperature. Although 3 alpha-pregnanolone has sedative activities, there is no change in sleep quality during the luteal phase due to their low serum levels. It could be demonstrated that performance on tests of articulatory and fine motor skills are enhanced in the late follicular phase as compared to the menstruation phase, while spatial ability was better during menses. Estrogens may influence mood and well-being in a favorable manner, while in predisposed women progesterone may cause symptoms of premenstrual syndrome. In most women there are, however, no cycle-dependent mood changes. An increase in appetite can be observed during the periovulatory phase and before menses, while sexual interest increases in the follicular phase. Somatic complaints (back pain, abdominal pain, breast tenderness) which are highest before and during menstruation, are probably associated with a lowered pain threshold due to a fall in the beta-endorphin levels in the CNS.
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PMID:[Influence of the ovarian cycle on the central nervous system]. 1201 35


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