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)

Delta-9-tetrahydrocannabinol (THC) was administered to young male Fischer-344 (CDF) and Sprague-Dawley (CD) rats on days 30-50 of age. Doses of THC consisted of 20, 10 or 5 doses of 10 mg/kg spaced over the 20-day period. On day 140 animals were exposed to a 15 sec 1.5 mA scrambled foot-shock. Latency for withdrawal from 55 degrees C water was used as a measure for analgesia. Both CDF and CD rats showed a foot-shock induced analgesia (FSIA). Animals which had received 5 or 10 doses of THC in youth showed an enhanced response to foot-shock in the CDF rat. The foot-shock was then paired with an unconditioned stimulus (shock environment) and a conditioned analgesia developed over 4 days. At weekly intervals thereafter animals were tested in the shock environment only for extinction of the analgesic response. Over 4 weeks, analgesia did not show extinction in the CDF rat. Extinction of the response was observed in the veh and 20 dose groups in the CD rat; whereas a resistance to extinction was observed in the other groups. The CDF rats were then sacrificed following the last extinction trial and serum corticosterone and prolactin measured. Five and 10 doses of THC decreased prolactin levels; stress, however, increased these levels above the levels in VEH treated animals exposed to stress. Extinction of a fixed ratio 10 as well as exposure to fixed ratio strain in the CD rat were not affected by THC. These data suggest that THC administered during postweaning development alters endogenous systems which mediate the animals response to stress.
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PMID:Effects of postweaning administration of delta-9-tetrahydrocannabinol (THC) on adult behavioral and neuroendocrine function in Sprague-Dawley and Fischer-344 rats. 302 Apr 62

The hypothalamic paraventricular nucleus (PVN) has been implicated in a remarkable number of functions including control of pituitary-adrenocortical activity in response to stress, body fluid homeostasis, milk ejection reflex, prolactin secretion, thyroid hormone secretion, analgesia, food intake, gastrointestinal functions, cardiovascular functions, and control of pineal melatonin synthesis. Paraventricular neurons produce hormones of key importance in neuroendocrine regulation such as vasopressin (VP), oxytocin (OX), 41-residue corticotropin releasing factor (CRF), thyrotropin releasing hormone (TRH), somatostatin (SOM) and the putative prolactin releasing factor vasoactive intestinal polypeptide (VIP). Three recent advances pertinent to the organization of the PVN include: (1) the evidence that the structure of the PVN is compartmental in nature, topographically segregated cellular units seem to carry out different functions; (2) the discovery that paraventricular neurons are capable of expressing a multitude of neuromediators simultaneously, thus cellular units can be best specified by a certain combination of neuromediators; (3) evidence that the composition of the neuromediator "cocktail" in individual neurons is variable and depends on the physiological status of the animal. Hence, the PVN may be best considered as a dynamic mosaic of chemically specified subgroups of neurons. The flexibility of neurotransmitter status in paraventricular neurons may play a central role of a functional plasticity of fixed anatomical circuits.
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PMID:Dynamism of chemoarchitecture in the hypothalamic paraventricular nucleus. 304 19

The effect of calcium chloride and nifedipine on prolactin-(PRL) induced analgesia was studied by chemical assay and compared with other analgesics like morphine, thyrotrophin-releasing hormone (TRH) and clonidine. Nifedipine potentiated the analgesic effect of PRL similar to morphine while that of clonidine and TRH remained unaltered. Further, calcium chloride administration antagonized the analgesic effect of PRL and of morphine. These data suggest that PRL, similar to morphine, may alter calcium movements across the membrane to produce analgesia.
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PMID:Role of calcium in prolactin analgesia. 309 70

