To understand the basis of clinical heterogeneity in SCN2A -associated disorders, the biophysical consequences of Na v 1.2 channel mutations and their impact on action potential firing and neuronal excitability must be clarified. Representative current traces from Chinese hamster ovary (CHO) cells transiently expressing wild-type or mutant Na v 1.2 channels are shown in Fig. 1 B . Peak sodium current ( I Na ) densities in cells expressing L1563V channels were similar to those of wild-type channels, whereas I Na densities were decreased in cells harboring R853Q channels and increased in cells harboring R1882Q channels (Fig. 1 C and Table 2). The effects of mutations on Na v 1.2 channel gating over a range of membrane potential ( V m ) values are shown in Fig. 1 D . Relative to wild-type, the activation curves of R853Q and L1563V channels exhibited small but statistically significant hyperpolarizing or depolarizing shifts, respectively. R1882Q channel activation was more severely affected, resulting in a 6-mV hyperpolarizing shift of the V 0.5,act value, a change that results in increased sodium-channel availability compared with the wild-type (Fig. 1 D and Table 2). In all mutants, the V 0.5,inact values were significantly changed compared with wild-type (Fig. 1 D and Table 2). In cells expressing R853Q channels, the hyperpolarizing shift of V 0.5,inact stabilizes inactivation and leads to reduced sodium-channel availability at physiologically relevant V m values. Conversely, the depolarizing shift of V 0.5,inact increases sodium-channel availability for L1563V and R1882Q variants.
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