scholarly journals Aging alters voltage-gated calcium channels in prefrontal cortex pyramidal neurons in the HIV brain

2017 ◽  
Vol 24 (1) ◽  
pp. 113-118 ◽  
Author(s):  
Christina E. Khodr ◽  
Lihua Chen ◽  
Lena Al-Harthi ◽  
Xiu-Ti Hu
Keyword(s):  
Prefrontal Cortex ◽  
Calcium Channels ◽  
Pyramidal Neurons ◽  
Voltage Gated ◽  
Voltage Gated Calcium Channels

scholarly journals 1,25-Dihydroxyvitamin D modulates L-type voltage-gated calcium channels in a subset of neurons in the developing mouse prefrontal cortex

2019 ◽  
Vol 9 (1) ◽  
Author(s):  
Helen Gooch ◽  
Xiaoying Cui ◽  
Victor Anggono ◽  
Maciej Trzaskowski ◽  
Men Chee Tan ◽  
...  
Keyword(s):  
Risk Factors ◽  
Vitamin D ◽  
Prefrontal Cortex ◽  
Calcium Channels ◽  
Brain Maturation ◽  
Genome Wide Association Studies ◽  
Voltage Gated ◽  
Voltage Gated Calcium Channels ◽  
Enhanced Activity ◽  
Activity Dependent

Abstract Schizophrenia has been associated with a range of genetic and environmental risk factors. Here we explored a link between two risk factors that converge on a shared neurobiological pathway. Recent genome-wide association studies (GWAS) have identified risk variants in genes that code for L-type voltage-gated calcium channels (L-VGCCs), while epidemiological studies have found an increased risk of schizophrenia in those with neonatal vitamin D deficiency. The active form of vitamin D (1,25(OH)2D) is a secosteroid that rapidly modulates L-VGCCs via non-genomic mechanisms in a range of peripheral tissues, though its non-genomic effects within the brain remain largely unexplored. Here we used calcium imaging, electrophysiology and molecular biology to determine whether 1,25(OH)2D non-genomically modulated L-VGCCs in the developing prefrontal cortex, a region widely implicated in schizophrenia pathophysiology. Wide-field Ca2+ imaging revealed that physiological concentrations of 1,25(OH)2D rapidly enhanced activity-dependent somatic Ca2+ levels in a small subset of neurons in the developing PFC, termed vitamin D-responsive neurons (VDRNs). Somatic nucleated patch recordings revealed a rapid, 1,25(OH)2D-evoked increase in high-voltage-activated (HVA) Ca2+ currents. Enhanced activity-dependent Ca2+ levels were mediated by L-VGCC but not associated with any changes to Cacna1c (L-VGCC pore-forming subunit) mRNA expression. Since L-VGCC activity is critical to healthy neurodevelopment, these data suggest that suboptimal concentrations of 1,25(OH)2D could alter brain maturation through modulation of L-VGCC signalling and as such may provide a parsimonious link between epidemiologic and genetic risk factors for schizophrenia.

scholarly journals Impact of calcium-activated potassium channels on NMDA spikes in cortical layer 5 pyramidal neurons

2016 ◽  
Vol 115 (3) ◽  
pp. 1740-1748 ◽  
Author(s):  
Tobias Bock ◽  
Greg J. Stuart
Keyword(s):  
Potassium Channels ◽  
Calcium Channels ◽  
Pyramidal Neurons ◽  
Cortical Layer ◽  
Sk Channels ◽  
Spike Generation ◽  
Voltage Gated ◽  
Voltage Gated Calcium Channels ◽  
Basal Dendrites ◽  
Calcium Activated Potassium Channels

Active electrical events play an important role in shaping signal processing in dendrites. As these events are usually associated with an increase in intracellular calcium, they are likely to be under the control of calcium-activated potassium channels. Here, we investigate the impact of calcium-activated potassium channels on N-methyl-d-aspartate (NMDA) receptor-dependent spikes, or NMDA spikes, evoked by glutamate iontophoresis onto basal dendrites of cortical layer 5 pyramidal neurons. We found that small-conductance calcium-activated potassium channels (SK channels) act to reduce NMDA spike amplitude but at the same time, also decrease the iontophoretic current required for their generation. This SK-mediated decrease in NMDA spike threshold was dependent on R-type voltage-gated calcium channels and indicates a counterintuitive, excitatory effect of SK channels on NMDA spike generation, whereas the capacity of SK channels to suppress NMDA spike amplitude is in line with the expected inhibitory action of potassium channels on dendritic excitability. Large-conductance calcium-activated potassium channels had no significant impact on NMDA spikes, indicating that these channels are either absent from basal dendrites or not activated by NMDA spikes. These experiments reveal complex and opposing interactions among NMDA receptors, SK channels, and voltage-gated calcium channels in basal dendrites of cortical layer 5 pyramidal neurons during NMDA spike generation, which are likely to play an important role in regulating the way these neurons integrate the thousands of synaptic inputs they receive.