D-Met2, Pro5-enkephalinamide (DMPEA) is an opioid peptide having analgesic activity in animals more potent after intravenous administration than morphine. It is less toxic but in animals it showed a higher dependence capacity than morphine. Besides analgesia DMPEA produces in rodent behavioral symptoms similar to those evoked by morphine or beta-endorphin, resembling the actions of neuroleptica. In human trials DMPEA was found to produce unpleasant sensations, no euphoria, and sometimes even dysphoria. DMPEA increases the serum levels of prolactin, growth hormone and, to a less extent, of TSH. Those effect of DMPEA on pituitary hormones. Finally, the human studies indicated that DMPEA antagonized pain (measured with the submaximum effort tourniquet technique), but did not affect adversely and even improved attention and short-term memory; it had no effect on the long-term memory. As the subjective effects of DMPEA are not pleasant, and no patient desired to obtain another treatment, some optimism as to low habit-forming properties of DMPEA may be justified.
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PMID:Pharmacological and human studies with a highly potent opioid peptide, D-Met2, Pro5-enkephalinamide. 333 15

Electrical stimulation of the ventral midbrain periaqueductal grey (PAG) elicits an opioidergic antinociception against noxious heat and pressure in freely moving rats. Recurrent stimulation was associated with a gradual decline and eventual loss of this stimulation-produced antinociception (SPA). This could be reinstated by an increase in current intensity and this reinstatement was preventable by naloxone. The current intensity--antinociception (dose--response) curve was shifted to the right in recurrently stimulated rats and parallel to that in naive animals. The loss of SPA upon repetitive simulation did not represent a conditioning phenomenon. Thus, tolerant rats exposed to all cues which accompanied stimulation revealed no (compensatory) hyperalgesic response--but rather a slight antinociception. Further, SPA recovered spontaneously in tolerant rats. Moreover, 'extinction' by repeated exposure to all cues accompanying stimulation did not restore or accelerate the recovery of SPA in tolerant animals. Tolerant rats showed no depletion in midbrain PAG or other CNS or hypophyseal pools of beta-endorphin, Met-enkephalin or dynorphin indicating that a depletion of endogenous opioid peptides does not underlie the tolerance which develops to stimulation. In fact recurrently stimulated rats did not show any of the pronounced effects upon CNS pools of opioid peptides which are seen with long-term stress. Moreover, repetitively stimulated rats revealed no indications of stress as judged by a diversity of stress-sensitive parameters; basal nociceptive threshold, core temperature, ingestive behaviour, body weight, adrenal weight and hypophyseal secretion of beta-endorphin and prolactin. The data offer two major conclusions. Firstly, the gradual loss of analgesia upon recurrent stimulation of the midbrain PAG does not reflect a generalized debilitation or stress and neither a conditioning phenomenon nor a depletion of pools of endogenous opioid peptides. Rather it closely corresponds to the pharmacological definition of tolerance and may reflect a process occurring at the level of the opioid receptor and coupled processes. This finding explains the cross-tolerance which we observe recurrently stimulated rats to display to morphine. Secondly, this SPA is not a form of stress-induced analgesia and rats undergoing recurrent stimulation reveal no indications of stress as judged by biochemical, physiological and behavioural parameters.
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PMID:An analysis of the 'tolerance' which develops to analgetic electrical stimulation of the midbrain periaqueductal grey in freely moving rats. 342 72

The effects of analgesic, thermoregulatory and endocrine functions of administering morphine sulphate (0.3 mg) into the lateral cerebral ventricle via an Ommaya catheter were assessed in eight patients with cancer pain. Satisfactory control of intractable pain was obtained in these patients, without any change in other sensory modalities. The delay in the onset of pain relief and the duration of analgesia ranged, respectively, from 20 to 40 min and from 12 to 16 h after drug injection. In addition, intraventricular administration of morphine caused a reduction in rectal temperature in these patients at an ambient temperature of 24 degrees C. The hypothermia in response to the injection of morphine was due to cutaneous vasodilation and sweating. There was no change in metabolism or in respiratory evaporative heat loss after morphine injection. Further, 10 to 20 min after intraventricular administration of morphine, the blood levels of prolactin, growth hormone and glucose were elevated in these patients. The changes in temperature and endocrine levels lasted for 1-3 h. In addition to the pain relief, these side-effects of morphine treatment were short-lasting and disappeared as the morphine treatment continued. The results indicate that activation of opiate receptors in the brain produced pain relief, hypothermia (due to cutaneous vasodilation and sweating), and increased blood levels of prolactin, growth hormone and glucose in patients with cancer pain.
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PMID:Intraventricular morphine produces pain relief, hypothermia, hyperglycaemia and increased prolactin and growth hormone levels in patients with cancer pain. 343 Jan 86

