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Bandhan Mukherjee, Qi Yuan
The interactions of L-type calcium channels (LTCCs) and NMDA receptors (NMDARs) in memories are poorly understood. Here we investigated the specific roles of anterior piriform cortex (aPC) LTCCs and NMDARs in early odor preference memory in mice. Using calcium imaging in aPC slices, LTCC activation was shown to be dependent on NMDAR activation. Either D-APV (NMDAR antagonist) or nifedipine (LTCC antagonist) reduced somatic calcium transients in pyramidal cells evoked by lateral olfactory tract stimulation. However, nifedipine did not further reduce calcium in the presence of D-APV...
October 14, 2016: Scientific Reports
Bruce A Berkowitz, Tiffany Schmidt, Robert H Podolsky, Robin Roberts
Purpose: In humans, rodents, and pigeons, the dark → light transition signals nonretinal brain tissue to increase choroidal thickness, a major control element of choroidal blood flow, and thus of photoreceptor and retinal pigment epithelium function. However, it is unclear which photopigments in the retina relay the light signal to the brain. Here, we test the hypothesis that melanopsin (Opn4)-regulated phototransduction modulates light-evoked choroidal thickness expansion in mice. Methods: Two-month-old C57Bl/6 wild-type (B6), 4- to 5-month-old C57Bl/6/129S6 wild-type (B6 + S6), and 2-month-old melanopsin knockout (Opn4-/-) on a B6 + S6 background were studied...
October 1, 2016: Investigative Ophthalmology & Visual Science
Richard Cv Tyser, Antonio Ma Miranda, Chiann-Mun Chen, Sean M Davidson, Shankar Srinivas, Paul R Riley
The mammalian heartbeat is thought to begin just prior to the linear heart tube stage of development. How the initial contractions are established and the downstream consequences of the earliest contractile function on cardiac differentiation and morphogenesis have not been described. Using high-resolution live imaging of mouse embryos, we observed randomly distributed spontaneous asynchronous Ca(2+)-oscillations (SACOs) in the forming cardiac crescent (stage E7.75) prior to overt beating. Nascent contraction initiated at around E8...
October 11, 2016: ELife
Martin Laasmaa, Rikke Birkedal, Marko Vendelin
In cardiac excitation-contraction coupling (ECC), calcium enters the cytosol via L-type Ca(2+) channels (LTCC) and reverse Na(+)/Ca(2+)-exchange (NCXrev), or is released from the sarcoplasmic reticulum (SR) by Ca(2+)-induced Ca(2+)-release (CICR). The magnitude of Ca(2+) influx via the different pathways varies with the state of the cell and is difficult to assess quantitatively, because changes in Ca(2+) influx through one pathway affects the others. In rainbow trout ventricular myocytes, the role of the SR has been uncertain for decades...
October 1, 2016: Journal of Molecular and Cellular Cardiology
Jennifer J DuPont, Amy McCurley, Ana P Davel, Joseph McCarthy, Shawn B Bender, Kwangseok Hong, Yan Yang, Jeung-Ki Yoo, Mark Aronovitz, Wendy E Baur, Demetra D Christou, Michael A Hill, Iris Z Jaffe
Hypertension is nearly universal yet poorly controlled in the elderly despite proven benefits of intensive treatment. Mice lacking mineralocorticoid receptors in smooth muscle cells (SMC-MR-KO) are protected from rising blood pressure (BP) with aging, despite normal renal function. Vasoconstriction is attenuated in aged SMC-MR-KO mice, thus they were used to explore vascular mechanisms that may contribute to hypertension with aging. MicroRNA (miR) profiling identified miR-155 as the most down-regulated miR with vascular aging in MR-intact but not SMC-MR-KO mice...
September 8, 2016: JCI Insight
Jose L Sanchez-Alonso, Anamika Bhargava, Thomas O'Hara, Alexey V Glukhov, Sophie Schobesberger, Navneet Bhogal, Markus B Sikkel, Catherine Mansfield, Yuri E Korchev, Alexander R Lyon, Prakash P Punjabi, Viacheslav O Nikolaev, Natalia A Trayanova, Julia Gorelik
RATIONALE: Disruption in subcellular targeting of Ca(2+) signaling complexes secondary to changes in cardiac myocyte structure may contribute to the pathophysiology of a variety of cardiac diseases, including heart failure (HF) and certain arrhythmias. OBJECTIVE: To explore microdomain-targeted remodeling of ventricular L-type Ca(2+) channels (LTCCs) in HF. METHODS AND RESULTS: Super-resolution scanning patch-clamp, confocal and fluorescence microscopy were used to explore the distribution of single LTCCs in different membrane microdomains of nonfailing and failing human and rat ventricular myocytes...
