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L-type Ca2+ (l-type + ca2+)

Distribution by Scientific Domains
Medical Sciences75%

Terms modified by L-type Ca2+

  • l-type ca2+ channel
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  • l-type ca2+ current
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    Selected Abstracts

    Activity-dependent formation and functions of chondroitin sulfate-rich extracellular matrix of perineuronal nets

    DEVELOPMENTAL NEUROBIOLOGY, Issue 5 2007
    Alexander Dityatev
    Abstract Extracellular matrix molecules,including chondroitin sulfate proteoglycans, hyaluronan, and tenascin-R,are enriched in perineuronal nets (PNs) associated with subsets of neurons in the brain and spinal cord. In the present study, we show that similar cell type-dependent extracellular matrix aggregates are formed in dissociated cell cultures prepared from early postnatal mouse hippocampus. Starting from the 5th day in culture, accumulations of lattice-like extracellular structures labeled with Wisteria floribunda agglutinin were detected at the cell surface of parvalbumin-expressing interneurons, which developed after 2,3 weeks into conspicuous PNs localized around synaptic contacts at somata and proximal dendrites, as well as around axon initial segments. Physiological recording and intracellular labeling of PN-expressing neurons revealed that these are large fast-spiking interneurons with morphological characteristics of basket cells. To study mechanisms of activity-dependent formation of PNs, we performed pharmacological analysis and found that blockade of action potentials, transmitter release, Ca2+ permeable AMPA subtype of glutamate receptors or L-type Ca2+ voltage-gated channels strongly decreased the extracellular accumulation of PN components in cultured neurons. Thus, we suggest that Ca2+ influx via AMPA receptors and L-type channels is necessary for activity-dependent formation of PNs. To study functions of chondroitin sulfate-rich PNs, we treated cultures with chondroitinase ABC that resulted in a prominent reduction of several major PN components. Removal of PNs did not affect the number and distribution of perisomatic GABAergic contacts but increased the excitability of interneurons in cultures, implicating the extracellular matrix of PNs in regulation of interneuronal activity. © 2007 Wiley Periodicals, Inc. Develop Neurobiol, 2007 [source]

    Effects of 4-piperidinomethyl-2-isopropyl-5-methylphenol on oxidative stress and calcium current

    JOURNAL OF PHARMACY AND PHARMACOLOGY: AN INTERNATI ONAL JOURNAL OF PHARMACEUTICAL SCIENCE, Issue 9 2005
    Mei-Han Huang
    4-Piperidinomethyl-2-isopropyl-5-methylphenol (THPI) was synthesized by reaction of thymol with piperidine and formaldehyde. The biological effect of THPI on superoxide anion scavenging activity, antiplatelet activity and calcium current inhibition were investigated. THPI (50 ,m) was shown to be a scavenger of superoxide radicals in human neutrophils stimulated with N -formyl-Met-Leu-Phe (66% inhibition). Since superoxide anions are essential for platelet aggregation and L-type Ca2+ -channel activity, we further found that THPI inhibited platelet aggregation induced by arachidonic acid (IC50 46.80 ± 6.88 ,m). The effect of THPI on Ca2+ current in NG108,15 cells was investigated using the whole-cell voltage-clamp technique. THPI inhibited voltage-dependent L-type Ca2+ current (ICa,L). The IC50 value of THPI-induced inhibition of ICa,L was 3.60 ± 0.81 ,m. THPI caused no change in the overall shape of the current-voltage relationship of ICa,L. This indicates that THPI is an inhibitor of ICa,L in NG108,15 cells. Therefore, the channel-blocking properties of THPI may contribute to the underlying mechanism by which it affects neuronal or neuroendocrine function. Furthermore, no significant cytotoxic effects of THPI (0.3,50 ,m) were observed in NG108,15 cells. The results indicate that THPI is a potential reactive oxygen species scavenger and may prevent platelet aggregation or inhibit L-type Ca2+ -channel activity, possibly by scavenging reactive oxygen species. [source]

    New Expression Profiles of Voltage-gated Ion Channels in Arteries Exposed to High Blood Pressure

    MICROCIRCULATION, Issue 4 2002
    Robert H. Cox
    The diameters of small arteries and arterioles are tightly regulated by the dynamic interaction between Ca2+ and K+ channels in the vascular smooth muscle cells. Calcium influx through voltage-gated Ca2+ channels induces vasoconstriction, whereas the opening of K+ channels mediates hyperpolarization, inactivation of voltage-gated Ca2+ channels, and vasodilation. Three types of voltage-sensitive ion channels have been highly implicated in the regulation of resting vascular tone. These include the L-type Ca2+ (CaL) channels, voltage-gated K+ (KV) channels, and high-conductance voltage- and Ca2+ -sensitive K+ (BKCa) channels. Recently, abnormal expression profiles of these ion channels have been identified as part of the pathogenesis of arterial hypertension and other vasospastic diseases. An increasing number of studies suggest that high blood pressure may trigger cellular signaling cascades that dynamically alter the expression profile of arterial ion channels to further modify vascular tone. This article will briefly review the properties of CaL, KV, and BKCa channels, present evidence that their expression profile is altered during systemic hypertension, and suggest potential mechanisms by which the signal of elevated blood pressure may result in altered ion channel expression. A final section will discuss emerging concepts and opportunities for the development of new vasoactive drugs, which may rely on targeting disease-specific changes in ion channel expression as a mechanism to lower vascular tone during hypertensive diseases. [source]

    ELECTROPHYSIOLOGICAL EFFECTS OF KETAMINE ON HUMAN ATRIAL MYOCYTES AT THERAPEUTICALLY RELEVANT CONCENTRATIONS

    CLINICAL AND EXPERIMENTAL PHARMACOLOGY AND PHYSIOLOGY, Issue 12 2008
    Chun-Yu Deng
    SUMMARY 1Ketamine is widely used for the induction of anaesthesia in high-risk patients with cardiovascular instability or severe hypovolaemia. However, the ionic mechanisms involved in the effects of ketamine at therapeutically relevant concentrations in human cardiac myocytes are unclear. The present study was designed to investigate the effects of ketamine on L-type Ca2+ (ICa), transient outward K+ (Ito), ultra-rapid delayed rectifier K+ (IKur) and inward rectifier potassium (IK1) currents, as well as on action potentials, in human isolated atrial myocytes. 2Atrial myocytes were isolated enzymatically from specimens of human atrial appendage obtained from patients undergoing coronary artery bypass grafting. The action potential and membrane currents were recorded in both current- and voltage-clamp modes using the patch-clamp technique. 3Ketamine inhibited ICa with an IC50 of 1.8 µmol/L. In addition, 10 µmol/L ketamine decreased the ICa peak current at +10 mV from 5.1 ± 0.3 to 2.1 ± 0.4 pA/pF (P < 0.01), but did not change the threshold potential, peak current potential and reverse potential. 4Ketamine had no effect on Ito, IKur or IK1, but it reversibly shortened the duration of the action potential in human atrial myocytes. 5In conclusion, ketamine, at a clinically relevant concentration, shortens the action potential duration of the human atrial myocytes, probably by inhibiting ICa. [source]