scholarly journals Activity-dependent increases in [Ca2+]i contribute to digital-analog plasticity at a molluscan synapse

2017 ◽  
Vol 117 (6) ◽  
pp. 2104-2112 ◽  
Author(s):  
Bjoern Ch. Ludwar ◽  
Colin G. Evans ◽  
Monica Cambi ◽  
Elizabeth C. Cropper
Keyword(s):  
Synaptic Transmission ◽  
Intracellular Calcium ◽  
Time Constant ◽  
Calcium Concentration ◽  
Low Frequency ◽  
Intracellular Calcium Concentration ◽  
Calcium Signal ◽  
Presynaptic Neuron ◽  
Calcium Dependent ◽  
Long Time

In a type of short-term plasticity that is observed in a number of systems, synaptic transmission is potentiated by depolarizing changes in the membrane potential of the presynaptic neuron before spike initiation. This digital-analog form of plasticity is graded. The more depolarized the neuron, the greater the increase in the efficacy of synaptic transmission. In a number of systems, including the system presently under investigation, this type of modulation is calcium dependent, and its graded nature is presumably a consequence of a direct relationship between the intracellular calcium concentration ([Ca2+]i) and the effect on synaptic transmission. It is therefore of interest to identify factors that determine the magnitude of this type of calcium signal. We studied a synapse in Aplysia and demonstrate that there can be a contribution from currents activated during spiking. When neurons spike, there are localized increases in [Ca2+]i that directly trigger neurotransmitter release. Additionally, spiking can lead to global increases in [Ca2+]i that are reminiscent of those induced by subthreshold depolarization. We demonstrate that these spike-induced increases in [Ca2+]i result from the activation of a current not activated by subthreshold depolarization. Importantly, they decay with a relatively slow time constant. Consequently, with repeated spiking, even at a low frequency, they readily summate to become larger than increases in [Ca2+]i induced by subthreshold depolarization alone. When this occurs, global increases in [Ca2+]i induced by spiking play the predominant role in determining the efficacy of synaptic transmission. NEW & NOTEWORTHY We demonstrate that spiking can induce global increases in the intracellular calcium concentration ([Ca2+]i) that decay with a relatively long time constant. Consequently, summation of the calcium signal occurs even at low firing frequencies. As a result there is significant, persistent potentiation of synaptic transmission.

Heterogeneous response of microvascular endothelial cells to shear stress

2006 ◽  
Vol 290 (6) ◽  
pp. H2498-H2508 ◽  
Author(s):  
D. Hong ◽  
D. Jaron ◽  
D. G. Buerk ◽  
K. A. Barbee
Keyword(s):  
Endothelial Cells ◽  
Shear Stress ◽  
Intracellular Calcium ◽  
Purinergic Receptors ◽  
Calcium Concentration ◽  
Intracellular Calcium Concentration ◽  
Calcium Signal ◽  
Calcium Waves ◽  
Aortic Endothelial Cells ◽  
Atp Concentration

We investigated changes in calcium concentration in cultured bovine aortic endothelial cells (BAECs) and rat adrenomedulary endothelial cells (RAMECs, microvascular) in response to different levels of shear stress. In BAECs, the onset of shear stress elicited a transient increase in intracellular calcium concentration that was spatially uniform, synchronous, and dose dependent. In contrast, the response of RAMECs was heterogeneous in time and space. Shear stress induced calcium waves that originated from one or several cells and propagated to neighboring cells. The number and size of the responding groups of cells did not depend on the magnitude of shear stress or the magnitude of the calcium change in the responding cells. The initiation and the propagation of calcium waves in RAMECs were significantly suppressed under conditions in which either purinergic receptors were blocked by suramin or extracellular ATP was degraded by apyrase. Exogenously applied ATP produced similarly heterogeneous responses. The number of responding cells was dependent on ATP concentration, but the magnitude of the calcium change was not. Our data suggest that shear stress stimulates RAMECs to release ATP, causing the increase in intracellular calcium concentration via purinergic receptors in cells that are heterogeneously sensitive to ATP. The propagation of the calcium signal is also mediated by ATP, and the spatial pattern suggests a locally elevated ATP concentration in the vicinity of the initially responding cells.

Activity-induced elevations of intracellular calcium concentration in pyramidal and nonpyramidal cells of the CA3 region of rat hippocampal slice cultures

1992 ◽  
Vol 68 (3) ◽  
pp. 961-963 ◽  
Author(s):  
T. Knopfel ◽  
B. H. Gahwiler
Keyword(s):  
Intracellular Calcium ◽  
Time Course ◽  
Calcium Concentration ◽  
Potassium Conductance ◽  
Pyramidal Cells ◽  
Calcium Transients ◽  
Intracellular Calcium Concentration ◽  
Calcium Signal ◽  
Cell Somata ◽  
Ca3 Region

1. Depolarization-induced elevations of intracellular calcium concentration ([Ca2+]i) were examined in slice-cultured hippocampal pyramidal and nonpyramidal cells of the CA3 region by combined intracellular and multisite fura-2 recording techniques. 2. In pyramidal cells, spiking activity induced by depolarizing current pulses (200–800 ms) induced transient elevations of somatic as well as of proximal dendritic [Ca2+]i. The calcium signals from the proximal dendrites were larger in amplitude and decayed much faster than those from the soma. Depolarization of presumed interneurons induced comparable somatic and dendritic calcium transients, which decayed faster than those observed in pyramidal cell somata. 3. The calcium transients of pyramidal cells, but not those of nonpyramidal cells, were associated with a slow afterhyperpolarization (sAHP), whose time course was correlated with that of the somatic calcium signal. We conclude that the lack of a sAHP in non-pyramidal cells cannot be explained by the absence of an efficient rise in [Ca2+]i but rather by the absence of the potassium conductance underlying the sAHP in pyramidal cells.

