Fast Inactivation of CaV2.2 Channels Is Prevented by the Gβ1 Subunit in Rat Sympathetic Neurons

Reyes-Vaca, Arturo; Cruz, Lizbeth de la; Garduño, Julieta; Arenas, Isabel; García, David

doi:10.1007/s12031-017-0988-8

Cited by 2 publications

(2 citation statements)

References 30 publications

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“…Specific Gβ subunits have been shown to be responsible for the Ca V 2 channel modulation in different neurons. In rat SCG neurons Ca V 2.2 channels are differentially modulated by different types of Gβ subunits, with Gβ 1 and Gβ 2 being most effective, Gβ 5 showing weaker modulation, and Gβ 3 and Gβ 4 being ineffective [33,34,35]. In contrast, in rat stellate ganglion neurons, Gβ 2 and Gβ 4 but not Gβ 1 subunit are responsible for the coupling of Ca V 2.2 channels with noradrenaline receptors [36].…”

Section: Intracellular Molecules Modulate Presynaptic Ca2+ Channelmentioning

confidence: 99%

Presynaptic Calcium Channels

Mochida

2019

IJMS

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Presynaptic Ca2+ entry occurs through voltage-gated Ca2+ (CaV) channels which are activated by membrane depolarization. Depolarization accompanies neuronal firing and elevation of Ca2+ triggers neurotransmitter release from synaptic vesicles. For synchronization of efficient neurotransmitter release, synaptic vesicles are targeted by presynaptic Ca2+ channels forming a large signaling complex in the active zone. The presynaptic CaV2 channel gene family (comprising CaV2.1, CaV2.2, and CaV2.3 isoforms) encode the pore-forming α1 subunit. The cytoplasmic regions are responsible for channel modulation by interacting with regulatory proteins. This article overviews modulation of the activity of CaV2.1 and CaV2.2 channels in the control of synaptic strength and presynaptic plasticity.

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Section: Intracellular Molecules Modulate Presynaptic Ca2+ Channelmentioning

confidence: 99%

Presynaptic Calcium Channels

Mochida

2019

IJMS

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“…Neurons were dissociated from the SCG by mechanical and enzymatic methods, as previously described [14]. Pancreatic β-cells were also obtained as previously described [5].…”

Section: Cell Culturementioning

confidence: 99%

Sympathetic Voltage-Independent Regulation of Voltage- Gated Calcium Channels in Pancreatic β-Cells

Cruz¹,

Reyes-Vaca²,

Garduño³

et al. 2018

JED

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Voltage-gated calcium (Ca V ) channels are regulated by G proteins via voltage-dependent and independent pathways. Voltage-independent regulation of calcium channels is important for intracellular calcium concentration and insulin secretion. Voltage dependence of each pathway can be elucidated by a prepulse facilitation protocol. Using this experimental approach, we compared Ca V regulation by GTPγS and noradrenaline (NA) in rat pancreatic β-cells and rat superior cervical ganglion (SCG) neurons. The SCG neuron is a model in which the bases of Ca V channel regulation by G proteins have been established. Ca V channel regulation through activation of the sympathetic nervous system has been poorly studied in native insulin-secreting cells. We recorded Ca V channel currents by means of the patch-clamp technique in the whole-cell configuration. We found that application of both GTPγS (a nonspecific activator of G proteins) by cell dialysis and noradrenaline (NA)-exposure reduced Ca V current amplitude in pancreatic β-cells and in SCG neurons. However, the inhibition of Ca V channel currents in GTPγS-dialyzed SCG neurons was relieved by a strong depolarizing pulse. By contrast, in pancreatic β-cells, the inhibition was maintained after a strong depolarizing pulse. In SCG neurons, the Ca V channel inhibition by NA is predominantly voltage-dependent, whereas in pancreatic β-cells it is only 40%. Thus, it appears that Ca V channels in rat pancreatic β-cells are regulated mainly through a voltage-independent pathway. The signaling pathway for Ca V channel regulation by NA in pancreatic β-cells appears to differ from the classic signaling pathway described in SCG neurons. Therefore, voltage-independent regulation of Ca 2+ entry through Ca V channels is a critical step in understanding the pathophysiology of type 2 diabetes.

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Fast Inactivation of CaV2.2 Channels Is Prevented by the Gβ1 Subunit in Rat Sympathetic Neurons

Cited by 2 publications

References 30 publications

Presynaptic Calcium Channels

Presynaptic Calcium Channels

Sympathetic Voltage-Independent Regulation of Voltage- Gated Calcium Channels in Pancreatic β-Cells

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