Brain research
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Central inflammation is an integral component and contributor of the pathology of many debilitating diseases and has been shown to produce spontaneous pain and hyperalgesia. Recently, administration of lipopolysaccharide (LPS) into the lateral ventricle of rats was shown to elicit both thermal hyperalgesia and tactile allodynia [K. Walker, A. ⋯ Immunohistochemical studies indicated an increased expression of activated macrophages in the brain parenchyma of primed rats but not in unprimed rats. Intraperitoneal (i.p., 2 mg/kg) administration of LPS had no significant effect on either thermal or mechanical thresholds in the first few hours after injection; however, priming rats via i.p. (0.2 mg/kg) or i.c.v. (0.2 microgram) LPS produced a reduction in both thermal nociceptive thresholds and mechanical response thresholds in rats given a subsequent i.p. injection of LPS. This study demonstrates that priming is an effective protocol for the induction of central inflammation and increases the duration of these behaviors after i.c. v. administration.
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In 49 halothane-anesthetized rats, we characterized the responses of single neurons in the ventrolateral orbital cortex (VLO) to a noxious visceral stimulus (colorectal balloon distension, CRD), and studied the effects of intravenous morphine on these responses using standard extracellular microelectrode recording techniques. One hundred and four neurons were isolated on the basis of spontaneous activity. Fifty-seven (55%) responded to CRD, of which 32% had excitatory and 68% had inhibitory responses. ⋯ Naloxone (0.4 mg/kg i.v.) reversed the effects of morphine. Morphine and naloxone had no significant effects on spontaneous activity. These data support the involvement of VLO neurons in visceral nociception.