September 30, 2016: Circulation Research
Javier Ávila-Medina, Eva Calderón-Sánchez, Patricia González-Rodríguez, Francisco Monje-Quiroga, Juan Antonio Rosado, Antonio Castellano, Antonio Ordóñez, Tarik Smani
Voltage-dependent CaV1.2 L-type Ca(2+) channels (LTCC) are the main route for calcium entry in vascular smooth muscle cells (VSMC). Several studies have also determined the relevant role of store-operated Ca(2+) channels (SOCC) in vascular tone regulation. Nevertheless, the role of Orai1- and TRPC1-dependent SOCC in vascular tone regulation and their possible interaction with CaV1.2 are still unknown. The current study sought to characterize the co-activation of SOCC and LTCC upon stimulation by agonists, and to determine the possible crosstalk between Orai1, TRPC1, and CaV1...
September 30, 2016: Journal of Biological Chemistry
Alejandra Z Vielma, Luisa León, Ignacio C Fernández, Daniel R González, Mauricio P Boric
S-nitrosylation of several Ca2+ regulating proteins in response to β-adrenergic stimulation was recently described in the heart; however the specific nitric oxide synthase (NOS) isoform and signaling pathways responsible for this modification have not been elucidated. NOS-1 activity increases inotropism, therefore, we tested whether β-adrenergic stimulation induces NOS-1-dependent S-nitrosylation of total proteins, the ryanodine receptor (RyR2), SERCA2 and the L-Type Ca2+ channel (LTCC). In the isolated rat heart, isoproterenol (10 nM, 3-min) increased S-nitrosylation of total cardiac proteins (+46±14%) and RyR2 (+146±77%), without affecting S-nitrosylation of SERCA2 and LTCC...
2016: PloS One
Ling He, Xiao-Tong Hu, Yu-Jie Lai, Yan Long, Lu Liu, Bing-Lin Zhu, Guo-Jun Chen
L-type calcium channel (LTCC) gene Cav1.2 is believed to play an important role in the alteration of Ca(2+) homeostasis in brain astrocytes. Increasing evidence shows that alteration of intracellular Ca(2+) concentration is related to the effect of 17β-estradiol (E2) in a variety of neurophysiological and neuropathological conditions. In this study, we measured immunoreactivity of Cav1.2 protein expression in rat primary cortical astrocytes by using Western blots. We demonstrated that E2 upregulated Cav1.2 expression in a dose- and time-dependent manner and the effect of E2 on Cav1...
October 2016: Journal of Molecular Neuroscience: MN
Francesca Rusconi, Paola Ceriotti, Michele Miragoli, Pierluigi Carullo, Nicolò Salvarani, Marcella Rocchetti, Elisa Di Pasquale, Stefano Rossi, Maddalena Tessari, Silvia Caprari, Magali Cazade, Paolo Kunderfranco, Jean Chemin, Marie-Louise Bang, Fabio Polticelli, Antonio Zaza, Giuseppe Faggian, Gianluigi Condorelli, Daniele Catalucci
BACKGROUND: L-type calcium channels (LTCCs) play important roles in regulating cardiomyocyte physiology, which is governed by appropriate LTCC trafficking to and density at the cell surface. Factors influencing the expression, half-life, subcellular trafficking, and gating of LTCCs are therefore critically involved in conditions of cardiac physiology and disease. METHODS: Yeast 2-hybrid screenings, biochemical and molecular evaluations, protein interaction assays, fluorescence microscopy, structural molecular modeling, and functional studies were used to investigate the molecular mechanisms through which the LTCC Cavβ2 chaperone regulates channel density at the plasma membrane...
