scholarly journals Voltage-Gated Calcium Channels: Key Players in Sensory Coding in the Retina and the Inner Ear

2018 ◽  
Vol 98 (4) ◽  
pp. 2063-2096 ◽  
Author(s):  
Tina Pangrsic ◽  
Joshua H. Singer ◽  
Alexandra Koschak
Keyword(s):  
Calcium Influx ◽  
Spatial Relationship ◽  
Spatial Arrangement ◽  
Sensory Receptor ◽  
Factors Affecting ◽  
Efficient Coding ◽  
Voltage Gated ◽  
Ribbon Synapses ◽  
Voltage Gated Calcium Channels ◽  
Sensory Receptor Cells

Calcium influx through voltage-gated Ca (CaV) channels is the first step in synaptic transmission. This review concerns CaV channels at ribbon synapses in primary sense organs and their specialization for efficient coding of stimuli in the physical environment. Specifically, we describe molecular, biochemical, and biophysical properties of the CaV channels in sensory receptor cells of the retina, cochlea, and vestibular apparatus, and we consider how such properties might change over the course of development and contribute to synaptic plasticity. We pay particular attention to factors affecting the spatial arrangement of CaV channels at presynaptic, ribbon-type active zones, because the spatial relationship between CaV channels and release sites has been shown to affect synapse function critically in a number of systems. Finally, we review identified synaptopathies affecting sensory systems and arising from dysfunction of L-type, CaV1.3, and CaV1.4 channels or their protein modulatory elements.

Inhibition of Dendritic Calcium Influx by Activation of G-Protein–Coupled Receptors in the Hippocampus

1997 ◽  
Vol 78 (6) ◽  
pp. 3484-3488 ◽  
Author(s):  
Huanmian Chen ◽  
Nevin A. Lambert
Keyword(s):  
Calcium Channels ◽  
Action Potential ◽  
G Protein ◽  
Pyramidal Neuron ◽  
Action Potentials ◽  
Calcium Influx ◽  
G Protein Coupled Receptors ◽  
Voltage Gated ◽  
Voltage Gated Calcium Channels ◽  
G Protein Coupled

Chen, Huanmian and Nevin A. Lambert. Inhibition of dendritic calcium influx by activation of G-protein–coupled receptors in the hippocampus. J. Neurophysiol. 78: 3484–3488, 1997. Gi proteins inhibit voltage-gated calcium channels and activate inwardly rectifying K+ channels in hippocampal pyramidal neurons. The effect of activation of G-protein–coupled receptors on action potential-evoked calcium influx was examined in pyramidal neuron dendrites with optical and extracellular voltage recording. We tested the hypotheses that 1) activation of these receptors would inhibit calcium channels in dendrites; 2) hyperpolarization resulting from K+ channel activation would deinactivate low-threshold, T-type calcium channels on dendrites, increasing calcium influx mediated by these channels; and 3) activation of these receptors would inhibit propagation of action potentials into dendrites, and thus indirectly decrease calcium influx. Activation of adenosine receptors, which couple to Gi proteins, inhibited calcium influx in cell bodies and proximal dendrites without inhibiting action-potential propagation into the proximal dendrites. Inhibition of dendritic calcium influx was not changed in the presence of 50 μM nickel, which preferentially blocks T-type channels, suggesting influx through these channels is not increased by activation of G-proteins. Adenosine inhibited propagation of action potentials into the distal branches of pyramidal neuron dendrites, leading to a three- to fourfold greater inhibition of calcium influx in the distal dendrites than in the soma or proximal dendrites. These results suggest that voltage-gated calcium channels are inhibited in pyramidal neuron dendrites, as they are in cell bodies and terminals and thatG-protein–mediated inhibition of action-potential propagation can contribute substantially to inhibition of dendritic calcium influx.

Abstract 488: Arteriolar Smooth Muscle Calcium Waves Depend on Calcium Influx through Voltage-gated Calcium Channels

Hypertension ◽  
2012 ◽  
Vol 60 (suppl_1) ◽  
Author(s):  
William F Jackson ◽  
Erika B Westcott
Keyword(s):  
Smooth Muscle ◽  
Striated Muscle ◽  
Calcium Influx ◽  
Ryanodine Receptors ◽  
Myogenic Tone ◽  
Voltage Gated ◽  
Voltage Gated Calcium Channels ◽  
Bayk 8644 ◽  
Muscle Calcium ◽  
Arteriolar Diameter

