Transmission in spinal reflex pathways from the toes to the ankle flexor tibialis anterior (TA) and to the knee flexor semitendinosus (ST), and from the heel to the ankle extensor medial gastrocnemius (MG), has been studied during antigen-induced inflammation due to subcutaneous injection of ovalbumin at the heel or at the toes in pre-immunized, pentobarbitone-anesthetized rabbits. The ovalbumin challenge induced a mild swelling at the injection site that developed over 6 h. Inflammation at the toes facilitated both flexor reflexes evoked from the toes and inhibited MG extensor responses to stimulation at the heel, with effects usually developing within 75 min of the initial injection and persisting to the end of the 6 h post-injection recording period.
View Article and Find Full Text PDFWithdrawal reflexes are the simplest centrally organized responses to painful stimuli, making them popular models for the study of nociception. Until recently, it was believed that withdrawal was a single reflex response involving excitation of all flexor muscles in a limb with concomitant inhibition of extensors. However, recent findings suggest that withdrawal reflexes are tailored to produce the most appropriate movement according the site at which the stimulus is applied, which could require extensors to act as the primary movers.
View Article and Find Full Text PDFInhibition of spinal and trigeminal withdrawal reflexes by morphine and by the cannabinoid agonist HU 210 has been studied in anaesthetized and in decerebrated rabbits. In intact, pentobarbitone-anaesthetized animals, the jaw-depressor reflex (JDR) evoked by stimulation of the tongue, and the reflex elicited in the ankle flexor tibialis anterior (TA) by stimulation of the toes were inhibited to the same extent by morphine (1-30 mg kg(-1) i.v.
View Article and Find Full Text PDFThe role of 5-HT(1B/1D), 5-HT(2) and 5-HT(3) receptors in mediating descending inhibition of spinal reflexes activated by application of fentanyl to the fourth ventricle has been studied in rabbits decerebrated under N(2)O/isoflurane anaesthesia. In the control state, intraventricular fentanyl (3-30 microg kg(-1)) depressed, to an equal extent, short- and long-latency reflexes in the medial gastrocnemius muscle nerve evoked by electrical stimulation of all sural nerve afferents. Inhibition of reflexes resulted from a decreased base line excitability in the reflex pathway accompanied by a reduction in the rate of temporal summation of responses.
View Article and Find Full Text PDFThe present study examined the possible contribution of endogenous opioids to inhibition of spinal reflexes by an alpha(2)-adrenoceptor agonist. In rabbits decerebrated and spinalised under halothane/nitrous oxide anaesthesia, the selective alpha(2)-adrenoceptor agonist dexmedetomidine (3-30 microg intrathecal) induced significant decreases in short- and long-latency reflex responses evoked in medial gastrocnemius (MG) motoneurones by stimulation of the sural nerve. After recovery from dexmedetomidine, the mu-opioid receptor antagonist beta-funaltrexamine (beta-FNA; 100 microg intrathecal) significantly enhanced short-latency but not long-latency MG reflex responses.
View Article and Find Full Text PDFSpatial aspects of central sensitisation were investigated by studying the effects on three hind limb withdrawal reflexes of an acute noxious stimulus (20 % mustard oil) applied to a number of locations around the body in decerebrate and in anaesthetised rabbits. Reflex responses to electrical stimulation of the toes were recorded from the ankle flexor tibialis anterior (TA) and the knee flexor semitendinosus (ST), whereas responses to stimulation of the heel were recorded from the ankle extensor medial gastrocnemius (MG). In non-spinalised, decerebrated, pentobarbitone-sedated preparations, flexor reflexes were facilitated significantly from sites on the plantar surface of the ipsilateral foot but were either inhibited or unaffected by stimulation of sites away from this location.
View Article and Find Full Text PDFThe selective opioid OP3(mu)-receptor agonist fentanyl was administered via the intravenous, intrathecal and intraventricular routes to decerebrated rabbits in doses from 1-30 microg/kg. Reflexes evoked in medial gastrocnemius motoneurones by electrical stimulation of the sural nerve were depressed by fentanyl given by all three routes. The opioid was most potent when given intrathecally and least potent when given into the fourth ventricle.
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