The effect of exogenous prolactin on the development of acute tolerance to and dependence on morphine was studied. As described elsewhere, analgesia induced by prolactin was subject to tolerance. Pretreatment with prolactin enhanced the development of tolerance to analgesia induced by morphine while it effectively suppressed the withdrawal symptoms. These results indicate that prolactin behaves like an opioid agonist and suggest that it may have therapeutic implications in the management of opioid dependence.
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PMID:Effect of prolactin on tolerance and dependence to acute administration of morphine. 358 24

In 18 patients scheduled for lower intraabdominal surgery (hysterectomy), changes in thyreotropin (TSH) thyroxine (T4), triiodothyronine (T3) binding of thyroid hormones to plasma proteins (T3-uptake) and glucose in serum were evaluated. In eight patients afferent neurogenic impulses from the surgical area were blocked (Th4-S5) with bupivacaine 0.5% infused continuously into the epidural space from the start of the operation until 6 h postoperatively. All patients received general anaesthesia with thiopentone, pethidine, pancuronium and nitrous-oxide plus oxygen. The patients receiving epidural analgesia had no increase in plasma-TSH, compared to the other group, which had a significant (P less than 0.05) increase peroperatively. The patients receiving epidural analgesia were pain-free and the normal stress-induced increase in plasma-glucose was abolished. Concerning T3 we found a significant decrease in both groups and a steady level of T4- and T3-uptake without significant fluctuations. Thus it can be concluded that the effects of surgical trauma on plasma-TSH concentration are markedly similar to the effects of other anterior pituitary hormones, i.e. HGH, prolactin and ACTH.
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PMID:Per- and postoperative changes in the concentration of serum thyreotropin under general anaesthesia, compared to general anaesthesia with epidural analgesia. 359 Dec 53

Endogenous hyperprolactinaemia, as induced by pituitary homografts under the kidney capsule, was followed by an inhibition of heroin self-administration in rats. This effect was mimicked by intracerebroventricular (i.c.v.) injection of rat prolactin (PRL) or peripheral administration of a hyperprolactinaemia-inducing drug, domperidone. I.c.v. injection of anti-PRL serum totally abolished the effect of hyperprolactinaemia on heroin self-administration behavior and facilitated it in rats with normal plasma PRL levels. The development of tolerance to morphine was facilitated in hyperprolactinaemic animals or in rats injected i.c.v. with rat PRL. This effect was abolished in hyperprolactinaemic animals by i.c.v. injection of anti-PRL serum. Furthermore, rats with normal plasma PRL levels showed an inhibited development of tolerance to morphine after i.c.v. injection of anti-PRL serum. Morphine-induced analgesia appeared to be potentiated in hyperprolactinaemic rats tested in the hot-plate test. It is concluded that endogenous hyperprolactinaemia can affect opiate-induced behavioral changes in rats, possibly through central mechanisms involving opioid transmission.
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PMID:Effects of endogenous hyperprolactinaemia on opiate-induced behavioral changes in rats. 400 82

The development of acute tolerance to prolactin-induced analgesia in mice was identified by using the writhing test. This tolerance was antagonised by naltrexone pretreatment indicating a role of an opioid mechanism. Cross-tolerance between morphine and prolactin was observed with regard to analgesia. These data show that prolactin mimics morphine properties as far as analgesia is concerned and serve as evidence supporting prolactin-opioid interaction.
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PMID:Prolactin analgesia: tolerance and cross-tolerance with morphine. 401 36


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