| 1. |
- Gustafson, I., et al.
(författare)
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Extracellular brain cortical levels of noradrenaline in ischemia : - Effects of desipramine and postischemic administration of idazoxan
- 1991
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Ingår i: Experimental Brain Research. - 0014-4819. ; 86:3, s. 555-561
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Tidskriftsartikel (refereegranskat)abstract
- Using microdialysis, extracellular noradrenaline (NA) levels in the rat cerebral cortex were studied under isoflurane/N2O anaesthesia before, during and for 6 hours following 10 min of forebrain ischemia in a 2-vessel occlusion model. A microdialysis probe was introduced into the parietal cortex and dorsal hippocampus in anaesthetized rats and continuously perfused with Krebs-Ringerbicarbonate buffer with or without the NA uptake inhibitor desipramine (DMI, 5 μM). Twenty min fractions were collected and the extracellular NA levels were measured in the dialysates using HPLC with electrochemical detection. The basal NA concentration in the dialysate was 10.5±1.8 (mean±SEM) pg/20 min fraction and increased to 39.3±4.8 pg/20 min fraction after local administration of DMI. During ischemia, NA increased to 38 times the basal level without DMI, and 6 times with DMI included during two hours' perfusion prior to ischemia. After recirculation NA levels returned to, or even transiently decreased below, preischemic values. With DMI present in the dialysis buffer, administration of idazoxan immediately following ischemia delayed the return to preischemic NA levels in the recirculation phase. In the absence of DMI, no effect of idazoxan on postischemic levels of NA was found. Local administration of DMI increases basal extracellular NA levels and reduces the ischemia-induced NA release. The latter effect may be a due to inhibition of the NA uptake system working in a reversed mode, or as a result of decreased synthesis of NA due to activation of presynaptic α2-receptors by the increased synaptic NA levels. Postischemic treatment with the α2-adrenoceptor antagonist idazoxan in combination with DMI prolongs the period of elevated extracellular NA levels, which may be of importance for the protective properties of idazoxan against ischemic cell injury.
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| 2. |
- Wieloch, T., et al.
(författare)
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Neuronal damage in the striatum following forebrain ischemia : lack of effect of selective lesions of mesostriatal dopamine neurons
- 1990
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Ingår i: Experimental Brain Research. - 0014-4819. ; 83:1, s. 159-163
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Tidskriftsartikel (refereegranskat)abstract
- Transient periods of global cerebral ischemia lead to selective neuronal damage in the striatum. We investigated the effects of unilateral 6-hydroxydopamine lesions of the mesostriatal dopamine (DA) system on the density and distribution of neuronal necrosis in the rat striatum following ischemia induced by bilateral occlusion of the common carotid arteries combined with hypotension. After both 12 and 15 min of ischemia, which caused slight and extensive striatal damage, respectively, there was no difference in the density of neuronal necrosis in the striatum between DA-lesioned and shamoperated animals. We conclude that the DA system alone does not modulate injury following complete cerebral ischemia, but may contribute significantly to damage following conditions such as during hypoglycemia and incomplete cerebral ischemia.
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