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When GABA Fails: Rundown on Chemokines

Commentary A hallmark feature of mesial temporal lobe epilepsy (MTLE) is that endogenous mechanisms that normally limit or reduce neuronal excitability become inefficient over time. Among those, GABAA receptor–mediated inhibitory currents have been shown to fail in MTLE, with several mechanisms accounting for this phenomenon, including a reversal of the electrochemical chloride gradient across the plasma membrane (1), altered composition of GABAA receptor subunits (2), and the use-dependent decrease (rundown) of GABA-evoked currents (IGABA) (3). The rundown of IGABA is a phenomenon in which the repeated exposure of the receptor to GABA results in a gradual decrease of the resulting currents; IGABA rundown is more pronounced in epileptogenic tissue. GABAA receptor function is also influenced by inflammatory processes (4). Because inflammatory processes, and in particular the activation glial cells, play a major role in epileptogenesis, endogenous and exogenous modulators of inflammation are of interest for our understanding of the pathophysiology of epilepsy. Chemokines are a specific class of small cytokines, which are paracrine messengers secreted by a large variety of cell types, and may trigger chemotaxis in nearby responsive cells. They have been grouped into four families (C, CX3C, CC, and CXC) based on structural motifs. All of these chemokines bind to specific G protein–coupled chemokine receptors. Among the chemokines, several interact with microglial chemokine receptors, modulate inflammatory responses, or have been implicated in epileptogenesis. Mounting evidence demonstrates that several chemokines interact with GABAergic signaling (5). Fractalkine/CX3CL1 Modulates GABAA Currents in Human Temporal Lobe Epilepsy.