scholarly journals Characterizing calcium influx via voltage- and ligand-gated calcium channels in embryonic Alligator neurons in culture

2013 ◽  
Vol 4 (3) ◽  
Author(s):  
Weina Ju ◽  
Jiang Wu ◽  
Michael Pritz ◽  
Rajesh Khanna
Keyword(s):  
Calcium Channels ◽  
Calcium Influx ◽  
Present Report ◽  
Initial Step ◽  
Nmda Receptor Antagonist ◽  
Brain Neurons ◽  
Calcium Deregulation ◽  
Voltage Gated Calcium Channels ◽  
Physiological Properties ◽  
Artificial Cerebrospinal Fluid

AbstractVertebrate brains share many features in common. Early in development, both the hindbrain and diencephalon are built similarly. Only later in time do differences in morphology occur. Factors that could potentially influence such changes include certain physiological properties of neurons. As an initial step to investigate this problem, embryonic Alligator brain neurons were cultured and calcium responses were characterized. The present report is the first to document culture of Alligator brain neurons in artificial cerebrospinal fluid (ACSF) as well as in standard mammalian tissue culture medium supplemented with growth factors. Alligator brain neuron cultures were viable for at least 1 week with unipolar neurites emerging by 24 hours. Employing Fura-2 AM, robust depolarizationinduced calcium influx, was observed in these neurons. Using selective blockers of the voltage-gated calcium channels, the contributions of N-, P/Q-, R-, T-, and L-type channels in these neurons were assessed and their presence documented. Lastly, Alligator brain neurons were challenged with an excitotoxic stimulus (glutamate + glycine) where delayed calcium deregulation could be prevented by a classical NMDA receptor antagonist.

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

scholarly journals Drosophila Mushroom Body Kenyon Cells Generate Spontaneous Calcium Transients Mediated by PLTX-Sensitive Calcium Channels

2005 ◽  
Vol 94 (1) ◽  
pp. 491-500 ◽  
Author(s):  
Shaojuan Amy Jiang ◽  
Jorge M. Campusano ◽  
Hailing Su ◽  
Diane K. O'Dowd
Keyword(s):  
Calcium Channels ◽  
Late Stage ◽  
Calcium Oscillations ◽  
Adult Brain ◽  
Calcium Transients ◽  
Mushroom Bodies ◽  
Brain Neurons ◽  
Voltage Gated ◽  
Voltage Gated Calcium Channels ◽  
Kenyon Cells

Spontaneous calcium oscillations in mushroom bodies of late stage pupal and adult Drosophila brains have been implicated in memory consolidation during olfactory associative learning. This study explores the cellular mechanisms regulating calcium dynamics in Kenyon cells, principal neurons in mushroom bodies. Fura-2 imaging shows that Kenyon cells cultured from late stage Drosophila pupae generate spontaneous calcium transients in a cell autonomous fashion, at a frequency similar to calcium oscillations in vivo (10–20/h). The expression of calcium transients is up regulated during pupal development. Although the ability to generate transients is a property intrinsic to Kenyon cells, transients can be modulated by bath application of nicotine and GABA. Calcium transients are blocked, and baseline calcium levels reduced, by removal of external calcium, addition of cobalt, or addition of Plectreurys toxin (PLTX), an insect-specific calcium channel antagonist. Transients do not require calcium release from intracellular stores. Whole cell recordings reveal that the majority of voltage-gated calcium channels in Kenyon cells are PLTX-sensitive. Together these data show that influx of calcium through PLTX-sensitive voltage-gated calcium channels mediates spontaneous calcium transients and regulates basal calcium levels in cultured Kenyon cells. The data also suggest that these calcium transients represent cellular events underlying calcium oscillations in the intact mushroom bodies. However, spontaneous calcium transients are not unique to Kenyon cells as they are present in approximately 60% of all cultured central brain neurons. This suggests the calcium transients play a more general role in maturation or function of adult brain neurons.

scholarly journals The Use of Fibrinolytic Therapy in Acute Ischemic Events

2020 ◽  
Vol 6 (2) ◽  
Author(s):  
Danny Del Duca
Keyword(s):  
Calcium Channels ◽  
Calcium Concentration ◽  
Calcium Influx ◽  
Tissue Perfusion ◽  
Fibrinolytic Therapy ◽  
High Concentration ◽  
Cytotoxic Effects ◽  
Voltage Gated Calcium Channels ◽  
Cerebrovascular Events ◽  
Ischemic Events

The loss of tissue perfusion represents the pathological basis underlying acute cerebrovascular events. The occlusion of the brain's blood supply by intravascular thrombotic and/or atherosclerotic phenomena results in a disruption in tissue oxygen and glucose delivery. This inevitably impairs the cell's capacity to synthesize ATP. Despite initial attempts to maintain consistent ATP stores through anaerobic glycolysis and adenosine release, the starving tissue experiences loss of membrane ionic gradients, secondary to the inactivation of the Na+/K+ ATPase pump. A significant increase in intracellular calcium concentration is triggered by the activation of voltage- gated calcium channels, the activation of ligand-gated calcium channels, and by the inactivation of the Na+/Ca+ exchanger. In addition, massive release of the main excitatory, inhibitory, and monoamine neurotransmitters (many of which become excitotoxins at high concentration) is also observed. The above excitatory transmitters, such as glutamine, for example, play an important role in the over-stimulation of the NMDA receptor, which in turn promotes excessive calcium influx (1). The cytotoxic effects of calcium are associated with the activation of lipases, proteases, and endonucleases, as well as xanthine oxidase and neuronal NO synthase, capable of either direct or indirect destruction of cellular structures (2).

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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