Persistent Enhancement of Neuron–Glia Signaling Mediated by Increased Extracellular K+ Accompanying Long-Term Synaptic Potentiation

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Abstract
Neuron–glia signaling is important for neural development and functions. This signaling may be regulated by neuronal activity and undergo modification similar to long-term potentiation (LTP) of neuronal synapses, a hallmark of neuronal plasticity. We found that tetanic stimulation of Schaffer collaterals (Sc) in the hippocampus that induced LTP in neurons also resulted in LTP-like persistent elevation of Sc-evoked slow depolarization in perisynaptic astrocytes. The elevated slow depolarization in astrocytes was abolished by NMDA receptor antagonist and K+ channel inhibitors, but not by Ca2+ chelator BAPTA loaded in the recorded astrocytes, suggesting involvement of an increased extracellular K+ accumulation accompanying LTP of neuronal synapses. The increased K+ accumulation and astrocyte depolarization after LTP induction may reduce the efficiency of glial glutamate transporters, which may contribute to the enhanced synaptic efficacy. The neuronal activity–induced persistent enhancement of neuron–glia signaling may thus have important physiological relevance.