The opioid peptide dynorphin has been demonstrated to be both nociceptive and antinociceptive. This article will review the potential mechanisms through which dynorphin contributes to spinally mediated nociception. Specifically, we will examine the interaction of dynorphin with multiple sites on the NMDA receptor complex. Dynorphin-induced opioid activity is generally inhibitory, with a tendenc...

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 ne...

The opioid peptide dynorphin has been demonstrated to be both nociceptive and antinociceptive. This article will review the potential mechanisms through which dynorphin contributes to spinally mediated nociception. Specifically, we will examine the interaction of dynorphin with multiple sites on the NMDA receptor complex. Dynorphin-induced opioid activity is generally inhibitory, with a tendenc...

Tissue injury and inflammation result in release of various mediators that promote ongoing pain or pain hypersensitivity against mechanical, thermal and chemical stimuli. Pro-nociceptive mediators activate primary afferent neurons directly or indirectly to enhance nociceptive signal transmission to the central nervous system. Excitation of primary afferents by peripherally originating mediators...

Nociceptive primary afferents have three surprising properties: they are highly complex in their expression of neurotransmitters and receptors and most probably participate in autocrine and paracrine interactions; they are capable of exerting tonic and activity-dependent inhibitory control over incoming nociceptive input; they can generate signals in the form of dorsal root reflexes that are tr...

Long-term potentiation of synaptic strength (LTP) in nociceptive pathways shares principle features with hyperalgesia including induction protocols, pharmacological profile, neuronal and glial cell types involved and means for prevention. LTP at synapses of nociceptive nerve fibres constitutes a contemporary cellular model for pain amplification following trauma, inflammation, nerve injury or w...

The role of L-DOPA in spinal nociceptive reflex activity has been re-evaluated. In high spinal cats, with supraspinal loops being excluded, the onset of reflex facilitation induced by noxious radiant heat is delayed after injection of L-DOPA by 4 to 10 s, i.e. the early component of nociceptive reflex facilitation is blocked, while the late component persisted. Further investigations have shown...

Research studies have begun to identify altered neurophysiological mechanisms that develop as a consequence of chronic painful knee arthritis. Neuroplastic changes may occur in nociceptive pathways, thereby contributing to heightened chronic pain and spread of symptoms, as well as diminished quality of life. One biomarker for examining central sensitization of nociceptive pathways is the measur...

Anti-nociceptive, anti-inflammatory and gastroprotective activities of the known C-glycosyl flavonoid, isoorientin, were studied in rats and mice. For the anti-nociceptive activity assessment the p-benzoquinone-induced writing test, for the anti-inflammatory activity the carrageenan-induced hind paw edema model in mice, and for the gastroprotective activity the EtOH-induced ulcerogenesis model ...

7 Introduction 9 Where do the estrogens come from? 9 a. Systemic synthesis of estrogens 9 b. Local synthesis of estrogens in the brain 10 By which cellular mechanisms do estrogens exert their effects? 11 a. Estrogen receptors 11 b. Alternative mechanisms of action 13 Where are the estrogen receptors located? 14 What physiological effects do estrogens have in the brain? 15 The nociceptive system...