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.

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.

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.

Simultaneous exposure to ATP and phenylephrine induces a sustained elevation in the intracellular calcium concentration in supraoptic neurons

2006 ◽  
Vol 291 (1) ◽  
pp. R37-R45 ◽  
Author(s):  
Zhilin Song ◽  
Sukumar Vijayaraghavan ◽  
Celia D. Sladek
Keyword(s):  
Intracellular Calcium ◽  
Calcium Concentration ◽  
Calcium Release ◽  
Calcium Influx ◽  
Intracellular Calcium Concentration ◽  
Calcium Stores ◽  
Simultaneous Exposure ◽  
Peak Response ◽  
Synergistic Response ◽  
Supraoptic Neurons

Vasopressin (VP) release from the hypothalamo-neurohypophyseal system (HNS) is stimulated by ATP activation of P2X purinergic receptors and by activation of α1-adrenergic receptors by phenylephrine (PE). These responses are potentiated by simultaneous exposure to ATP+PE. Potentiation was blocked by depleting intracellular calcium stores with thapsigargin. To test the hypothesis that the synergistic response to ATP+PE reflects alterations in the intracellular calcium concentration ([Ca2+]i), [Ca2+]i was monitored in supraoptic neurons in HNS explants loaded with fura 2-AM. Both ATP and PE induced rapid, but transient, elevations in [Ca2+]i. In 0.3 mM Ca2+, the peak response to ATP was greater than to PE but did not differ from the peak response to ATP+PE. A sustained elevation in [Ca2+]i was induced by ATP+PE, that was greater than ATP or PE alone. In 2 mM Ca2+, the peak response to ATP+PE was significantly greater than to either ATP or PE alone, and the sustained response to ATP+PE was greater than to either agent alone. Responses were comparable in the presence of TTX. The sustained elevation in [Ca2+]i was also observed when ATP+PE was removed after 1 min, but it was eliminated by either thapsigargin or removing external calcium, indicating that both calcium influx and calcium release from internal stores are required. Some cells were vasopressinergic based on a VP-induced increase in [Ca2+]i. These observations support the hypothesis that simultaneous exposure to ATP+PE induces a different pattern of [Ca2+]i than either agent alone that may initiate events leading to synergistic stimulation of VP release.

Sodium/lithium countertransport and intracellular calcium concentration in patients with essential hypertension and coronary heart disease

2003 ◽  
Vol 104 (3) ◽  
pp. 323-327
Author(s):  
Sybille GRUSKA ◽  
Ingo JENDRAL ◽  
Rainer RETTIG ◽  
Günter KRAATZ
Keyword(s):  
Coronary Heart Disease ◽  
Heart Disease ◽  
Essential Hypertension ◽  
Intracellular Calcium ◽  
Calcium Concentration ◽  
Calcium Signalling ◽  
Intracellular Calcium Concentration ◽  
Diabetic Patients ◽  
Hypertensive Patients ◽  
Increased Risk

The present study was designed to test the hypothesis that enhanced intracellular calcium signalling and increased sodium/lithium countertransport (Na+/Li+ CT) activity may be associated with coronary heart disease (CHD) in non-diabetic patients with essential hypertension. Platelet-activating factor (PAF)-evoked rises in the intracellular calcium concentration ([Ca2+]i) were measured in Epstein–Barr-virus-immortalized lymphoblasts from 62 hypertensive patients with CHD and 34 patients without CHD. Na+/Li+ CT activity was assessed in erythrocytes from 80 hypertensive patients with CHD and 46 patients without CHD. Baseline values of unstimulated and PAF-stimulated [Ca2+]i were not significantly different between hypertensive subjects with (baseline, 126±5nmol/l; stimulated, 550±43nmol/l) and without (baseline, 125±5nmol/l; stimulated, 654±105nmol/l) CHD. Similarly, Na+/Li+ CT activity was not significantly different between the two groups (patients with CHD, 219±8µmol·l-1·h-1; patients without CHD, 234±10µmol·l-1·h-1). We conclude that intracellular signal transduction, as indicated by PAF-induced rises in [Ca2+]i and Na+/Li+ CT activity, is not associated with an increased risk of CHD in non-diabetic patients with essential hypertension.

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
Sign in / Sign up

Export Citation Format

Share Document