Smooth muscle cells (SMCs) in arterioles from striated muscle display IP 3 receptor-dependent Ca 2+ waves that contribute to global myoplasmic Ca 2+ concentration and myogenic tone. However, the contribution of voltage-gated Ca 2+ channels (VGCC) to these arteriolar Ca 2+ signals is unknown. We tested the hypothesis that Ca 2+ waves depend on Ca 2+ influx through VGCC in cremaster muscle arterioles loaded with Fluo-4 and imaged by confocal microscopy. At rest, with vessels pressurized to 80 cm H 2 O in 2 mM Ca 2+ , arteriolar diameter was 28 ± 2 μm (n = 5), and SMCs displayed Ca 2+ waves with frequency (FREQ) = 0.21 ± 0.06 Hz, occurrence (OCC) = 3.5 ± 1.0 waves/SMC and amplitude (AMP) = 1.7 ± 0.1 F/Fo. Removal of extracellular Ca 2+ dilated the arterioles to 39 ± 1 μm, and inhibited Ca 2+ waves (FREQ = 0.1 ± 0.03, OCC = 1.7 ± 0.5 waves/SMC and AMP = 1.4 ± 0.06 F/Fo; p < 0.05 vs. rest) indicating that Ca 2+ waves depended, in part, on influx of extracellular Ca 2+ . Similarly, the VGCC antagonist, nifedipine (1 μM), dilated the arterioles to 34 ± 1.3 μm and also inhibited Ca 2+ waves (FREQ = 0.07 ± 0.02 Hz, OCC = 1.1 ± 0.5 waves/SMC, AMP = 1.4 ± 0.05 F/Fo; p < 0.05 vs. rest). Hyperpolarization of SMCs with the K + channel agonist, cromakalim (10 μM), dilated arterioles from 49 ± 3 to 59 ± 4 μm (n = 4, p < 0.05) and also reduced Ca 2+ wave FREQ (0.1 ± 0.04 to 0.03 ± 0.003 Hz), OCC (1.7 ± 0.04 to 0.5 ± 0.05 waves/SMC) and AMP (1.5 ± 0.04 to 1.2 ± 0.004 F/Fo) (p < 0.05). Conversely, depolarization of SMCs with the BK Ca channel blocker, TEA (1 mM), constricted arterioles from 28 ± 2 to 16 ± 1 μm (n = 5, p < 0.05) and increased wave FREQ (0.2 ± 0.1 to 0.5 ± 0.1 Hz, p < 0.05) and OCC (4 ± 1 to 8 ± 2 waves/SMC, p < 0.05), effects blocked by nifedipine (1μM) (p < 0.05). Similarly, in arterioles pressurized to 20 cm H 2 O to eliminate myogenic tone and reduce basal VGCC activity, application of the VGCC agonist, BayK 8644 (5 nM) constricted the arterioles from 14 ± 1 to 8 ± 1 μm and increased wave FREQ (0.2 ± 0.1 to 0.6 ± 0.1 Hz) and OCC (3 ± 1 to 10 ± 1 waves/SMC) (n = 6; p < 0.05), effects that were independent of ryanodine receptors, as Ca 2+ waves were unaffected by ryanodine (50 μM) in the absence or presence of BayK 8644 (n = 6; p > 0.05). These data support the hypothesis that Ca 2+ waves in arteriolar SMCs depend, in part, on Ca 2+ influx through VGCC.

scholarly journals Transthyretin oligomers induce calcium influx via voltage-gated calcium channels

2007 ◽  
Vol 100 (2) ◽  
pp. 446-457 ◽  
Author(s):  
Xu Hou ◽  
Helena C. Parkington ◽  
Harold A. Coleman ◽  
Adam Mechler ◽  
Lisandra L. Martin ◽  
...  
Keyword(s):  
Calcium Channels ◽  
Calcium Influx ◽  
Voltage Gated ◽  
Voltage Gated Calcium Channels

scholarly journals Regulation of fetoplacental vascular bed by hypoxia

2009 ◽  
pp. S87-S94
Author(s):  
V Hampl ◽  
V Jakoubek
Keyword(s):  
Experimental Data ◽  
Plasma Membrane ◽  
Vascular Resistance ◽  
Intrauterine Growth Restriction ◽  
Calcium Influx ◽  
Contractile Apparatus ◽  
Voltage Gated ◽  
Intrauterine Growth ◽  
Voltage Gated Calcium Channels ◽  
Vascular Bed

Important fetal and perinatal pathologies, especially intrauterine growth restriction (IUGR), are thought to stem from placental hypoxia-induced vasoconstriction of the fetoplacental vessels, leading to placental hypoperfusion and thus fetal undernutrition. However, the effects of hypoxia on the fetoplacental vessels have been surprisingly little studied. We review here available experimental data on acute hypoxic fetoplacental vasoconstriction (HFPV) and on chronic hypoxic elevation of fetoplacental vascular resistance. The mechanism of HFPV includes hypoxic inhibition of potassium channels in the plasma membrane of fetoplacental vascular smooth muscle and consequent membrane depolarization that activates voltage gated calcium channels. This in turn causes calcium influx and contractile apparatus activation. The mechanism of chronic hypoxic elevation of fetoplacental vascular resistance is virtually unknown except of signs of the involvement of morphological remodeling.

