Differential Distribution of Voltage‐Gated Sodium Channel a‐ and b‐Subunits in Human Brain

Whitaker, William R. J.; Clare, Jeffrey J.; Emson, Piers C.

doi:10.1111/j.1749-6632.1999.tb11278.x

Cited by 7 publications

(4 citation statements)

References 12 publications

(13 reference statements)

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“…Our results indicate that sodium channel ␣ and ␤ subunits have distinct regional expression patterns in the human CNS. These results have been reported previously in preliminary form (Whitaker et al, 1999).…”

supporting

confidence: 90%

Distribution of voltage-gated sodium channel ?-subunit and ?-subunit mRNAs in human hippocampal formation, cortex, and cerebellum

et al. 2000

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supporting

confidence: 90%

Distribution of voltage-gated sodium channel ?-subunit and ?-subunit mRNAs in human hippocampal formation, cortex, and cerebellum

et al. 2000

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“…So far, 4 different sodium channel subtypes have been identified in the rat brain: I, II, III, and VI [10][11][12] . The expression of α or β subunits in neurons can be altered during the epileptogenic process either in model rats or in during the epileptogenic process either in model rats or in human tissue [13][14][15][16][17][18][19][20] . In rodents, systemic administration of kainate, a glutamate receptor agonist, induces the development of the well-described model of limbic seizures which is accompanied by neuronal cell death, axonal sprouting and neosynaptogenesis in the hippocampus as well as the induction of specific genes [21] .…”

Section: Introductionmentioning

confidence: 99%

Kinetic changes and modulation by carbamazepine on voltage-gated sodium channels in rat CA1 neurons after epilepsy

Sun

Werkman

Wadman

2006

Acta Pharmacologica Sinica

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Aim: To study whether the functional properties of sodium channels, and subsequently the channel modulation by carbamazepine (CBZ) in hippocampal CA1 neurons can be changed after epileptic seizures. Methods: We used the acutely dissociated hippocampal CA1 pyramidal cells from epilepsy model rats 3 weeks and 3 months respectively after kainate injection, and whole-cell voltage-clamp techniques. Results: After long-term epileptic seizures, both sodium channel voltage-dependence of activation and steady-state inactivation shifted to more hyperpolarizing potentials, which resulted in the enlarged window current; the membrane density of sodium current decreased and the time constant of recovery from inactivation increased. CBZ displayed unchanged efficacy on sodium channels, with a similar binding rate to them, except that at higher concentrations, the voltage shift of inactivation was reduced. For the short-term kainate model rats, no differences were detected between the control and epilepsy groups. Conclusion: These results indicate that the properties of sodium channels in acutely dissociated hippocampal neurons could be changed following long-term epilepsy, but the alternation might not be enough to induce the channel resistance to CBZ.

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“…Fit parameters are shown in Table 1 tary distribution patterns, suggesting that αIIA can associate with β1 or β3 in different areas of the brain [19]. The αIIA subunit has also been reported to be highly expressed in human brain and shows a distribution pattern that overlaps with β1 expression [34]. The present study demonstrates that the human β3 subunit can functionally couple to αIIA.…”

Section: Discussionmentioning

confidence: 72%

Tissue distribution and functional expression of the human voltage-gated sodium channel β3 subunit

Stevens

Cox

Shah

et al. 2001

Pfl�gers Archiv European Journal of Physiology

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This study investigated the distribution of beta3 in human tissues and the functional effects of the human beta3 subunit on the gating properties of brain and skeletal muscle alpha subunits. Using RT-PCR of human cDNA panels, beta3 message was detected in brain, heart, kidney, lung, pancreas and skeletal muscle. Both alphaIIA and SkM1 expressed in Xenopus oocytes inactivated with a time course described by two exponential components representing fast and slow gating modes, while co-expression of human beta3 with alphaIIA or SkM1 significantly increased the proportion of channels operating by the fast gating mode. In the presence of beta3 a greater proportion of alphaIIA or SkM1 current was described by the fast time constant for both inactivation and recovery from inactivation. beta3 caused a hyperpolarizing shift in the voltage dependence of inactivation of alphaIIIA and reduced the slope factor. The voltage dependence of inactivation of SkM1 was described by a double Boltzmann equation. However, SkM1 co-expressed with beta3 was described by a single Boltzmann equation similar to one of the Boltzmann components for SkM1 expressed alone, with a small positive shift in V1/2 value and reduced slope factor. This is the first study demonstrating that beta3 is expressed in adult mammalian skeletal muscle and can functionally couple to the skeletal muscle alpha subunit, SkM1.

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Differential Distribution of Voltage‐Gated Sodium Channel a‐ and b‐Subunits in Human Brain

Cited by 7 publications

References 12 publications

Distribution of voltage-gated sodium channel ?-subunit and ?-subunit mRNAs in human hippocampal formation, cortex, and cerebellum

Distribution of voltage-gated sodium channel ?-subunit and ?-subunit mRNAs in human hippocampal formation, cortex, and cerebellum

Kinetic changes and modulation by carbamazepine on voltage-gated sodium channels in rat CA1 neurons after epilepsy

Tissue distribution and functional expression of the human voltage-gated sodium channel β3 subunit

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