Abstract

Three different intensities of swim stress produced stress-induced antinociception (SIA) in mice which was assessed either by the reduction in the number of abdominal constrictions produced by acetic acid or by an increase in reaction time on a hot-plate. The involvement of alpha-adrenoceptors in the three models of SIA was investigated using selective antagonists. SIA produced by the mild stress of a 30 s warm water swim was attenuated by idazoxan (0.5-1 mg kg-1), and by yohimbine at a dose (1 mg kg-1) which reduced antinociception produced by clonidine (12.5-50 micrograms kg-1). Indoramin (1-2 mg kg-1) did not affect this model of SIA, but reversed phenylephrine induced inhibition of the constrictions. A 3 min room temperature swim increased reaction times on the hot-plate and this naloxone-sensitive SIA was reduced significantly by prazosin (1-2 mg kg-1), idazoxan (0.5-1 mg kg-1) and yohimbine (0.5-1 mg kg-1) but enhanced by clonidine (0.5 mg kg-1) and noradrenaline (NA) (10 micrograms i.c.v.). Mice treated with 6-hydroxydopamine (60 + 60 micrograms i.c.v.) were hypersensitive to the hot-plate and did not develop SIA. Levels of noradrenaline in the brain (minus the cerebellum) were decreased after the room temperature swim SIA. The most severe stress of a cold water swim produced SIA on the hot-plate which was initially naloxone-insensitive.(ABSTRACT TRUNCATED AT 250 WORDS)

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