Abstract
Increase in the temperature from 36 to 40°C produces a membrane hyperpolarization associated with a decrease in input resistance and depresses the excitatory postsynaptic potential (EPSP) of CA1 neurons evoked by a stimulation of Schaffer collaterals in rat hippocampus. We examined whether the activation of adenosine A1 receptor contributes on those heat-induced responses in CA1 pyramidal neurons using the intracellular recording techniques. Parasaggital slices of the hippocampus (400μm thick) were obtained from male Wistar rats (130-360g). The slices were superfused with oxygenated artificial cerebral spinal fluid (ACSF) at 2ml/min. The temperature of the ACSF was initially kept at 36°C for 30min. Increasing the temperature to 40°C rapidly produced a membrane hyperpolarization associated with a decrease in input resistance regardless the presence of the DPCPX (1μM), an A1 receptor antagonist. DPCPX (1μM) blocked the rapid depression of the EPSP induced by the temperature increase to 40°C, which reached a peak within 6min. Application of adenosine (10μM) depressed the amplitude of the EPSP by more than 90% of control at 32°C. However, in the presence of the adenosine (10μM), the EPSP was not depressed by the temperature increase from 36 to 40°C. These results suggest that endogenous adenosine contributes to the heat-induced depression of the EPSP via the A1 receptors, not to the reduction of the membrane excitation in CA1 neurons. [J Physiol Sci. 2007;57 Suppl:S146]
