ISSN:
1573-6881
Keywords:
Neurons
;
VDCC
;
beta subunits
;
expression
;
assembly
;
development
;
differentiation
;
epilepsy
Source:
Springer Online Journal Archives 1860-2000
Topics:
Biology
,
Chemistry and Pharmacology
,
Physics
Notes:
Abstract Voltage-gated calcium channels (VDCC) are essential to neuronal maturation and differentiation. It is believed that important signaling information is encoded by VDCC-mediated calcium influx that has both spatial and temporal components. VDCC are multimeric complexes comprised of a pore-forming α1 subunit and auxiliary β and α2/δ subunits. Changes in the fractional contribution of distinct calcium conductances to the total calcium current have been noted in developing and differentiating neurons. These changes are anticipated to reflect the differential expression and localization of the pore-forming α1 subunits. However, as in vitro studies have established that β regulates the channel properties and targeting of α1, attention has been directed toward the developmental expression and assembly of β isoforms. Recently, changes in the β component of the omega-conotoxin GVIA (CTX)-sensitive N-type VDCC have indicated differential assembly of α1B with β in postnatal rat brain. In addition, unique properties of β4 have been noted with respect to its temporal pattern of expression and incorporation into N-type VDCC complexes. Therefore, the expression and assembly of specific α1/β complexes may reflect an elaborate cellular strategy for regulating VDCC diversity. The importance of these developmental findings is bolstered by a recent study which identified mutations in the β4 as the molecular defect in the mutant epileptic mouse (lethargic; lh/lh). As β4 is normally expressed in both forebrain and cerebellum, one may consider the impact of the loss of β4 upon VDCC assembly and activity. The importance of the βlb and β4 isoforms to calcium channel maturation and assembly is discussed.
Type of Medium:
Electronic Resource
URL:
http://dx.doi.org/10.1023/A:1021997924473
Permalink