Voltage-Gated Calcium Channels Mediate Intracellular Calcium Increase in Weaver Dopaminergic Neurons During Stimulation of D2 and GABAB Receptors

2004 ◽  
Vol 92 (6) ◽  
pp. 3368-3374 ◽  
Author(s):  
Ezia Guatteo ◽  
C. Peter Bengtson ◽  
Giorgio Bernardi ◽  
Nicola B. Mercuri
Keyword(s):  
Calcium Channels ◽  
Dopaminergic Neurons ◽  
Calcium Influx ◽  
Dopamine Neurons ◽  
Gabab Receptors ◽  
Voltage Gated ◽  
Voltage Gated Calcium Channels ◽  
Whole Cell Patch Clamp ◽  
Midbrain Dopaminergic Neurons ◽  
And Control

The weaver ( wv) mutation affects the pore-forming region of the inwardly rectifying potassium channel (GIRK) leading to degeneration of cerebellar granule and midbrain dopaminergic neurons. The mutated channel ( wvGIRK) loses its potassium selectivity, allowing sodium (Na+) and possibly calcium ions (Ca2+) to enter the cell. Here we performed whole cell patch-clamp recordings combined with microfluorometry to investigate possible differences in calcium ([Ca2+]i) dynamics in native dopaminergic neurons (expressing the wvGIRK2 subunits) in the midbrain slice preparation from homozygous weaver ( wv/wv) and control (+/+) mice. Under resting conditions, [Ca2+]i was similar in wv/wv compared with +/+ neurons. Activation of wvGIRK2 channels by D2 and GABAB receptors increased [Ca2+]i in wv/wv neurons, whereas activation of wild-type channels decreased [Ca2+]i in +/+ neurons. The calcium rise in wv/wv neurons was abolished by antagonists of the voltage-gated calcium channels (VGCC); voltage clamp of the neuron at −60 mV; and hyperpolarization of the neuron to −80 mV or more, in current clamp, and was unaffected by TTX. Therefore we propose that wvGIRK2 channels in native dopamine neurons are not permeable to Ca2+, and when activated by D2 and GABAB receptors they mediate membrane depolarization and an indirect Ca2+ influx through VGCC rather than via wvGIRK2 channels. Such calcium influx may be the trigger for calcium-mediated excitotoxicity, responsible for selective neuronal death in weaver mice.

scholarly journals Regulation of GABAA Receptors Induced by the Activation of L-Type Voltage-Gated Calcium Channels

Membranes ◽  
2021 ◽  
Vol 11 (7) ◽  
pp. 486
Author(s):  
María Clara Gravielle
Keyword(s):  
Calcium Channels ◽  
Gabaa Receptor ◽  
Gabaa Receptors ◽  
Intracellular Signaling ◽  
Calcium Influx ◽  
Normal Function ◽  
Receptor Subtypes ◽  
Voltage Gated ◽  
Voltage Gated Calcium Channels ◽  
Gabaa Receptor Subtypes

GABAA receptors are pentameric ion channels that mediate most synaptic and tonic extrasynaptic inhibitory transmissions in the central nervous system. There are multiple GABAA receptor subtypes constructed from 19 different subunits in mammals that exhibit different regional and subcellular distributions and distinct pharmacological properties. Dysfunctional alterations of GABAA receptors are associated with various neuropsychiatric disorders. Short- and long-term plastic changes in GABAA receptors can be induced by the activation of different intracellular signaling pathways that are triggered, under physiological and pathological conditions, by calcium entering through voltage-gated calcium channels. This review discusses several mechanisms of regulation of GABAA receptor function that result from the activation of L-type voltage gated calcium channels. Calcium influx via these channels activates different signaling cascades that lead to changes in GABAA receptor transcription, phosphorylation, trafficking, and synaptic clustering, thus regulating the inhibitory synaptic strength. These plastic mechanisms regulate the interplay of synaptic excitation and inhibition that is crucial for the normal function of neuronal circuits.

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