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Martin F. Schneider, PhD

Academic Title:

Professor

Primary Appointment:

Biochemistry and Molecular Biology

Secondary Appointment(s):

Biophysics

Additional Title:

Director, Interdisciplinary Program in Muscle Biology

Location:

108NG 229

Phone (Primary):

(410) 706-7812

Education and Training

 

  • Yale University, BS Biochemistry (honors; magna cum laude) 

  • Tufts University School of Medicine, completed 2 years of Medical School

  • University College, London, UK, 1 year as a special student in Biophysics and Physiology

  • Duke University, PhD in Physiology

  • Yale University School of Medicine, postdoctoral training in Physiology

 

 

 

Biosketch

Dr Schneider is an internationally known leader in skeletal muscle excitation-contraction coupling, the series of steps whereby electrical depolarization of the normally inside negative muscle membrane potential initiates release  of calcium ions (Ca2+) from their intracellular storage location, the muscle sarcoplasmic reticulum (SR), allowing Ca2+ ions bind to regulatory sites on muscle contractile filaments, which serves as a switch to permit contractile filament interaction, producing force development and muscle shortening.  In pioneering work in collaboration with his post doc mentor Dr W.K. Chandler (Yale University), Dr Schneider made the first measurements of tiny electrical currents (charge displacement currents or channel “gating” currents) due to the redistribution of charged voltage sensor proteins within the muscle membrane.  Such gating currents were previously predicted in the classic studies of Hodgkin and Huxley on voltage dependent channel activation underlying the action potential in nerve axons, and were first detected in any excitable cell membrane by Schneider and Chandler in skeletal muscle, where they control Ca2+ release from Ca2+ release channels in the spatially immediately adjacent SR membrane.  Analogous gating currents were subsequently identified by other groups for gating voltage dependent Na+, K+ and Ca2+ channels in other excitable cells. 

As an Assistant Professor and Associate Professor (tenured) in the Department of Physiology at the University of Rochester School of Medicine, Dr Schneider examined the functional role of muscle intramembrane charge movement in the regulation of Ca2+ release from the SR in skeletal muscle fibers, developing single and double gap techniques for doing voltage clamp studies on muscle fibers with maintained or suppressed contraction, respectively. He also developed procedures for using dyes which changed absorbance on Ca2+ binding to monitor Ca2+ release from intracellular stores (sarcoplasmic reticulum) in response to membrane depolarization and the ensuing membrane charge movement.  Dr Schneider also spent a year's sabbatical from the University of Rochester at the Neurobiology Laboratory, Ecole Normale Superieure, Paris, France, where he studied Na+ channel gating current, and its modification by several neuro toxins.

After moving to UMSOM, Dr Schneider investigated modulation of the coupling of voltage sensor charge displacement to the SR Ca2+ release channel activation in the process of excitation contraction coupling, including advanced imaging techniques with fluorescent Ca2+ indicators to characterize both global cytoplasmic Ca2+ signals during depolarization, as well as local Ca2+ release events, known as Ca2+ sparks. These local intracellular events were discovered and characterized in cardiac muscle cells by Dr Lederer at UM SOM, who collaborated with Dr Schneider in the initial studies on Ca2+ sparks in skeletal muscle. In addition, more recent work in the Schneider lab utilizes confocal fluorescence imaging to study nucleo-cytoplasmic movements of several transcriptional regulator molecules (NFAT, HDACs, Foxo) in skeletal muscle fibers.  In addition, Dr Schneider is the founding and current director and PI of the NIH/NIAMS-funded Interdisciplinary Training Program in Muscle Biology (now in year 21 of continuous funding), which provides support annually for 5 pre doc and 5 post doc trainees studying various aspects of skeletal, cardiac or smooth muscle biology and disease at UMSOM.  

Dr Schneider’s research contributions have been recognized by an NIH/NINDS Career Development Award, an NIH/NINDS Javits Neuroscience Investigator Award, an NIH/NIAMS MERIT Award (ongoing), chairmanship of a Gordon Research Conference on Muscle: Excitation-Contraction Coupling and an honorary degree from the University of Debrecen, Debrecen, Hungary.  His current NIH research grant has been continuously funded for 32 years.    

Research/Clinical Keywords

Skeletal muscle, calcium signaling, muscle cell signaling, excitation-contraction coupling, membrane voltage sensors, gating currents, Ca2+ channels, excitability, neuronal signaling, nucleo-cytoplasmic signaling, NFAT, HDAC, Foxo, cell membrane biophysics, cell electrical properties, muscle plasticity, muscle fiber type, muscle growth, muscular dystrophy, hypokalemic periodic paralysis, muscle membranes, muscle sarcoplasmic reticulum Ca2+ release, cytoplasmic Ca2+ transients, local Ca2+ signals, Ca2+ sparks, S100A1, calmodulin, calmodulation.

Highlighted Publications

 

S100A1 and calmodulin regulation of ryanodine receptor in striated muscle.

Prosser BL, Hernández-Ochoa EO, Schneider MF.

Cell calcium. 2011; 50(4):323-31. NIHMSID: NIHMS315208 PMID:21784520; PMCID:PMC3185186

 

Voltage clamp methods for the study of membrane currents and SR Ca(2+) release in adult skeletal muscle fibres.

Hernández-Ochoa EO, Schneider MF.

Progress in biophysics and molecular biology. 2012; 108(3):98-118. NIHMSID: NIHMS35243;  PMID:22306655;

PMCID:PMC3321118

 

Kinetics of nuclear-cytoplasmic translocation of Foxo1 and Foxo3A in adult skeletal muscle fibers.