August 16, 2016: Circulation
Weixia Zhong, Andrew J Picca, Albert S Lee, Nissar A Darmani
Cisplatin-like chemotherapeutics cause vomiting via calcium (Ca(2+))-dependent release of multiple neurotransmitters (dopamine, serotonin, substance P, etc.) from the gastrointestinal enterochromaffin cells and/or the brainstem. Intracellular Ca(2+) signaling is triggered by activation of diverse emetic receptors (including tachykininergic NK1, serotonergic 5-HT3, dopaminergic D2, cholinergic M1, or histaminergic H1), whose activation in vomit-competent species can evoke emesis. Other emetogens such as cisplatin, rotavirus NSP4 protein and bacterial toxins can also induce intracellular Ca(2+) elevation...
July 26, 2016: Autonomic Neuroscience: Basic & Clinical
Wei Li, Nai-Zhong Zheng, Qi Yuan, Ke Xu, Fan Yang, Lei Gu, Gu-Yan Zheng, Guo-Jie Luo, Chun Fan, Guang-Ju Ji, Bo Zhang, Huiqing Cao, Xiao-Li Tian
UNLABELLED: Entry of calcium into cardiomyocyte via L-type calcium channel (LTCC) is fundamental to cardiac contraction. CACNA1C, a type of LTCC and a hallmark of a matured ventricular myocyte, is developmentally regulated. Here, we identified 138 potential transcription factors by a comparative genomic study on 5-kb promoter regions of CACNA1C gene across eight vertebrate species, and showed that six factors were developmentally regulated with the expression of Cacna1c in mouse P19cl6 in vitro cardiomyocyte differentiation model...
September 2016: Journal of Molecular Medicine: Official Organ of the "Gesellschaft Deutscher Naturforscher und Ärzte"
Mark D Levin, Gautam K Singh, Hai Xia Zhang, Keita Uchida, Beth A Kozel, Phyllis K Stein, Atilla Kovacs, Ruth E Westenbroek, William A Catterall, Dorothy Katherine Grange, Colin G Nichols
Cantu syndrome (CS) is caused by gain-of-function (GOF) mutations in genes encoding pore-forming (Kir6.1, KCNJ8) and accessory (SUR2, ABCC9) KATP channel subunits. We show that patients with CS, as well as mice with constitutive (cGOF) or tamoxifen-induced (icGOF) cardiac-specific Kir6.1 GOF subunit expression, have enlarged hearts, with increased ejection fraction and increased contractility. Whole-cell voltage-clamp recordings from cGOF or icGOF ventricular myocytes (VM) show increased basal L-type Ca(2+) current (LTCC), comparable to that seen in WT VM treated with isoproterenol...
June 14, 2016: Proceedings of the National Academy of Sciences of the United States of America
Sulayma A Albarwani, Fathi Mansour, Abdul Aleem Khan, Intisar Al-Lawati, Abdulla Al-Kaabi, Al-Manar Al-Busaidi, Safa Al-Hadhrami, Isehaq Al-Husseini, Sultan Al-Siyabi, Musbah O Tanira
Calcium channel blockers (CCBs) are widely used to treat cardiovascular disease (CVD) including hypertension. As aging is an independent risk factor for CVD, the use of CCBs increases with increasing age. Hence, this study was designed to evaluate the effect of aging on the sensitivity of small mesenteric arteries to L-type voltage-gated calcium channel (LTCC) blockers and also to investigate whether there was a concomitant change in calcium current density. Third order mesenteric arteries from male F344 rats, aged 2...
2016: Frontiers in Physiology
A Cipriani, K Saunders, M-J Attenburrow, J Stefaniak, P Panchal, S Stockton, T A Lane, E M Tunbridge, J R Geddes, P J Harrison
l-type calcium channel (LTCC) antagonists have been used in bipolar disorder for over 30 years, without becoming an established therapeutic approach. Interest in this class of drugs has been rekindled by the discovery that LTCC genes are part of the genetic aetiology of bipolar disorder and related phenotypes. We have therefore conducted a systematic review of LTCC antagonists in the treatment and prophylaxis of bipolar disorder. We identified 23 eligible studies, with six randomised, double-blind, controlled clinical trials, all of which investigated verapamil in acute mania, and finding no evidence that it is effective...
