Modulation as an Acidosis-Evoked Current by A1 Adenosine Receptors in the CA1 Region of the Mouse Hippocampus
Acidosis, along with hypoxia and hypoglycemia are immediate metabolic consequences of reduced blood flow to the brain. Acidosis exacerbates ischemic brain injury by activating non-selective cation currents that induce neuronal damage in a calcium-dependent manner, independent of glutamate receptor activation. Adenosine is released during periods of metabolic stress and exerts a neuroprotective role mediated by adenosine A1 receptor stimulation. The purpose of this project was to study the effect of adenosine A1 receptor stimulation in an in vitro model of acidosis. The findings suggest that acidosis activates a non-selective sustained cation current which is directly inhibited by adenosine, consistent with the neuroprotective role of adenosine.