Voltage-gated calcium channels distribute throughout the dendrite of hippocampal CA1 pyramidal neurons

1991 ◽  
Vol 16 ◽  
pp. 4
Author(s):  
Miyakawa Hiroyoshi ◽  
David Jaffe ◽  
Daniel Johnston ◽  
John Lisman ◽  
Nechama Lasser-Ross ◽  
...  
Keyword(s):  
Calcium Channels ◽  
Pyramidal Neurons ◽  
Voltage Gated ◽  
Ca1 Pyramidal Neurons ◽  
Voltage Gated Calcium Channels ◽  
Hippocampal Ca1

Role of voltage-gated calcium channels in the generation of activity-induced extracellular pH transients in the rat hippocampal slice

1996 ◽  
Vol 75 (6) ◽  
pp. 2354-2360 ◽  
Author(s):  
P. Paalasmaa ◽  
K. Kaila
Keyword(s):  
Calcium Channels ◽  
Pyramidal Neurons ◽  
Hippocampal Slices ◽  
Extracellular Ph ◽  
Stratum Radiatum ◽  
Gamma Aminobutyric Acid ◽  
Voltage Gated ◽  
Voltage Gated Calcium Channels ◽  
Alkaline Shift

1. The role of voltage-gated calcium channels in the generation of activity-induced alkaline shifts in extracellular pH (pHo) was studied in rat hippocampal slices (area CAI) by means of Ca(2+)-and H(+)-selective microlectrodes inserted into the stratum pyramidale and/or stratum radiatum. 2. After complete pharmacological blockade of ionotropic glutamate receptors and gamma-aminobutyric acid-A (GABAA) receptors, trains (5-10 Hz, 5-10s) of antidromic spikes in pyramidal neurons were associated with a fast alkaline transient of up to 0.17 pH units and a fall in the extracellular Ca2+ concentration ([Ca2+]o). The alkaline shift was strongly enhanced upon inhibition of extracellular carbonic anhydrase. 3. Application of 100 microM Ni2+ plus 100 microM Cd2+ inhibited both the fall in [Ca2+]o and the alkaline transient triggered by antidromic spikes. The alkaline shift was abolished in the absence of extracellular Ca2+. 4. In the absence of postsynaptic receptor antagonists, alkaline transients linked to a given level of synaptic excitation in s. radiatum were strongly suppressed after blockade of somatic (and, consequently, of dendritic “backpropagating”) spikes by microdrop application of tetrodotoxin to the cell-body layer. 5. We have previously shown that activity-induced alkaline transients in the CAI region are due to an influx of Ca2+ into neurons, which triggers an influx of H+ ions probably caused by activation of a plasmalemmal Ca2+/H+ ATPase. The present results indicate that much (in s. pyramidale perhaps all) of the pH-changing influx of Ca2+ is mediated by voltage-gated Ca2+ channels.

Differential modulation of single voltage-gated calcium channels by cholinergic and adrenergic agonists in adult hippocampal neurons

1990 ◽  
Vol 64 (4) ◽  
pp. 1291-1302 ◽  
Author(s):  
R. Fisher ◽  
D. Johnston
Keyword(s):  
Calcium Channels ◽  
Hippocampal Neurons ◽  
Pyramidal Neurons ◽  
Single Channel ◽  
Mossy Fiber ◽  
Long Term Potentiation ◽  
High Threshold ◽  
Voltage Gated ◽  
Voltage Gated Calcium Channels ◽  
Ca3 Pyramidal Neurons

1. Pharmacologic agents known to modulate long-term potentiation (LTP) at the mossy fiber-to-CA3 pyramidal neuron synapse were tested for their effects on the activity of single voltage-gated calcium channels in adult CA3 pyramidal neurons. 2. Single-channel current recordings of three types of voltage-gated calcium channels were made from acutely exposed CA3 pyramidal neurons of the adult guinea pig hippocampus. 3. The beta-adrenergic agonist isoproterenol (10 microM), which is known to enhance LTP, increased the activity of the two high-threshold calcium channels (N and L) with no striking effect on the low-threshold (T) channel. 4. The muscarinic agonists carbachol and muscarine (1-10 microM), the latter of which has been shown to inhibit LTP, decreased the probability of opening of L channels, increased the probability of opening of T channels, and had no effect on N channels. The effects were blocked by 0.1 microM atropine. 5. These results are consistent with the hypothesis that neuromodulation of mossy fiber LTP occurs, at least in part, through the modulation of postsynaptic, voltage-gated calcium channels.

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