October 2016: Molecular Psychiatry
Man Li, Hong-Peng He, Hui-Qin Gong, Jian Zhang, Wen-Jian Ma, Hao Zhou, Dong-Sun Cao, Nan Wang, Tong-Cun Zhang
AIMS: Dysregulation of Ca(2+) is a central cause of cardiac hypertrophy. The α1C subunit of L-type Ca(2+) channel (LTCC) is a pore-forming protein which is responsible for the voltage-dependent channel gating and channel selectivity for Ca(2+). Myocardin and nuclear factor of activated T-cells c4 (NFATc4) are two key transcription factors in cardiac hypertrophy. We aimed to investigate the underlying mechanism of the transcriptional regulation of LTCC α1C by myocardin and NFATc4 in hypertrophic cardiomyocytes...
June 15, 2016: Life Sciences
Matthias Eden, Benjamin Meder, Mirko Völkers, Montatip Poomvanicha, Katrin Domes, M Branchereau, P Marck, Rainer Will, Alexander Bernt, Ashraf Rangrez, Matthias Busch, Martin Hrabě de Angelis, Christophe Heymes, Wolfgang Rottbauer, Patrick Most, Franz Hofmann, Norbert Frey
Calcium signalling plays a critical role in the pathogenesis of heart failure. Here we describe a cardiac protein named Myoscape/FAM40B/STRIP2, which directly interacts with the L-type calcium channel. Knockdown of Myoscape in cardiomyocytes decreases calcium transients associated with smaller Ca(2+) amplitudes and a lower diastolic Ca(2+) content. Likewise, L-type calcium channel currents are significantly diminished on Myoscape ablation, and downregulation of Myoscape significantly reduces contractility of cardiomyocytes...
2016: Nature Communications
Eef Dries, Demetrio J Santiago, Daniel M Johnson, Guillaume Gilbert, Patricia Holemans, Sanne M Korte, H Llewelyn Roderick, Karin R Sipido
In cardiac myocytes, β-adrenergic stimulation enhances Ca(2+) cycling through an integrated signalling cascade modulating L-type Ca(2+) channels (LTCC), phospholamban, and ryanodine receptors (RyRs). CaMKII and nitric oxide synthase1 (NOS1) are proposed as prime mediators for increasing RyR open probability. We investigate whether this pathway is confined to the high Ca(2+) microdomain of the dyadic cleft and thus to coupled RyRs. Pig ventricular myocytes are studied under whole-cell voltage-clamp and confocal line-scan imaging with Fluo-4 as a [Ca(2+) ]i indicator...
April 28, 2016: Journal of Physiology
Catherine B Xie, Lalarukh Haris Shaikh, Sumedha Garg, Gizem Tanriver, Ada E D Teo, Junhua Zhou, Carmela Maniero, Wanfeng Zhao, Soosung Kang, Richard B Silverman, Elena A B Azizan, Morris J Brown
Aldosterone-producing adenomas (APAs) vary in phenotype and genotype. Zona glomerulosa (ZG)-like APAs frequently have mutations of an L-type calcium channel (LTCC) CaV1.3. Using a novel antagonist of CaV1.3, compound 8, we investigated the role of CaV1.3 on steroidogenesis in the human adrenocortical cell line, H295R, and in primary human adrenal cells. This investigational drug was compared with the common antihypertensive drug nifedipine, which has 4.5-fold selectivity for the vascular LTCC, CaV1.2, over CaV1...
2016: Scientific Reports
Mireille Aline Santamaria-Herrera, Erick Benjamín Ríos-Pérez, Juan Antonio Manuel de la Rosa, Maricela García-Castañeda, Diana Stephanie Osornio-Garduño, Roberto Ramos-Mondragón, Teresa Mancilla-Percino, Guillermo Avila
In cardiac muscle cells both T-and L-type Ca(2+) channels (TTCCs and LTCCs, respectively) are expressed, and the latter are relevant to a process known as excitation-contraction coupling (ECC). Evidence obtained from docking studies suggests that isoindolines derived from α-amino acids bind to the LTCC CaV1.2. In the present study, we investigated whether methyl (S)-2-(1,3-dihydroisoindol-2-yl)-4-methylpentanoate (MDIMP), which is derived from L-leucine, modulates both Ca(2+) channels and ECC. To this end, mechanical properties, as well as Ca(2+) transients and currents, were all investigated in isolated cardiac myocytes...
June 15, 2016: European Journal of Pharmacology
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