Zhu_1993_Neurosci.Lett_155_128

Reference

Title : Adenosine release is a major cause of failure of synaptic transmission during hypoglycaemia in rat hippocampal slices - Zhu_1993_Neurosci.Lett_155_128
Author(s) : Zhu PJ , Krnjevic K
Ref : Neuroscience Letters , 155 :128 , 1993
Abstract :

Glucose-free medium (aglycaemia) caused a complete failure of CA1 population spikes (after 14.5 +/- 0.8 min) and field EPSPs (after 18.1 +/- 0.5 min). In the presence of the selective adenosine A1 antagonist, 8-(p-sulfophenyl)theophylline (10 microM), population spikes and EPSPs were decreased by only 13.8 +/- 11.9% and 32.4 +/- 11.6% at the end of 17.0 +/- 3.0 min and 19.8 +/- 1.7 min of aglycaemia, respectively. A similar effect was produced by caffeine (0.2 mM). The ATP-sensitive K+ channel blockers tolbutamide (1 mM) and glibenclamide (10 microM) had no significant effect on aglycaemic suppression of synaptic transmission. These observations indicate that endogenous adenosine, but not ATP-sensitive K+ conductance, plays a major role in hypoglycaemia failure of transmission.

PubMedSearch : Zhu_1993_Neurosci.Lett_155_128
PubMedID: 8397349

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Zhu PJ, Krnjevic K (1993)
Adenosine release is a major cause of failure of synaptic transmission during hypoglycaemia in rat hippocampal slices
Neuroscience Letters 155 :128

Zhu PJ, Krnjevic K (1993)
Neuroscience Letters 155 :128