Brain research
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The effects of low frequency-high intensity transcutaneous and intramuscular electrical nerve stimulation (TENS and IENS, respectively) on ipsilateral muscular pain threshold were studied in healthy volunteers. The combined effects of TENS (or IENS) and vibration as well as the effects of TENS applied to contralateral regions were also investigated. Muscular pain threshold was evaluated by the subjects' verbal reports in response to electrical stimulation (wire electrodes) of the vastus medialis muscle and by the appearance of blink response (startle reaction) without habituation. ⋯ TENS and vibration performed simultaneously induced increases in muscular pain threshold, which were greater than those obtained with each individual conditioning stimulation. TENS proved to be capable of enhancing muscular pain threshold even when applied to contralateral regions; however, these effects were smaller and of shorter duration. The results provide evidence that low frequency-high intensity TENS (or IENS) are effective in raising muscular pain threshold and support the hypothesis that this type of stimulation brings supraspinal control systems into action through the activation of group III afferent fibres.
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It has been previously demonstrated that rhythmically firing neurons (Pre-I neurons) preceding cervical root (C4 or C5) inspiratory activity, localized in the rostral ventrolateral medulla (RVL), are important in the generation of the basic respiratory rhythm in brainstem-spinal cord preparations from newborn rats. We examined the effects of single and continuous electrical stimulation applied to the RVL on Pre-I and C4 activities in these preparations. We verified that the phase of respiratory rhythm was reset when Pre-I firing was induced in both right and left RVL by single shock stimulation, whether C4 activity appeared or not. ⋯ After bilateral lesions of the caudal ventrolateral medulla, Pre-I neurons retained their rhythmic activity, while C4 activity disappeared. Present results further confirmed our hypothesis that Pre-I neurons are the primary generator of respiratory rhythm. We propose a hypothetical model of the generation of rhythmic respiratory activity.
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The lateral reticular nucleus (LRN) in the caudal ventrolateral medulla has been implicated in descending monoaminergic modulation of spinal nociceptive transmission. Experiments were undertaken to examine the organization of pontine and spinal pathways mediating inhibition of the tail-flick (TF) reflex from the LRN in rats lightly anesthetized with pentobarbital. Microinjections of the local anesthetic lidocaine ipsilaterally or bilaterally into the dorsolateral pons blocked stimulation-produced inhibition of the TF reflex from the nucleus locus coeruleus/subcoeruleus (LC/SC), but had no effect on descending inhibition produced by microinjection of glutamate into the LRN. ⋯ Neither lidocaine blocks nor transections of the DLFs completely blocked the descending inhibitory effects of electrical stimulation in the LRN. The DLFs appear to carry fibers mediating LRN stimulation-produced inhibition of the TF reflex as well as tonic descending inhibition of spinal reflexes. The results of the present study indicate that (1) adrenergic modulation of the nociceptive TF reflex from the LRN does not depend on a rostral loop through the pontine LC/SC, and (2) descending inhibitory influences from the LRN are contained in, but not confined to, the dorsal quadrants of the spinal cord.
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In the anesthetized rat, cocaine (25 mg/kg i.p.), enhanced the frequency potentiation of nociceptively evoked polysynaptic discharges but did not affect the polysynaptic reflex discharge to single nociceptive stimuli or the habituation of this reflex to repetitive pinch stimuli. The non-nociceptive, short-latency reflex discharge was suppressed for 10-15 min after cocaine administration. The neurogenic extravasation response to antidromic cutaneous C-fiber stimulation was unaffected by cocaine. These findings suggest that systemic cocaine, in doses analgesic for the rat, does not suppress spinal nociceptive reflexes.
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In opiate-naive rats, the endogenous opioid peptides, beta-endorphin, dynorphin(1-13) and Met-Enk-Arg-Phe (MEAP) and the synthetic enkephalin analogue D-Ala2-D-Leu5-Enk (DADLE) potently stimulated plasma corticosterone in a dose-dependent, naloxone reversible manner. To characterize their in vivo affinities, the effects of these peptides on plasma corticosterone release were tested in rats made tolerant to morphine, U50488H, DADLE/morphine or beta-endorphin. These cross-tolerance studies showed that dynorphin and MEAP exerted their action on plasma corticosterone release at kappa-opioid receptors. ⋯ These results indicate that there is independent modulation of the hypothalamic-pituitary-adrenal axis by endogenous opioid peptides at mu-, delta- and kappa-opioid receptors. In addition there may be modulation by beta-endorphin at a separate site that we suggest could be a central epsilon-receptor site. This cross-tolerance paradigm, using a neuroendocrine model, provides in vivo evidence for the action of centrally active endogenous opioid peptides at multiple and independent opioid receptors.