A novel molecular inactivation determinant of voltage-gated CaV1.2 L-type Ca2+ channel

Selective modulation of cellular voltage-dependent calcium channels by hyperbaric pressure—a suggested HPNS partial mechanism

“…Notwithstanding, no significant changes were observed in the Ʈ Decay Slow at HP in both channels, supporting the concept of different mechanisms for the fast and slow inactivation (Hering et al, 2000; Sokolov et al, 2000), which can also react differently to external treatment (Livneh et al, 2006). It was also demonstrated that the molecular structures responsible for these two types of inactivation are differently located in the VDCC's protein (Berjukow et al, 1999) and that the fast inactivation may act similarly to the “ball and chain” mechanism in the K + channel (Cens et al, 1999), while the slow inactivation seems to be at least partially dependent on the interaction between α 1 and β subunits (Sokolov et al, 2000).…”

Selective pressure modulation of synaptic voltage‐dependent calcium channels—involvement in HPNS mechanism

“…Although generally s Decay Fast and s Decay Slow were affected similarly by HP for each channel separately (Table 2), both in Ca V 2.2 and Ca V 2.2 +c2 , s Decay Slow was affected differentially than s Decay Fast at HP for membrane potentials below V Imax (DV <0 mV). This further supports the well-established concept of different mechanisms for the fast and slow inactivation [65,66], which can also react differently to external treatment [67]. It was also demonstrated that the molecular structures responsible for these two types of inactivation are differently located in the VDCC's protein [68] and that the fast inactivation may act similarly to the 'ball and chain' mechanism in the K + channel [69], while the slow inactivation seems to be at least partially dependent on the interaction between a 1 and b subunits [66].…”

Desynchronization of Glutamate Release Prolongs Synchronous CA3 Network Activity

“…Sr 2ϩ could prolong bursts by other effects, such as by reducing calcium-dependent inactivation of high-voltage calcium channels (Lee et al 1985), which might prolong dendritic plateau potentials. However, Sr 2ϩ effects on the inactivation rates of neuronal high-voltage-gated calcium channels (Livneh et al 2006;McNaughton and Randall 1997) are insufficient to explain the observed increases in burst duration. The nature of the plateau potential that occurs during CA3 bursts is controversial (Johnston and Brown 1986) and may include contributions from as-yet uncharacterized voltage-dependent calcium channels whose kinetics may be more substantially altered by Sr 2ϩ , so we cannot completely exclude an effect on calcium channels as a mechanism of burst prolongation, although at this time there is no evidence supporting this mechanism.…”