期刊
JOURNAL OF NEUROSCIENCE RESEARCH
卷 96, 期 1, 页码 31-44出版社
WILEY
DOI: 10.1002/jnr.24088
关键词
connexin; pannexin; synaptic plasticity; epilepsy; seizure; hemichannel; gap junction; gliotransmission; purinergic signaling; electrical synapse; pan-glial network; neuronal excitability; astrocyte
资金
- National Multiple Sclerosis Society [NMSS-RG-4853A3/2]
- National Institute of Health [NIH R01-7R01NS081141]
In the central nervous system (CNS), connexin (Cx)s and pannexin (Panx)s are an integral component of homeostatic neuronal excitability and synaptic plasticity. Neuronal Cx gap junctions form electrical synapses across biochemically similar GABAergic networks, allowing rapid and extensive inhibition in response to principle neuron excitation. Glial Cx gap junctions link astrocytes and oligodendrocytes in the pan-glial network that is responsible for removing excitotoxic ions and metabolites. In addition, glial gap junctions help constrain excessive excitatory activity in neurons and facilitate astrocyte Ca2+ slow wave propagation. Panxs do not form gap junctions in vivo, but Panx hemichannels participate in autocrine and paracrine gliotransmission, alongside Cx hemichannels. ATP and other gliotransmitters released by Cx and Panx hemichannels maintain physiologic glutamatergic tone by strengthening synapses and mitigating aberrant high frequency bursting. Under pathological depolarizing and inflammatory conditions, gap junctions and hemichannels become dysregulated, resulting in excessive neuronal firing and seizure. In this review, we present known contributions of Cxs and Panxs to physiologic neuronal excitation and explore how the disruption of gap junctions and hemichannels lead to abnormal glutamatergic transmission, purinergic signaling, and seizures.
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