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 Al antagonist, 8-( p-sulfophenyl)theophylline (10 μM), 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 μM) 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.
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