1982
DOI: 10.1161/01.str.13.1.74
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Abstract: SUMMARY Responses to monoamines perfused over the cortical surface through modified pial windows were monitored in 106 cats. Norepinephrine (NE) and serotonin (5-HT) were diluted in mock CSF to concentrations of 50 and 500 ng/ml respectively, levels at or near the maximum concentrations to which the cortical surface might be exposed in subarachnoid hemorrhage or damage to nearby neurons. Each cat had simultaneous one-hour perfusions of monoamine solution over one hemisphere and a control solution over the othe… Show more

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Cited by 25 publications
(10 citation statements)
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References 73 publications
(10 reference statements)
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“…This conclusion was supported by the observations of Stein and Cracco 10 that the topical application of catecholamines to cortical tissue has toxic effects even in the absence of ischemia. These investigations led Clemens and Phebus 8 and Globus et al 11 to propose that extracellular accumulation of dopamine, or its metabolites, may have a mechanistic role in the pathogenesis of ischemic striatal neuronal injury.…”
Section: Biphasic Striatal Dopamine Release During Transient Ischemiasupporting
confidence: 63%
“…This conclusion was supported by the observations of Stein and Cracco 10 that the topical application of catecholamines to cortical tissue has toxic effects even in the absence of ischemia. These investigations led Clemens and Phebus 8 and Globus et al 11 to propose that extracellular accumulation of dopamine, or its metabolites, may have a mechanistic role in the pathogenesis of ischemic striatal neuronal injury.…”
Section: Biphasic Striatal Dopamine Release During Transient Ischemiasupporting
confidence: 63%
“…Furthermore, there is some evidence that extraneuronal catecholamines may be toxic to neuronal structures: When norepinephrine is injected into the capillaries of a pial window, regional necrosis of cerebral tissue occurs. 16 Necrosis does not occur when 5-HT is injected, even with an equivalent amount of regional ischemia. 16 Acute release of endogenous catecholamine does not explain the delayed damage to nerve terminals that occurs after eight hours of ischemia, though it may be involved in the initial damaging process.…”
Section: Discussionmentioning
confidence: 98%
“…This high extracellular NE concentration is intensely neurotoxic (Stein and Cracco, 1982;Globus et al, 1989) and may play a key role in ischemic neuronal damage . The mechanism of this release under ischemic conditions involves Na ϩ -dependent reversal of the monoamine uptake carrier (Vizi, 2000;Sumiya et al, 2001).…”
Section: Reducing Ne Release Is Protectivementioning
confidence: 99%