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Query: UMLS:C0344307 (analgesia)
 28,200 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Pain sensitivity of food and/or water-deprived male mice was tested on a hotplate. The most pronounced analgesia ensued in animals given no food and water, and no food but water ad libitum, the least one in water-deprived mice. The magnitude of the rise in pain threshold depended on the duration of deprivation and was correlated with the increase in the blood plasma beta-endorphin level. In the hypothalamus beta-endorphin level increased after 72-h food deprivation only. The level of dynorphin remained unchanged. Naloxone (10 mg/kg) almost completely reversed food or water-deprivation induced analgesia.
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PMID:The effect of food and water deprivation on post-stress analgesia in mice and levels of beta-endorphin and dynorphin in blood plasma and hypothalamus. 242 64

Fischer-344 rat pups were injected with either 10 mg/kg delta 9-tetrahydrocannabinol (THC) or vehicle on postnatal days 4,6 and 8. Pups were then allowed to mature. On day 129 of age rats were exposed to a stress paradigm which consisted of inescapable electric foot-shock administered at 1 mA for 15 sec daily for 8 days. Analgesia induced by foot-shock was measured by tail withdrawal from 55 degree C water. On the 9th day rats were exposed to the shock environment only. Fifteen minutes following measurement of tail withdrawal, animals were sacrificed. Plasma corticosterone and prolactin were measured. Levels of norepinephrine, dopamine and 5-hydroxytryptamine and metabolites were determined in frontal cortex, hippocampus and hypothalamus. Neonatal exposure to THC produced an increase in baseline tail withdrawal latency. No effect of THC exposure was seen on acute stress-induced analgesia. Rats exposed to THC required a greater number of conditioning trials to develop conditioned analgesia than animals treated neonatally with vehicle. The conditioned stress increased plasma corticosterone without affecting prolactin. Stress increased hypothalamic 5HT and 5HIAA while decreasing 5HT turnover in this area. Dopamine and DOPAC levels in the hypothalamus and frontal cortex were increased by stress; dopamine turnover in the frontal cortex was elevated by stress. Neonatal THC and stress elevated norepinephrine above control levels in the hypothalamus, while increasing 5HT in the hippocampus and frontal cortex. The stress-induced increase in DOPAC in the frontal cortex was decreased by THC exposure. These data suggest that long-term neurochemical changes may occur with neonatal administration of THC.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Neonatal administration of delta-9-tetrahydrocannabinol (THC) alters the neurochemical response to stress in the adult Fischer-344 rat. 244 11

Analgesic and discriminative stimulus effects of phencyclidine (PCP), ketamine, dextrorphan, (+)-N-allyl-normetazocine [(+)-SKF 10,047] and (+)-5-methyl-10,11-dihydro-5H-dibenzo(a,d) cyclohepten-5,10-amine maleate (MK-801) were studied in rhesus monkeys. All five compounds increased in a dose-related manner the latency for monkeys to remove their tails from warm water with the order of potency being MK-801 greater than PCP greater than ketamine greater than (+)-SKF 10,047 greater than dextrorphan. Moreover, these effects were temperature-dependent with larger doses required to produce a maximum response when higher temperatures (i.e., 55 degrees C) were studied. The effects of PCP, ketamine, dextrorphan, (+)-SKF 10,047 and MK-801 were not attenuated by a dose (1.0 mg/kg) of the opioid antagonist quadazocine that antagonized the analgesic effects of the opioid mu agonist alfentanil and kappa agonist U-50,488. MK-801, PCP, (+)-SKF 10,047 and dextrorphan also substituted in a dose-related manner for the ketamine discriminative stimulus (1.78 mg/kg) and their relative potency as discriminative stimuli was the same as their relative potency in the tail withdrawal procedure. The apparent analgesic effects of PCP-like drugs occurred at doses 2- to 8-fold larger than doses required for discriminative stimulus effects and 3- to 10-fold smaller than doses required for anesthesia. These results support the notion that PCP-like drugs produce analgesic effects at subanesthetic doses. Moreover, the analgesic effects of PCP and related drugs in rhesus monkeys were not mediated by actions at the opioid receptors known to be associated with analgesia.
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PMID:Analgesic effects of phencyclidine-like drugs in rhesus monkeys. 250 76

