Mouse models to study L-type calcium channel function

Moosmang, Sven; Lenhardt, Peter; Haider, Nicole; Hofmann, Franz; Wegener, Jörg W.

doi:10.1016/j.pharmthera.2004.12.003

Cited by 67 publications

(53 citation statements)

References 69 publications

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“…Therefore, we hypothesized that NMDAR-independent, L-type Ca 2ϩ channel-dependent synaptic plasticity might, in parallel to NMDAR-activated processes, be necessary for spatial learning in the behaving animal. Although the pharmacological analysis of cultured cells and slice preparations has provided much insight into the regulation and function of L-type Ca 2ϩ channels in neurons (for review, see Hofmann et al, 1999;Striessnig, 1999;Moosmang et al, 2005), their significance in vivo is far less clear because of several problems associated with the currently available pharmacological tools. Most importantly, all L-type Ca 2ϩ channel blockers affect the function of the cardiovascular system to some extent, which may have substantial input on the function of the CNS.…”

Section: Discussionmentioning

confidence: 99%

Role of Hippocampal Ca_v1.2 Ca²⁺Channels in NMDA Receptor-Independent Synaptic Plasticity and Spatial Memory

Moosmang¹,

Haider²,

Klugbauer³

et al. 2005

J. Neurosci.

393

357

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Current knowledge about the molecular mechanisms of NMDA receptor (NMDAR)-independent long-term potentiation (LTP) in the hippocampus and its function for memory formation in the behaving animal is limited. NMDAR-independent LTP in the CA1 region is thought to require activity of postsynaptic L-type voltage-dependent Ca2+channels (Cav1.x), but the underlying channel isoform remains unknown. We evaluated the function of the Cav1.2 L-type Ca2+channel for spatial learning, synaptic plasticity, and triggering of learning-associated biochemical processes using a mouse line with an inactivation of theCACNA1C(Cav1.2) gene in the hippocampus and neocortex (Cav1.2HCKO). This model shows (1) a selective loss of protein synthesis-dependent NMDAR-independent Schaffer collateral/CA1 late-phase LTP (L-LTP), (2) a severe impairment of hippocampus-dependent spatial memory, and (3) decreased activation of the mitogen-activated protein kinase (MAPK) pathway and reduced cAMP response element (CRE)-dependent transcription in CA1 pyramidal neurons. Our results provide strong evidence for a role of L-type Ca2+channel-dependent, NMDAR-independent hippocampal L-LTP in the formation of spatial memory in the behaving animal and for a function of the MAPK/CREB (CRE-binding protein) signaling cascade in linking Cav1.2 channel-mediated Ca2+influx to either process.

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Section: Discussionmentioning

confidence: 99%

Role of Hippocampal Ca_v1.2 Ca²⁺Channels in NMDA Receptor-Independent Synaptic Plasticity and Spatial Memory

Moosmang¹,

Haider²,

Klugbauer³

et al. 2005

J. Neurosci.

393

357

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“…In comparison, sodium channels play a major role in supporting the action potentials [Stephan and Agnew 1991] and calcium channels are voltage-gated channels. These open in response to plasma membrane depolarization and have been shown to regulate a broad range of physiological processes (for a review see [Moosmang et al 2005]). …”

Section: Ion Currentsmentioning

confidence: 99%

Ion currents modulating oocyte maturation in animals

Tosti

Boni

Gallo

et al. 2013

Systems Biology in Reproductive Medicine

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Growing oocytes are arrested at the first prophase of meiosis which is morphologically identified by the presence of a large and vesicular nucleus, called the germinal vesicle. The dissolution of the germinal vesicle marks the resumption of meiosis during which the oocyte undergoes massive modifications up to the second meiotic block, which is removed at fertilization. The interval between the first and the second meiotic block is defined as maturation and the events occurring during this period are crucial for ovulation, fertilization, and embryo development. Oocytes are excitable cells that react to stimuli by modifying their electrical properties as a consequence of ion currents flowing through ion channels on the plasma membrane. These electrical changes have been largely described at fertilization whereas little information is available during oocyte maturation. The aim of this review is to give an overview on the involvement of ion channels and ion currents during oocyte maturation in species from invertebrates to mammals. The results summarized here point to the possible functional role of ion channels underlying oocyte growth and maturation.

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“…Subunit α1c is the primary isoform found in the heart and gives rise to high-voltageactivated L-type Ca 2+ currents (I Ca,L ). 11,12) Ca 2+ overload in cardiomyocytes could induce mitochondrial Ca 2+ overload and depletion of tissue ATP stores. 13) Our previous studies have shown that Leo decreased intracellular Ca 2+ 3,4) and exerted mitochondrial protective effect both in cardiomyocytes and brain.…”

mentioning

confidence: 99%

Effects of <i>Leonurine</i> on L-Type Calcium Channel in Rat Ventricular Myocytes

Hong

Wang

et al. 2012

Biological & Pharmaceutical Bulletin

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Leonurine (Leo) is a special alkaloid principle of Herba leonuri that has recently been suggested to improve cardiovascular functions. To date, there is no direct ionic evidence of Leo on regulating calcium channels in the heart. In the present study, we examined the effects of Leo on action potentials and membrane currents recorded from isolated rat ventricular myocytes with the whole-cell patch clamp technique. Leo 100 µM shortened the action potential duration in a dose-dependent manner. Leo up to 200 µM had no significant effect on the Na current (I Na ) and K current (I K ). However, Leo depressed the L-type Ca 2 current (I Ca,L ). In the presence of 20 and 100 µM Leo, the current density was decreased and the voltage at half maximal inactivation V 0.5 shift to more negative potential. The recovery time constant was also delayed. In addition, the transcription and protein expression levels of L-type calcium channel (Ca v1.2 ) in primary cultured neonatal myocytes from Sprague-Dawley rats were reduced by Leo treatment in a dose-dependent fashion as assessed by reverse transcription-polymerase chain reaction (RT-PCR) and Western blot assays. We conclude that Leo inhibits L-type calcium channels in cardiomyocytes.

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Mouse models to study L-type calcium channel function

Cited by 67 publications

References 69 publications

Role of Hippocampal Ca_v1.2 Ca²⁺Channels in NMDA Receptor-Independent Synaptic Plasticity and Spatial Memory

Role of Hippocampal Ca_v1.2 Ca²⁺Channels in NMDA Receptor-Independent Synaptic Plasticity and Spatial Memory

Ion currents modulating oocyte maturation in animals

Effects of <i>Leonurine</i> on L-Type Calcium Channel in Rat Ventricular Myocytes

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Mouse models to study L-type calcium channel function

Cited by 67 publications

References 69 publications

Role of Hippocampal Cav1.2 Ca2+Channels in NMDA Receptor-Independent Synaptic Plasticity and Spatial Memory

Role of Hippocampal Cav1.2 Ca2+Channels in NMDA Receptor-Independent Synaptic Plasticity and Spatial Memory

Ion currents modulating oocyte maturation in animals

Effects of <i>Leonurine</i> on L-Type Calcium Channel in Rat Ventricular Myocytes

Contact Info

Product

Resources

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Role of Hippocampal Ca_v1.2 Ca²⁺Channels in NMDA Receptor-Independent Synaptic Plasticity and Spatial Memory

Role of Hippocampal Ca_v1.2 Ca²⁺Channels in NMDA Receptor-Independent Synaptic Plasticity and Spatial Memory