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)

Tolerance to morphine analgesia was induced in rats by chronic treatment with morphine (5-30 mg/kg, t.i.d. for 6 days). Intracerebroventricular (i.c.v.) injection of antiserum against cholecystokinin octapeptide (CCK-8) reversed tolerance to morphine by 50% (P less than 0.001). Intrathecal (ith) injection of the CCK-8 antiserum produced a similar, although less marked, reversal of tolerance to morphine. Rats made tolerant to analgesia induced by morphine developed a cross tolerance to electroacupuncture-induced analgesia. This cross tolerance was also reversed by the CCK-8 antiserum by more than 50% (P less than 0.001). Intracerebroventricular or intrathecal injection of the CCK-8 antiserum per se produced no significant changes in the basal level of the latency of the tail flick response, nor did it affect the analgesia induced by morphine in naive rats. The results suggest that prolonged activation of opioid receptors may trigger the CCK-8 system in the central nervous system to exert a negative feedback control, which may constitute one of the mechanisms for the development of tolerance to opioids.
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PMID:Reversal of tolerance to morphine but no potentiation of morphine-induced analgesia by antiserum against cholecystokinin octapeptide. 349 37

The analgesic effect produced by electroacupuncture (EA) stimulation in the rat was dose-dependently antagonized by cholecystokinin octapeptide (CCK-8) administered intracerebroventricularly (i.c.v.) or intrathecally (i.th) at a dose range of 0.25-4 ng. This effect had an immediate onset and lasted for at least 4 h. CCK-8 per se, however, did not affect baseline tail flick latency. Rats subjected to prolonged EA stimulation developed EA tolerance as well as cross-tolerance to morphine. These tolerances could be postponed or reversed by i.c.v. or i.th injection of antiserum against CCK-8. While CCK-8 antagonized opioid analgesia, it did not affect analgesia induced by 5-hydroxytryptamine (5-HT) or norepinephrine (NE). Moreover, CCK-8 antiserum did not alter the basic level of nociception, nor did it potentiate EA analgesia in naive rats. It is concluded that prolonged EA stimulation results in a profound release of opioids which may trigger the release of CCK-8 in the central nervous system to counteract the opioid component of EA analgesia. This mechanism may account, at least in part, for the development of EA tolerance.
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PMID:Cholecystokinin octapeptide (CCK-8): antagonism to electroacupuncture analgesia and a possible role in electroacupuncture tolerance. 349 55

A tabular synopsis is presented for articles concerned with the effects of peptides on the central nervous system that appeared in the journal Peptides from 1980-1985. A table arranged alphabetically by peptide and one arranged by effects, both listing routes of injection, species, direction of change, and qualifying notes, provides easy cross-referencing of peptides and their effects. Over 80 peptides and over 135 effects are listed. The list of peptides includes, but is not limited to: ACTH, angiotensin, bombesin, bradykinin, calcitonin, casomorphin, CCK, ceruletide, CGRP, CRF, dermorphin, DSIP, dynorphin, endorphins, enkephalins, GRF, gastrin, LHRH, litorin, metkephamid, MIF-l, motilin, MSH, NPY, NT, oxytocin, ranatensin, sauvagine, substances P and K, somatostatin, TRH, VIP, vasopressin, and vasotocin. The list of effects includes, but is not limited to: aggression, alcohol, analgesia, attention, avoidance, behavior, cardiovascular regulation, catalepsy, conditioned behavior, convulsions, dopamine binding and metabolism, discrimination, drinking, EEG, exploration, feeding, fever, gastric secretion, GI motility, grooming, learning, locomotor behavior, mating, memory, neuronal activity, open field, operant behavior, rearing, respiration, satiety, scratching, seizure, sleep, stereotypy, temperature, thermoregulation and tolerance.
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PMID:Central nervous system effects of peptides, 1980-1985: a cross-listing of peptides and their central actions from the first six years of the journal Peptides. 353 8

The C-terminal octapeptide of cholecystokinin (CCK 8) was administered intrathecally to rats. Doses in the nanogram range produced weak but significant antinociception in the paw pressure test five minutes after injection whereas microgram doses of CCK 8 produced hyperalgesia. The CCK 8-induced analgesia or hyperalgesia was not seen in the tail flick test and was not associated with motor incapacitation or any other noticeable side effects. The C-terminal tetrapeptide of CCK (CCK 4) and pentagastrin were found to be ineffective in all tests but caerulein and molluscan cardioexcitatory neuropeptide (FMRF-amide), like CCK 8, produced antinociception in the paw pressure test.
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PMID:CCK 8 analgesia and hyperalgesia after intrathecal administration in the rat: comparison with CCK-related peptides. 367 May 69