Alterations in nociceptive reactivity, opiate receptor binding, and other behavioral responses occur in rats exposed to morphine either in utero or post-natally. The present study examined whether post-natal morphine (0, 1 or 20 micrograms, days 1-7) altered analgesia on the tail-flick and jump tests induced by nonopioid-mediated continuous cold-water swims (CCWS), opioid-mediated intermittent cold-water swims (ICWS) or morphine (2.5 and 5.0 mg/kg, SC) in adult male and female rats. Changes in body weight, developmental signs (e.g., eye opening), basal pain thresholds, and both CCWS and ICWS hypothermia were also assessed. Previously-reported gender differences occurred for all forms of analgesia in control rats. Post-natal morphine treatment transiently increased ICWS analgesia and hypothermia, and transiently decreased CCWS analgesia and hypothermia, suggesting that these effects were not specific to pain inhibition. Post-natal morphine treatment significantly increased the magnitude of morphine analgesia on both tests in females, and significantly decreased the magnitude of morphine analgesia on both tests in males, thereby acting to vitiate the observed gender differences in morphine analgesia. Such effects could not be explained by concomitant changes in other measures. These data indicate that post-natal morphine treatment exerts highly selective effects upon specific analgesic responses which are gender sensitive.
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PMID:Post-natal morphine differentially affects opiate and stress analgesia in adult rats. 250 92

This study demonstrates that pre-exposure to stress influences subsequent effects of stress on pain sensitivity (stress-induced analgesia) and on plasma corticosterone and brain catecholamine activity. Animals exposed to a 30 min shock session (S1 = 8, 5.0 s shocks) 10 days earlier showed a significant attenuation of shock-induced analgesia, as measured by increased latency of tail withdrawal from a hot water bath immediately after a 40 s, 1.6 mA footshock (S2). Animals exposed to shock 10 days before testing also exhibited a higher plasma corticosterone response to testing than did all other groups. Norepinephrine (NE) levels in the frontal cortex and dopamine (DA) and dihydroxyphenylacetic acid (DOPAC) levels in the frontal cortex and nucleus accumbens were not altered in any group. However, the DOPAC/DA ratio in the frontal cortex was increased by analgesia testing, and this increase was enhanced only by the combination of shock 10 days before testing and shock immediately before the test (S1 + S2). These results are consistent with previous reports from this laboratory which indicate that an animal's acute response to stress is strongly influenced by its past history of stress.
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PMID:Prior stress attenuates the analgesic response but sensitizes the corticosterone and cortical dopamine responses to stress 10 days later. 250 60

A lot of researches indicate that central nervous system not only exist endogenous opiate analgesic system but also possess endogenous nonopiate analgesic system. The opiate and nonopiate analgesic systems can be selectively activated by different environmental or artificial manipulations and modulated the stimulation-produced analgesia, acupuncture analgesia and stress-induced analgesia, including the foot shock-induced analgesia, tail-shock-produced analgesia, ear-shock-induced analgesia, analgesia of cold water swim, analgesia of immobilization or of restraint and analgesia of a-Deoxy-D- glucose and so on. The existence and description of these modulatory mechanisms have it's multiplicity and important clinical implications for the treatment of pain.
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PMID:[The endogenous opiate and nonopiate analgesic system]. 251 18

