Nociceptive threshold and analgesic response to morphine in aged and young adult rats as determined by thermal radiation and intracerebral electrical stimulation.
ABSTRACT The present experiment compared the nociceptive threshold and analgesic response to morphine in young (4-5 months) and aged (24 months) rats using peripheral thermal stimulation and intracerebral electrical stimulation. Responses to thermal stimuli were assessed using both the classical tail-flick procedure in which latency of response is the dependent variable and a new method in which threshold in calories of heat is the dependent variable. In the intracerebral nociceptive threshold procedure, electrical stimuli were delivered via an electrode implanted in the mesencephalic reticular formation (MRF), a pain pathway, and the animals were trained to terminate the stimulation by turning a cylindrical manipulandum embedded in one wall of the experimental chamber. For the classical tail-flick method, the aged rats required a greater intensity of stimulation to produce a basal response latency that was between 2.5 and 3.5 s. Using the new psychophysical method for determining the tail-flick threshold, the aged rats' basal thresholds were significantly higher than that of the young rats. However, the basal thresholds obtained by direct stimulation of the MRF failed to show a significant age effect, suggesting that the registration of pain is not different between young and aged rats. These age-related differences in baseline tail-flick response may be due to changes in the spinal reflex associated with aging. Although, there was no difference in the analgesic effects of morphine between young and aged rats using the latency of the tail-flick response, evidence for decreased analgesic response was seen using the tail-flick threshold measure and the intracerebral stimulation threshold method.
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- "In order to evaluate the intensity of clinical pain, patients are often asked to judge the intensity of their pain on a 10 point scale with a score of 10 being the worst pain they ever felt or could imagine and 0 being the score for no pain . "
ABSTRACT: Background: Animal models comparing rat behaviours are often used in studies characterizing addiction and stress. Aim of this study was evaluation of five or ten days forced treadmill exercise effect on morphine addiction-induced hypoalgesia in young male rats. Materials and Methods: In this study we used twenty four male Wistar rats weighing 200-300 g. Addicted and non-addicted rats have run as forced exercise on motorized treadmill one hour daily for ten days. Tail-flick latency was tested for each rat three times daily with 10 min intervals at a day before, 5 and 10 days after running on treadmill. A sham group consisted of animals placed on treadmill while its motor was off but electrical shock turned on. Mean of tail-flick latencies was analyzed statistically in sham, ran addicted and non-addicted rats. Results: The tail-flick latencies were no significant alteration between all groups during 24 hours before forced running (1080 m distances daily). Animals ran 5400 m and 10800 m during 5 and 10 days on treadmill, respectively. Tail- flick latencies showed that pain reflex latency was increased significantly (pJournal of Clinical and Diagnostic Research 12/2007; 1(6):555 - 560. · 0.23 Impact Factor
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ABSTRACT: This paper is the 29th consecutive installment of the annual review of research concerning the endogenous opioid system, now spanning 30 years of research. It summarizes papers published during 2006 that studied the behavioral effects of molecular, pharmacological and genetic manipulation of opioid peptides, opioid receptors, opioid agonists and opioid antagonists. The particular topics that continue to be covered include the molecular-biochemical effects and neurochemical localization studies of endogenous opioids and their receptors related to behavior (Section 2), and the roles of these opioid peptides and receptors in pain and analgesia (Section 3); stress and social status (Section 4); tolerance and dependence (Section 5); learning and memory (Section 6); eating and drinking (Section 7); alcohol and drugs of abuse (Section 8); sexual activity and hormones, pregnancy, development and endocrinology (Section 9); mental illness and mood (Section 10); seizures and neurological disorders (Section 11); electrical-related activity and neurophysiology (Section 12); general activity and locomotion (Section 13); gastrointestinal, renal and hepatic functions (Section 14); cardiovascular responses (Section 15); respiration and thermoregulation (Section 16); and immunological responses (Section 17).Peptides 01/2008; 28(12):2435-513. DOI:10.1016/j.peptides.2007.09.002 · 2.61 Impact Factor
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ABSTRACT: Mahnaz Kesmati1, Maryem Rezaie1, Hadi Fathi-Moghaddam21Department of Biology, Faculty of Sciences, Shahid Chamran University, Ahvaz; 2Department of Physiology and Persian Gulf Physiology Research Center, School of Medicine, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, IranBackground: The aim of this study was to examine the relationship between the glucocorticoid and opioid systems in the modulation of nociception in young and adult rats.Materials and methods: The experiments were done in young and adult Wistar rats, using morphine 5 mg/kg, and naloxone 2 mg/kg as a µ-opioid receptor agonist. Dexamethasone 1 mg/kg and mifepristone (RU486) 20 mg/kg were used as a glucocorticoid receptor agonist and antagonist, respectively. Hind paw licking latency was measured by hot plate after intraperitoneal administration of drugs.Results: The results showed that morphine and dexamethasone had significant analgesic effects (P < 0.001, P < 0.01, respectively) in both age groups. Coadministration of morphine and dexamethasone did not induce a greater analgesic effect in comparison with morphine alone in either age group. Mifepristone prevented the analgesic effect of morphine in the adult animals (P < 0.001), but had no effect in young animals. The analgesic effect of dexamethasone was inhibited by naloxone in both groups (P < 0.01).Conclusion: These results suggest that glucocorticoids regulate opioid-induced analgesia from the age of puberty, but opioids regulate glucocorticoid-induced analgesia in prepubescent animals. Thus, there is a clear overlapping effect between the two pain modulation systems.Keywords: opioid, glucocorticoid, naloxone, mifepristone, hot plateOpen Access Animal Physiology 01/2010;