Spreading depolarizations (SDs) are massive breakdowns of ion homeostasis in the brain’s gray matter and are a necessary pathologic mechanism for lesion development in various injury models. However, injury-induced SDs also propagate into remote, healthy tissue where they do not cause cell death, yet their functional long-term effects are unknown. Here we induced SDs in uninjured cortex and hippocampus of Sprague–Dawley rats to study their impact on glutamate receptor subunit expression after three days. We find that both cortical and hippocampal tissue exhibit changes in glutamate receptor subunit expression, including GluA1 and GluN2B, suggesting that SDs in healthy brain tissue may have a role in plasticity. This study is the first to show prolonged effects of SDs on glutamate signaling and has implications for neuroprotection strategies aimed at SD suppression.

扩散去极化 (SDs) 是大脑灰质中离子稳态的大规模破坏，是各种损伤模型中病变发展的必要病理机制。然而，损伤诱导的 SD 也会传播到远处的健康组织中，在那里它们不会导致细胞死亡，但它们的功能性长期影响尚不清楚。在这里，我们在 Sprague-Dawley 大鼠未受伤的皮层和海马中诱导 SD，以研究它们在三天后对谷氨酸受体亚基表达的影响。我们发现皮质和海马组织都表现出谷氨酸受体亚基表达的变化，包括 GluA1 和 GluN2B，这表明健康脑组织中的 SD 可能在可塑性中起作用。