Eighty-three women experiencing low back pain in the 1st stage of labor were given intracutaneous nociceptive stimulation (INS) by means of sterile water papules injected intracutaneously over sacrum. There was instant and complete relief of the low back pain in all but 6 women, this effect lasting in many cases as long as 3 h, after which INS could be repeated. A reduction in total pain-score from 6.05 to 2.92 was seen after 1 hour with no further analgesia given, and half the women required no further analgesia during the 1st stage. The method was well tolerated and 67 of the 83 women said they would like to have INS analgesia for their next delivery. Possible mechanisms behind the analgesic effect of INS are discussed.
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PMID:Relief of low back pain in labor by using intracutaneous nerve stimulation (INS) with sterile water papules. 253 52

MR2266 (MR), an opioid antagonist that binds to kappa and mu receptors, was examined for its ability to influence the aversively motivated behaviors conditioned by electric shock and the drinking induced by water deprivation or the availability of a palatable saccharin/glucose solution. The intraperitoneal (ip) and intracerebroventricular (icv) administration routes were contrasted. After both ip and icv administration, MR was able to reverse conditional analgesia as measured by the formalin test. MR enhanced the Pavlovian conditional freezing response when administered icv prior to shock exposure but reduced freezing if given ip prior to shock. A related benzomorphan-derived opioid antagonist, MR1452, also reduced freezing when given ip prior to shock. MR2266 was a potent antidipsogenic agent when administered ip but had no such effect when administered icv. It is concluded that separable opioid systems are involved in the modulation of appetitively and aversively motivated behaviors.
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PMID:Modulation of appetitively and aversively motivated behavior by the kappa opioid antagonist MR2266. 254 7

This study was designed to evaluate whether or not rats that were tolerant to the analgesic action of morphine were also tolerant to stress-induced potentiation of morphine-induced analgesia. Rats were trained to drink either solutions of morphine (0.5 mg/ml) or drug-free tap water on a limited access schedule (10 min every 6 hr). The daily intake of morphine averaged 46 mg/kg. Nontolerant and rats tolerant to morphine were tested for morphine-induced analgesia (tail-flick assay), while either unstressed or stressed (i.e. immobilized in Plexiglas cylinders). Morphine produced dose- and time-dependent increases in tail-flick latencies in all groups. Increased sensitivity to analgesia induced by morphine was evident for both nontolerant and tolerant, stressed rats, when compared to their unstressed counterparts. Stress-induced potentiation of morphine-induced analgesia was characterized by dose-related increases in the peak effect and duration of the effect. Stress potentiated the analgesic effect of morphine, comparably in nontolerant (1.7-fold) and tolerant (1.5-fold) rats. Differential tolerance to analgesia induced by morphine and to stress-induced potentiation of morphine-induced analgesia suggests that different mechanisms mediate these two effects.
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PMID:Stress-induced potentiation of morphine-induced analgesia in morphine-tolerant rats. 256 74

This study was undertaken to examine the thermal pain thresholds over a wide area of the lower body surface following the intrathecal administration of capsaicin in rats. Thermal nociceptive thresholds measured under light halothane anesthesia were determined as skin twitch or escape response latencies to the heat stimulation (52.0 degrees C) by a thermal probe. Capsaicin (50 micrograms in 10 microliters) was injected through a chronically implanted catheter whose tip was near the lumbar enlargement of the spinal cord. The hot-plate test (52.0 degrees C) was also performed in all rats tested. Increase in thermal pain thresholds were consistently observed in the low back and abdominal region, while the hind paws did not always respond with prolonged skin twitch or escape latencies. Intensities of thermal analgesia at the sole of hind paws measured by hot-plate test correlated well with those by thermal probe test. In conclusion, intrathecal capsaicin definitely produced thermal analgesia, but its intensity was considerably variable in the hind paws. These results are in keeping with our previous finding that there was much variability in the effect of capsaicin assessed by the hot-plate test, indicating a possibility that capsaicin does not spread uniformly in the CSF because of its water insolubility or difficulty in penetrating to the large nerve roots innervating the hind paws.
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PMID:[Thermal analgesia following intrathecal capsaicin administration in rats--detailed measurements of thermal analgesia over the lower body by a thermal probe]. 258 99


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