Ischemic stroke remains the third leading cause of death and leading cause of adult disability worldwide. A key event in the pathophysiology of stroke is the anoxic depolarization (AD) of neurons in the ischemic core. Previous studies have established that both the latency to AD and the time spent in AD prior to re-oxygenation are predictors of neuronal death. The present studies used hippocampal slices from male and female mice to investigate the electrophysiological events that affect latency to AD after oxygen deprivation. The results confirm that the epoch between AD and re-oxygenation largely determines the magnitude of synaptic recovery after anoxic challenge. Using a selective antagonist of adenosine A₁ receptors, we also confirmed that adenosine released during anoxia (ANOX) suppresses synaptic glutamate release; however, this action has no effect on AD latency or the potential for post-anoxic recovery of synaptic transmission. In contrast, antagonism of AMPA- and NMDA-type glutamate receptors significantly prolongs the latency to AD and alters the speed and synchrony of associated depolarizing waves. Experiments using slices with fields Cornu ammonis 3 (CA3) and Cornu ammonis 1 (CA1) disconnected showed that AD latency is longer in CA1 than in CA3; however, the early AD in CA3 is propagated to CA1 in intact slices. Finally, AD latency in CA1 was found to be longer in slices from female mice than in those from age-matched male mice. The results have implications for stroke prevention and for understanding brain adaptations in hypoxia-tolerant animals.

缺血性中风仍然是全球第三大死亡原因和成人残疾的主要原因。中风病理生理学中的一个关键事件是缺血核心神经元的缺氧去极化（AD）。以前的研究已经确定，AD 的潜伏期和再氧合之前在 AD 中花费的时间都是神经元死亡的预测因素。本研究使用雄性和雌性小鼠的海马切片来研究影响缺氧后 AD 潜伏期的电生理事件。结果证实，AD 和再氧合之间的时期在很大程度上决定了缺氧挑战后突触恢复的幅度。使用腺苷 A _{1的选择性拮抗剂}受体，我们还证实了在缺氧（ANOX）过程中释放的腺苷抑制了突触谷氨酸的释放；然而，这一行动对 AD 潜伏期或突触传递的缺氧后恢复的潜力没有影响。相比之下，AMPA 型和 NMDA 型谷氨酸受体的拮抗作用显着延长了 AD 的潜伏期，并改变了相关去极化波的速度和同步性。使用未连接的 Cornu ammonis 3 (CA3) 和 Cornu ammonis 1 (CA1) 场的切片的实验表明，CA1 的 AD 潜伏期比 CA3 长；然而，CA3 中的早期 AD 在完整切片中传播到 CA1。最后，发现雌性小鼠切片中 CA1 的 AD 潜伏期比年龄匹配的雄性小鼠切片中的要长。