Progress in neurobiology
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Progress in neurobiology · Jun 1993
ReviewAntinociception induced by alpha-2-adrenoceptor agonists, with special emphasis on medetomidine studies.
Alpha-2-adrenoceptor agonists can activate varying antinociceptive mechanisms depending on the dose and the route of administration, although the main site for their antinociceptive effect in physiological pain conditions seems to be the spinal dorsal horn. In this paper the investigations on the underlying mechanisms are reviewed, with particular emphasis on novel studies using a highly selective and potent alpha-2-adrenoceptor agonist medetomidine. In behavioral studies alpha-2-adrenoceptor agonists, including medetomidine, produce antinociception following systemic administration or local application to the spinal cord. ⋯ Thus, the higher sensitivity of supraspinal neuronal responses and their behavioral correlates to the antinoceptive effect of medetomidine obviously reflects the cumulative effect of medetomidine at several areas along the polysynaptic pathway to the rostral parts of the brain. Paradoxically, the response of immediate early genes in the medial thalamic neurons is only slightly, influenced by antinociceptive doses of medetomidine. Alpha-2-adrenoceptors have significant interactions with other receptors (e.g. opioid, serotonin and muscarine) in producing antinociception at the spinal cord level.
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Progress in neurobiology · Jan 1992
ReviewPeripheral and central mechanisms of cutaneous hyperalgesia.
Hyperalgesia after cutaneous injury can be divided into two phenomena: Primary hyperalgesia occurs at the site of injury and is characterized by hyperalgesia to mechanical and heat stimuli. Secondary hyperalgesia occurs outside the injury site and is characterized by mechanical hyperalgesia only. Hyperalgesia in inflammatory processes corresponds to primary hyperalgesia. ⋯ This form of sensitization may account for the pain to light touch associated with neuropathic pain. Receptive field plasticity is a prevalent property of dorsal horn neurons and probably plays a vital role with regard to hyperalgesia. The molecular mechanisms of synaptic plasticity are currently subject to intense experimental investigation and may provide new insights on the mechanisms of pain and hyperalgesia.
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Relations between brain damage and memory disturbance are outlined with emphasis on the so-called amnesic syndrome. Following a brief introduction into forms of memory and memory failures, the basic causes of brain damaage (with relevance to amnestic failures) are described. Thereafter, the two best-known forms of brain damage-amnesia relations are reviewed: the consequences of damage to medial temporal lobe structures and to diencephalic regions. ⋯ The contribution of animal models of human amnesia is critically reviewed and discrepancies are analyzed between human and animal memory disturbances. This section emphasizes the value of investigating inter-dependencies between brain structures by pointing out that relations between memory disturbances and brain damage may be more complicated than apparent from a simple structure-function assignment. This aspect is further followed up in the conclusions.