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. 2022 Mar 7;37(Suppl 1):83–101. doi: 10.1007/s12028-021-01431-w

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© The Author(s) 2022

Open AccessThis article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/.

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Fig. 1 — Intracellular recordings from single rodent neurons undergoing SD in live brain slices. Neurons in the higher brain briskly undergo SD while most neurons in the lower brain respond slowly and then consistently recover. A, In response to 5-min 9.6 mM K⁺, a rat neocortical pyramidal cell depolarizes to − 73 mV then repolarizes in control aCSF. Exposure to 26 mM K⁺ elicits more depolarization with spiking and then spike inactivation, before a plateau of − 48 mV is reached. SD onset (arrow) is aborted just as control aCSF reaches the slice. A third K⁺ exposure again evokes firing and spike inactivation, reaching a plateau at − 48 mV. A steep depolarization then coincides with SD onset (arrow). Modified from [107]. B, Typical membrane potential changes (Vm) of a neocortical neuron (somatosensory cortex; mouse) shown in the upper trace with a simultaneous extracellular field potential recording (FP) acquired near the recorded neuron in the lower trace. After application of KCl in layer I/II of the neocortex, neurons in layer V depolarize abruptly during CSD as the negative DC shift initiates. The inset shows a brief burst of high-frequency population spikes recorded during the early DC deflection. Modified from [228]. C A rat hippocampal CA1 pyramidal neuron undergoes a terminal SD induced by 10 min of OGD. Typically, higher neurons in neocortex, thalamus, striatum and hippocampus reduce their firing during OGD before undergoing rapid SD to near-zero millivolts, with no recovery. D A ‘lower’ locus ceruleus neuron, like most neurons in hypothalamus and brainstem, only slowly depolarizes in response to OGD. As action potentials inactivate, the membrane potential slowly continues to near-zero millivolts (Weak SD). On return to control aCSF, the neuron slowly recovers, dramatically different from higher neurons post-OGD. C and D modified from [107]