Biphasic striatal dopamine release during transient ischemia and reperfusion in gerbils.

Abstract

To clarify the nature of ischemic striatal dopamine release during the earliest periods of neuronal injury, we used chronoamperometry to measure dopamine levels every 60 seconds during various durations of ischemia in 32 gerbils. Catecholamine-selective electrodes were implanted into the brains of anesthetized gerbils subjected to 2, 5, or 10 minutes of transient forebrain ischemia or permanent forebrain ischemia. Four control animals showed a stable chronoamperometric baseline. In the six gerbils subjected to permanent ischemia, dopamine release was rapid during early ischemia and slowed with time. The four animals subjected to 2 minutes of ischemia showed minimal dopamine release. The six gerbils subjected to 5 minutes of ischemia demonstrated a noticeable dopamine release during ischemia, and three of the six developed a massive secondary dopamine release during reperfusion. All six animals subjected to 10 minutes of ischemia demonstrated a similar biphasic dopamine release twice the size of that observed in the 5-minute group. Pretreatment with pargyline in six additional gerbils subjected to 10 minutes of ischemia failed to modify significantly this biphasic pattern of dopamine release. We conclude that dopamine release occurs very early during ischemia and that its magnitude correlates with the duration of an ischemic insult. Reperfusion is associated with an even larger striatal dopamine release. This previously unreported biphasic dopamine release phenomenon may have important clinical implications in the management of cerebral ischemia. (Stroke 1991;22:674-679) R ecently, attention has been focused on the role of neurotransmitters in the pathogenesis of ischemic cerebral injury. This area of research arose because investigators using microdialysis and in vivo electrochemical techniques in the striatum of experimental animals have long noted that a massive increase in the extracellular concentration of dopamine occurs shortly after

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“…Striatal dopamine release has also been demonstrated in response to ischaemia. Ahn et al. (1991) studied the effect of cerebral ischemia on dopamine release in gerbils and found that both early ischaemia and reperfusion resulted in biphasic dopamine release within the striatum.…”

“…Striatal dopamine release has also been demonstrated in response to ischaemia. Ahn et al (1991) studied the effect of cerebral ischemia on dopamine release in gerbils and found that both early ischaemia and reperfusion resulted in biphasic dopamine release within the striatum. It could be postulated that the high volume CED infusions in this study resulted in a period of relative hypoxia within the putamen resulting in dopamine release.…”

Increased Activation of L‐Type Voltage‐Dependent Calcium Channels Is Associated with Glycine Enhancement of N‐Methyl‐d‐Aspartate‐Stimulated Dopamine Release in Global Cerebral Ischemia/Reperfusion

“…Both excessive entry of calcium into neurons and increased DA release (Ahn et al ., 1991 ;Akiyama et al, 1991 ;Bhardwaj et al, 1990) have been shown to contribute to neuronal damage in ischemia. Some degree of neuroprotection has been achieved with modifiers of both processes (Clemens and Phebus, 1987;Bielenberg and Burkhardt, 1991).…”

“…NMDA receptors are normally activated by endogenous glutamate and its coagonist glycine (Gly) (Kleckner and Dingledine, 1988), acting at its own receptor within the NMDA receptor/ channel complex . Extracellular DA levels are elevated in striata of animals that have undergone ischemia (Harik et al ., 1986 ;Brannan et al ., 1987 ;Ahn et al ., 1991 ;Koorn et al ., 1992) . Using in vitro measurements of [3 H]DA release from striatal slices under conditions in which changes in uptake of [ 3 H]DA were excluded, we have previously shown that NMDA-stimulated [3 H]DA release is enhanced in tissue from animals subjected to 10 min of ischemia, and up to 24 h of reperfusion (Werling et al ., 1993) .…”

Dynamic study of the effect of electroacupuncture on dopamine in the striatum for rats with cerebral ischemia and reperfusion

“…It is not clear that whether dopamine protect or aggravate the damage after cerebral ischemia and reperfusion [1][2][3][4][5][6] . Therefore, study of the alterations in dopamine may lead to improvements in the treatment of cerebral ischemia.…”