SLC29A1 and status epilepticus: Under the condition of ischemia and hypoxia, ENT1 was over expressed and could reduce extracellular adenosine levels in mouse neurons [41], while ENT1 inhibitor (NBTI) could prolong onset latency for the development of seizures and status epilepticus in the epileptic animal models through increasing extracellular adenosine levels [21–23], and reduce evoked EPSC in lamina II neurons of rat spinal dorsal horn [24], suggesting that NBTI could reduce the excitability of neurons though adenosine signaling.