Neuroscience
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Although the importance of the rostral ventromedial medulla in pain modulation is generally accepted, the recognition that it can exert both pain facilitating and pain inhibiting influences, and that its constituent neuronal population is physiologically and pharmacologically heterogeneous, is relatively recent. A class of neuron which may be a source of facilitating influences from the rostral ventromedial medulla has been identified in electrophysiological experiments. These neurons, termed "on-cells," are characterized by a sudden burst of activity beginning just before nocifensive reflexes. ⋯ Spontaneous activity of other medullary neurons was unchanged. These data demonstrate that release of an endogenous excitatory amino acid neurotransmitter is necessary for the activation of on-cells that is associated with nocifensive reflexes. In contrast, these receptors evidently play a much less significant role in maintaining the ongoing activity of any cell class in the rostral ventromedial medulla in lightly anaesthetized rats.
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Chronic inflammatory conditions produce a state of hyperalgesia which is evident from a few hours to days after administration of an inflammatory stimulus. The molecular mechanisms involved in the initiation of hyperalgesia are not well understood and in this study we have investigated the role of prostaglandins in this process in the rat. Unilateral intraplantar injection of Freund's complete adjuvant produces an immediate localized swelling (oedema) with the development of altered pain responses in the ipsilateral paw such as a reduced threshold to noxious stimuli (hyperalgesia) and lowered thresholds such that normally innocuous stimuli produce a pain response (allodynia). ⋯ The marked increase in cyclooxygenase-2 messenger RNA in the lumbar spinal cord following intraplantar Freund's complete adjuvant suggests that the cyclooxygenase enzyme and its product may have a role in the adaptive response that occurs in the lumbar spinal cord during a peripheral inflammatory reaction. Pharmacological analysis reveals that prostaglandins are directly involved in the development of allodynia. However, these studies show that the development of mechanical hyperalgesia does not require the production of prostaglandins indicating that more than one pathway mediates the altered pain responses associated with a peripheral inflammatory lesion.