Abstract
The effects of prolonged swim-stress (2 h and 1 h) upon brain opioid receptor binding of tritiated [3H]diprenorphine were investigated in male Sprague-Dawley rats. This was accomplished by injecting the label intravenously immediately following the swim, then allowing 20 min for tracer washout from non-specific binding sites, sacrificing the animal, dissecting the brain into several discrete areas (medulla-pons, mid-brain, mesolimbic, caudate, thalamus, and hypothalamus), and subsequently preparing homogenates from each brain area. Data were obtained from scintillation counting of the homogenates. A separate support experiment measured circulating beta-endorphin endorphin like immunoreactivity immediately following 2 h of swim-stress. Blood-borne beta-endorphin levels were significantly enhanced by the swim. Additionally, [3H]diprenorphine binding was insignificantly elevated following the 1-h swim and significantly greater in 5 of 6 brain areas examined subsequent to the 2-h swim. Greater availability of opioid receptors to allow enhanced binding of [3H]diprenorphine may have been caused by decreased competition for available receptors from endogenously produced peptides or possibly by alterations in receptor-binding characteristics. These proposed explanations await further investigation. As a result of these studies, we conclude: exercise-induced enhancement of peripheral beta-endorphin probably does not have a supraspinal action; and prolonged swim-stress apparently alters opioid receptor occupancy in the rat brain, and this effect may be dependent upon exercise duration.
Published Version
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