Calcium Influx through Voltage-gated Calcium Channels Regulates 5-HT3 Receptor Channel Desensitization in NG108-15 Cells

1998 ◽  
Vol 861 (1 ADVANCES IN S) ◽  
pp. 253-254 ◽  
Author(s):  
S. JONES ◽  
J. L. YAKEL
Keyword(s):  
Calcium Channels ◽  
Calcium Influx ◽  
Voltage Gated ◽  
Voltage Gated Calcium Channels ◽  
Receptor Channel

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.

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

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.

scholarly journals Preoperative Pregabalin Prolongs Duration of Spinal Anesthesia and Reduces Early Postoperative Pain

QJM ◽  
2020 ◽  
Vol 113 (Supplement_1) ◽  
Author(s):  
G A A Elkady ◽  
S I Ghaly ◽  
A M Elansary ◽  
A M Ismail
Keyword(s):  
Postoperative Pain ◽  
Calcium Channels ◽  
Spinal Anesthesia ◽  
Calcium Influx ◽  
Aminobutyric Acid ◽  
Effective Dosage ◽  
Preoperative Pain ◽  
Voltage Gated ◽  
Voltage Gated Calcium Channels ◽  
Acid Analog

Abstract Background Various adjuvants have been used to prolong spinal anesthesia, with the additional advantages of delaying the onset of postoperative pain and reducing postoperative analgesic requirements. Pregabalin is an R-aminobutyric acid analog that binds to the α2-δ subunit of presynaptic voltage-gated calcium channels. Objective The aim of this work is to evaluate the efficacy of a single dose of pregabalin in terms of spinal blockade duration and its potential opioid-sparing effect during the first 24 hours postoperatively Patients and Methods There were limitations to the present study. First, since only 1 dosage of pregabalin was evaluated, we could not determine the most effective dosage. Second, clinically meaningful improvements in recovery were not assessed. Adequate postoperative pain control provides early postsurgical mobilization, shortened hospitalization, and increased patient satisfaction. Third, preoperative pain and anxiety scores were not recorded. Pregabalin might affect the preoperative pain, mood, and anxiety scores, and these factors can be related to the postoperative pain score. Results The mechanisms by which pregabalin premedication prolongs motor and sensory blocks using local anesthetics in spinal anesthesia are not fully understood. There may be several reasons for the prolongation of spinal anesthesia. Gabapentinoids are an r-aminobutyric acid analog that binds to α2-δ subunit of presynaptic voltage-gated calcium channels, and this inhibition decreases postsynaptic excitability by reducing potassium-evoked excitatory transmitter release. These medications provide antiepileptic, anxiolytic, and analgesic features by modulating both GABAergic neurotransmission and calcium influx. Gabapentinoid compounds produce a significant and clinically important improvement in preoperative anxiety scores. Since patients may be anxious in the perioperative period, the anxiolytic effects and euphorigenic effects of pregabalin may be beneficial.

AMPA Induces NO-Dependent cGMP Signals in Hippocampal and Cortical Neurons via L-Type Voltage-Gated Calcium Channels

2019 ◽  
Vol 30 (4) ◽  
pp. 2128-2143 ◽  
Author(s):  
Jan Giesen ◽  
Ernst-Martin Füchtbauer ◽  
Annette Füchtbauer ◽  
Klaus Funke ◽  
Doris Koesling ◽  
...  
Keyword(s):  
Calcium Channels ◽  
Cortical Neurons ◽  
Calcium Influx ◽  
Hippocampal Slices ◽  
Resonance Energy Transfer ◽  
Resonance Energy ◽  
Voltage Gated ◽  
Voltage Gated Calcium Channels ◽  
Acute Hippocampal Slices ◽  
The Impact

Abstract The nitric oxide (NO)/cGMP signaling cascade has an established role in synaptic plasticity. However, with conventional methods, the underlying cGMP signals were barely detectable. Here, we set out to confirm the well-known NMDA-induced cGMP increases, to test the impact of AMPA on those signals, and to identify the relevant phosphodiesterases (PDEs) using a more sensitive fluorescence resonance energy transfer (FRET)-based method. Therefore, a “knock-in” mouse was generated that expresses a FRET-based cGMP indicator (cGi-500) allowing detection of cGMP concentrations between 100 nM and 3 μM. Measurements were performed in cultured hippocampal and cortical neurons as well as acute hippocampal slices. In hippocampal and cortical neurons, NMDA elicited cGMP signals half as high as the ones elicited by exogenous NO. Interestingly, AMPA increased cGMP independently of NMDA receptors and dependent on NO synthase (NOS) activation. NMDA- and AMPA-induced cGMP signals were not additive indicating that both pathways converge on the level of NOS. Accordingly, the same PDEs, PDE1 and PDE2, were responsible for degradation of NMDA- as well as AMPA-induced cGMP signals. Mechanistically, AMPAR induced calcium influx through L-type voltage-gated calcium channels leading to NOS and finally NO-sensitive guanylyl cyclase activation. Our results demonstrate that in addition to NMDA also AMPA triggers endogenous NO formation and hence cGMP production.

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