Lesions of the hypothalamic arcuate nucleus produce a temporary hyperalgesia and attenuate stress-evoked analgesia

摘要: Abstract In an attempt to elucidate the role of β-endorphin in modulation ‘basal’ nociceptive threshold and mediation antinociception (analgesia) evoked by stress, a series lesions arcuate nucleus, origin central system β-endorphinergic neurones, were performed. These produced ∼80% depression level immunoreactivity both hypothalamus periventricular fibre-containing tissue. A 50% decrease neurointermediate lobe content immunoreactivity, but no change levels this anterior was also observed. Arcuate lesioned rats significantly hyperalgesic comparison sham animals on day 4 post-operation, days 10 12, basal groups did not differ significantly. On 12 post-surgery upon exposure 5 min foot-shock developed smaller increase tail-flick latency than animals. data are evidential importance nucleus determination generation analgesia which accompanies stress are, further, suggestive these processes.