Phe-Met-Arg-Phe-NH2 (FMRF-NH2) was initially isolated from the macrocallista nimbosa clam and subsequently existence of FMRF-NH2-like immunoreactivity (FMRF-NH2-IR) was detected in mammalian CNS. Due to the structural similarity between FMRF-NH2 and the C-terminal extended form of met5-enkephalin, met5-enkephalin-arg6-phe7 (YGGFMRF), a possible interaction between these two peptides was explored. FMRF-NH2 injected intrathecally decreases the antinociceptive action of YGGFMRF or morphine. However, the FMRF-NH2-IR present in rat and bovine brains differs from FMRF-NH2. Intrathecally injected FMRF-NH2-IR partially purified from bovine brain reduces YGGFMRF antinociception. The antagonism elicited by FMRF-NH2 can be reversed by proglumide, which was reported to act as a CCK antagonist. In order to characterize the biological profile of FMRF-NH2-IR, the effect of proglumide and of the FMRF-NH2 antibody on morphine analgesia was tested. Both the IgG isolated from FMRF-NH2 antiserum and proglumide were found to potentiate the morphine analgesia. The results taken together suggest that endogenous FMRF-NH2-IR modulates opioid antinociception; perhaps by acting as an endogenous naloxone.
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PMID:Are Phe-Met-Arg-Phe-NH2 immunoreactive peptides endacoids modulating opiate antinociception? 390 60

The decapeptide from the frog Hyla caerulea, caerulein (caerulein diethylammonium hydrate, ceruletide, CER) is chemically closely related to the C-terminal octapeptide of cholecystokinin (CCK-8). Like CCK-8, CER and some of its analogues produce many behavioural effects in mammals: inhibition of intake of food and water; antinociception; sedation; catalepsy; ptosis, antistereotypic, anticonvulsive and tremorolytic effects; inhibition of self-stimulation. Effects of CER in man comprise sedation, satiety, changes in mood, analgesia and antipsychotic effects. A modulation of central dopaminergic functions appears to be one possible mechanism of CER and its analogues. A common denominator for all effects of CER is, at present, not evident.
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PMID:Caerulein and its analogues: neuropharmacological properties. 391 10

Cholecystokinin octapeptide (CCK-8), given intracerebroventricularly (icv) or intrathecally (ith) at the dose range of 0.25-4.0 ng, dose-dependently antagonised the effect of morphine analgesia and electroacupuncture analgesia (EAA) in the rat. That CCK-8 antiserum was capable of reversing the tolerance to EAA and changing the non-responders of EAA into responders suggest CCK-8 to be the endogenous anti-opioid substrate and that blocking the effect of CCK-8 may prove to be a powerful way of augmenting the effect of morphine analgesia and EA analgesia.
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PMID:Is cholecystokinin octapeptide (CCK-8) a candidate for endogenous anti-opioid substrates? 400 Apr 12

The effect of cholecystokinin octapeptide (CCK-8) and its analogue, ceruletide on release of acetylcholine (ACh) from the cerebral cortex was investigated in urethane-anaesthetized and in unanaesthetized rats. Cholecystokinin octapeptide and ceruletide markedly stimulated output of ACh at doses of 1.5 and 5.0 micrograms/kg (i.p.), respectively. This effect was prevented by proglumide (160 mg/kg i.p.), a specific cholecystokinin receptor antagonist. At doses of 10 micrograms/kg (i.p.) and more, both CCK-8 and ceruletide decreased output of ACh from the cerebral cortex. The decrease was prevented by naloxone (1 mg/kg, s.c.), and replaced by a short-lasting increase. Cholecystokinin octapeptide and ceruletide appear therefore to affect the activity of cortical cholinergic fibres by acting upon both specific and opiate receptors. The interaction between CCK-8 and ceruletide, and opiate receptors either direct or through the release of endogenous opiates, was also demonstrated by the antagonism between ceruletide (1, 5 and 10 micrograms/kg, i.p.) and analgesia induced by morphine (5 mg/kg, s.c.), evaluated by the tail-flick test in the rat.
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PMID:Effect of cholecystokinin octapeptide and ceruletide on release of acetylcholine from cerebral cortex of the rat in vivo. 609 46

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

The effect of intrathecal injections of morphine and the two peptides, caerulein and cholecystokinin octapeptide (CCK-8), on the activity in ascending axons of the spinal cord evoked by electrical stimulation of primary nociceptive afferents was studied in spinal rats with decerebration. Morphine (20 microgram) depressed the spontaneous activity and the activity evoked from either A delta-or C-fibres. The co-activation by A delta-fibre stimulation of ascending axons activated by stimulation of C-fibres and the activity in ascending axons activated by stimulation of afferent A beta-fibres were not influenced by morphine. C-Fibre-evoked ascending activity was also depressed by morphine (10 microgram and 5 microgram). Ascending nociceptive activity was not changed by caerulein (30 ng) and CCK-8 300 ng, but it was depressed by a subsequent injection of morphine (20 microgram). The depressant effects of morphine were abolished by an intravenous injection of concluded that: (i) an intrathecal injection of morphine selectively depressed the ascending nociceptive activity; (ii) the depression produced by morphine is an equivalent for spinal analgesia following intrathecal injection of morphine to man; and (iii) the two components of the spinal nociceptive system, the motor and the sensory path, can independently be influenced by drugs.
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PMID:Analgesic effect of intrathecal morphine demonstrated in ascending nociceptive activity in the rat spinal cord an in effectiveness of caerulein and cholecystokinin octapeptide. 627 33


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