An Active Role for Astrocytes in Synaptic Plasticity?

2010 ◽  
Vol 104 (3) ◽  
pp. 1216-1218 ◽  
Author(s):  
Ian Wenker
Keyword(s):  
Synaptic Plasticity ◽  
Transgenic Mice ◽  
Intracellular Calcium ◽  
Calcium Concentration ◽  
Active Role ◽  
Intracellular Calcium Concentration ◽  
Synaptic Potentiation ◽  
Calcium Dependent

Recently, Henneberger and colleagues blocked hippocampal long-term synaptic potentiation (LTP) induction by “clamping” intracellular calcium concentration of individual CA1 astrocytes, suggesting calcium-dependent gliotransmitter release from astocytes plays a role in hippocampal LTP induction. However, using transgenic mice to manipulate astrocytic calcium, Agulhon and colleagues demonstrated no effect on LTP induction. Until the question of how intracellular calcium causes gliotransmitter release is answered, the role of astrocytes in synaptic plasticity will be incompletely understood.

Intracellular calcium concentration during low-frequency fatigue in isolated single fibers of mouse skeletal muscle

1993 ◽  
Vol 75 (1) ◽  
pp. 382-388 ◽  
Author(s):  
H. Westerblad ◽  
S. Duty ◽  
D. G. Allen
Keyword(s):  
Sarcoplasmic Reticulum ◽  
Intracellular Calcium ◽  
Calcium Concentration ◽  
Low Frequency ◽  
Intracellular Calcium Concentration ◽  
Low Frequencies ◽  
Single Fibers ◽  
Control Comparison ◽  
Low Frequency Fatigue ◽  
Tetanic Tension

Low-frequency fatigue is a form of muscle fatigue that follows intense muscle activity and is characterized by reduced tetanic tension at low frequencies of stimulation while tetanic tension at high stimulus frequencies is close to normal. The present experiments were performed on isolated single fibers of mouse in which tension and intracellular calcium concentration ([Ca2+]i) were measured. Fatigue was produced by intermittent short tetani continued until tension had declined to 30% of control. Comparison of low- (30- and 50-Hz) and high- (100-Hz) frequency tetani under control conditions and after 30 min of recovery from fatigue showed that low-frequency fatigue was present. During low-frequency fatigue, tetanic [Ca2+]i was substantially reduced at all stimulus frequencies but there was no change in Ca2+ sensitivity or maximum Ca(2+)-activated tension. One possible cause of the reduced tetanic [Ca2+]i is failure of conduction of the action potential in the T tubule, leading to reduced [Ca2+]i in the center of the fiber. However, imaging of [Ca2+]i across the fiber during low-frequency fatigue did not show any such gradient, suggesting that Ca2+ release is uniform across the fiber. Another possible mechanism is that changes in the Ca2+ pumping ability of the sarcoplasmic reticulum might affect tetanic [Ca2+]i. Measurements of the sarcoplasmic reticulum pump function showed a small slowing of Ca2+ uptake rate during low-frequency fatigue, which is unlikely to cause the reduced tetanic [Ca2+]i. In conclusion, the immediate cause of low-frequency fatigue appears to be a reduced tetanic [Ca2+]i, which is probably a consequence of a reduced Ca2+ release from the sarcoplasmic reticulum.

scholarly journals The interdependence of endothelin-1 and calcium: a review

2010 ◽  
Vol 119 (9) ◽  
pp. 361-372 ◽  
Author(s):  
Nathan R. Tykocki ◽  
Stephanie W. Watts
Keyword(s):  
Intracellular Calcium ◽  
Calcium Concentration ◽  
Calcium Influx ◽  
Calcium Signalling ◽  
Intracellular Calcium Concentration ◽  
Future Research ◽  
Endothelin 1 ◽  
Calcium Dependent ◽  
Amino Acid Peptide ◽  
Physiological Processes

The 21-amino-acid peptide ET-1 (endothelin-1) regulates a diverse array of physiological processes, including vasoconstriction, angiogenesis, nociception and cell proliferation. Most of the effects of ET-1 are associated with an increase in intracellular calcium concentration. The calcium influx and mobilization pathways activated by ET-1, however, vary immensely. The present review begins with the basics of calcium signalling and investigates the different ways intracellular calcium concentration can increase in response to a stimulus. The focus then shifts to ET-1, and discusses how ET receptors mobilize calcium. We also examine how disease alters calcium-dependent responses to ET-1 by discussing changes to ET-1-mediated calcium signalling in hypertension, as there is significant interest in the role of ET-1 in this important disease. A list of unanswered questions regarding ET-mediated calcium signals are also presented, as well as perspectives for future research of calcium mobilization by ET-1.

β-Amyloid-induced increase in the resting intracellular calcium concentration gives support to tell Alzheimer lymphocytes from control ones

2002 ◽  
Vol 58 (2) ◽  
pp. 203-205 ◽  
Author(s):  
András Palotás ◽  
János Kálmán ◽  
Miklós Palotás ◽  
Anna Juhász ◽  
Zoltán Janka ◽  
...  
Keyword(s):  
Intracellular Calcium ◽  
Calcium Concentration ◽  
Intracellular Calcium Concentration ◽  
Β Amyloid
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