Direct evidence of acute, massive striatal dopamine release in gerbils with unilateral strokes.

Brannan, Timothy; Weinberger, Jesse; Knott, P. J.; Taff, I; Kaufmann, Horacio; Togasaki, Daniel M.; Nieves-Rosa, J; Maker, Howard S.

doi:10.1161/01.str.18.1.108

Cited by 83 publications

(32 citation statements)

References 17 publications

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“…Brannan et al 2 used in vivo electrochemistry to demonstrate a massive unilateral striatal dopamine release in gerbils surviving unilateral stroke. Later, Slivka et al, 3 using the technique of microdialysis, confirmed the findings of Brannan et al 2 Subsequently, Phebus and Clemens, 4 Globus et al, 5 and Ogura et al 6 demonstrated that ischemic periods as brief as 20-30 minutes effectively cause striatal dopamine release during the period of transient ischemia. Additionally, Globus et al 7 demonstrated that ischemic catecholamine release is not confined to the striatum, but is also seen in the hippocampus during transient ischemia.…”

Section: Biphasic Striatal Dopamine Release During Transient Ischemiamentioning

confidence: 72%

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

Ahn

Blaha

Alkire

et al. 1991

Stroke

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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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Section: Biphasic Striatal Dopamine Release During Transient Ischemiamentioning

confidence: 72%

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

Ahn

Blaha

Alkire

et al. 1991

Stroke

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“…Various electrochemical processes, such as redox reactions with reduced and oxidised species present in the same phase [6,14,[21][22][23][24][25][26][27][28][29][30][31][32][33][34][35], adsorption on surfaces of electrodes [36][37][38], electrodeposition [39][40][41][42][43][44][45][46][47][48] or electrodissolution [49][50][51] were analysed by means of semi-differentiation or semi-integration. The most extensive mathematical treatment related to these methods was applied to the electrochemical reactions were both oxidised and reduced form are soluble in the electrolyte phase and their transport proceeds under conditions of semi-infinite linear diffusion [4].…”

Section: Introductionmentioning

confidence: 99%

Semi-differential analysis of irreversible voltammetric peaks

Grdeń

2016

J Solid State Electrochem

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Voltammetric peaks obtained by simulation of electrochemical reactions under conditions of linear semi-infinite diffusion with an irreversible electron transfer process are analysed using a semi-differentiation procedure. Obtained semi-derivative peaks, separated or overlapped, are fitted with appropriate mathematical functions. The functions used for data fitting include a function describing symmetrical peaks, proposed by several authors for fitting irreversible semiderivative peaks, and two alternative functions that express asymmetric shape of the irreversible semi-derivative signals. When applied to the overlapped irreversible semi-derivative peaks, the latter two functions allow calculating certain electrochemical parameters with a better accuracy as compared with the function derived for the symmetrical peaks.

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“…It has also been hypothesized that the release of vasoactive neurotransmitters causes vasoconstriction of the cerebral vasculature. 17 However, neurotransmitter release occurs almost immediately after the induction of ischemia, 20 prior to the onset of diaschisis.…”

Section: Time (Hours)mentioning

confidence: 99%

Cerebral blood flow in the evolution of infarction following unilateral carotid artery occlusion in Mongolian gerbils.

Weinberger¹,

Nieves-Rosa²

1987

Stroke

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Cerebral blood flow (CBF) was measured in gerbils 2, 4, 7, and 12 hours after unilateral irreversible carotid artery ligation to determine if the delayed ischemic damage to nerve terminals that occurs over 8 hours after stroke could be due to changes in CBF. [ 14 C]butanol (4.5 ^Ci in 45 /xl 0.9% saline) was injected into the femoral vein, and cpm accumulating in the cerebrum and in a catheter inserted in the abdominal aorta were measured. CBF (ml/100 g/min, mean ± SEM) in sham-operated control gerbils was 108.4 ± 37.5 in the left hemisphere and 123.8 ± 37.1 in the right. CBF in the ischemic left cerebrum was 41.0 ± 7.7 at 2 hours (n = 7), 21.6 ± 7.2 at 4 hours (n = 4), 26.2 ± 4.6 at 7 hours (n = 7), and 9.7 ± 3.1 at 12 hours (n = 6). CBF in the nonligated right hemisphere was 115.0 ± 15.3 at 2 hours, 70.4 ± 23.3 at 4 hours, 80.4 ± 14.6 at 7 hours, and 50.9 ± 20.1 at 12 hours. As expected, CBF was significantly reduced in the ischemic left cerebral hemisphere compared with the nonligated right cerebral hemisphere at each time, but CBF in the ischemic left cerebral hemisphere was also significantly lower at 12 hours than at 2 hours (p = 0.002) and at 7 hours (p = 0.014). CBF in the nonligated right cerebral hemisphere was also lower at 12 hours than at 2 hours (p = 0.02). No changes in Pco 2 or blood pressure accounted for these differences. The reduction in CBF 12 hours after stroke coincides with the time of ischemic damage to nerve terminals. (Stroke 1987;18:612-615)

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Direct evidence of acute, massive striatal dopamine release in gerbils with unilateral strokes.

Cited by 83 publications

References 17 publications

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

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

Semi-differential analysis of irreversible voltammetric peaks

Cerebral blood flow in the evolution of infarction following unilateral carotid artery occlusion in Mongolian gerbils.

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