Schachter TN, Shen T, Liu Y, Schneider MF.

American journal of physiology. Cell physiology. 2012; 303(9):C977-90.  PMID:22932683; PMCID:PMC3492827

 

β1a490-508, a 19-residue peptide from C-terminal tail of Cav1.1 β1a subunit, potentiates voltage-dependent calcium release in adult skeletal muscle fibers.

Hernández-Ochoa EO, Olojo RO, Rebbeck RT, Dulhunty AF, Schneider MF.

Biophysical journal. 2014; 106(3):535-47. PMID:24507594; PMCID:PMC3944469

 

Alternating bipolar field stimulation identifies muscle fibers with defective excitability but maintained local Ca(2+) signals and contraction.

Hernández-Ochoa EO, Vanegas C, Iyer SR, Lovering RM, Schneider MF.

Skelet Muscle. 2016 Feb 5;6:6. doi: 10.1186/s13395-016-0076-8. eCollection 2016. PMID: 26855765

Additional Publication Citations

iN CHRONOLOGICAL ORDER:

 

Linear electrical properties of the transverse tubules and surface membrane of skeletal muscle fibers.

Schneider MF.

The Journal of general physiology. 1970; 56(5):640-71.  PMID:5475999; PMCID:PMC2225972

 

Voltage dependent charge movement of skeletal muscle: a possible step in excitation-contraction coupling.

Schneider MF, Chandler WK.

Nature. 1973; 242(5395):244-6.  PMID:4540479

 

Calcium transients and intramembrane charge movement in skeletal muscle fibres.

Kovács L, Ríos E, Schneider MF.

Nature. 1979; 279(5712):391-6.  PMID:16068161

 

Membrane charge moved at contraction thresholds in skeletal muscle fibres.

Horowicz P, Schneider MF.

The Journal of physiology. 1981; 314:595-633.PMID:6975815; PMCID:PMC1249452

 

Time course of calcium release and removal in skeletal muscle fibers.

Melzer W, Rios E, Schneider MF.

Biophysical journal. 1984; 45(3):637-41.  PMID:6608964; PMCID:PMC1434889

 

Intramembrane charge movement and calcium release in frog skeletal muscle.

Melzer W, Schneider MF, Simon BJ, Szucs G.

The Journal of physiology. 1986; 373:481-511.  PMID:3489092; PMCID: PMC1182549

 

A general procedure for determining the rate of calcium release from the sarcoplasmic reticulum in skeletal muscle fibers.

Melzer W, Rios E, Schneider MF.

Biophysical journal. 1987; 51(6):849-63.  PMID:3496921; PMCID:PMC1330019

 

Inactivation of calcium release from the sarcoplasmic reticulum in frog skeletal muscle.

Schneider MF, Simon BJ.

The Journal of physiology. 1988; 405:727-45.  PMID:2855645; PMCID: PMC1191001

 

Caffeine slows turn-off of calcium release in voltage clamped skeletal muscle fibers.

Simon BJ, Klein MG, Schneider MF.

Biophysical journal. 1989; 55(4):793-7.  PMID: 2720072; PMCID: PMC1330563

 

Decline of myoplasmic Ca2+, recovery of calcium release and sarcoplasmic Ca2+ pump properties in frog skeletal muscle.

Klein MG, Kovacs L, Simon BJ, Schneider MF.

The Journal of physiology. 1991; 441:639-71.  PMID:1667802; PMCID: PMC1180218

 

 

Effects of low myoplasmic Mg2+ on calcium binding by parvalbumin and calcium uptake by the sarcoplasmic reticulum in frog skeletal muscle.

Jacquemond V, Schneider MF.

The Journal of general physiology. 1992; 100(1):115-35.  PMID:1512554; PMCID: PMC2229124

 

Two mechanisms of quantized calcium release in skeletal muscle.

Klein MG, Cheng H, Santana LF, Jiang YH, Lederer WJ, Schneider MF.

Nature. 1996; 379(6564):455-8.  PMID: 8559251

 

Voltage dependence of the pattern and frequency of discrete Ca2+ release events after brief repriming in frog skeletal muscle.

Klein MG, Lacampagne A, Schneider MF.

Proceedings of the National Academy of Sciences of the United States of America. 1997; 94(20):11061-6.  PMID:9380759; PMCID:PMC23600

 

Two mechanisms for termination of individual Ca2+ sparks in skeletal muscle.

Lacampagne A, Klein MG, Ward CW, Schneider MF.

Proceedings of the National Academy of Sciences of the United States of America. 2000; 97(14):7823-8.  PMID:10884414; PMCID: PMC16629

 

Effects of imperatoxin A on local sarcoplasmic reticulum Ca(2+) release in frog skeletal muscle.

Shtifman A, Ward CW, Wang J, Valdivia HH, Schneider MF.

Biophysical journal. 2000; 79(2):814-27.  PMID:10920014; PMCID:PMC1300980

 

Activity-dependent nuclear translocation and intranuclear distribution of NFATc in adult skeletal muscle fibers.

Liu Y, Cseresnyés Z, Randall WR, Schneider MF.

The Journal of cell biology. 2001; 155(1):27-39. PMID:11581284; PMCID: PMC2150785

 

Ca2+ sparks are initiated by Ca2+ entry in embryonic mouse skeletal muscle and decrease in frequency postnatally.

Chun LG, Ward CW, Schneider MF.

American journal of physiology. Cell physiology. 2003; 285(3):C686-97.  PMID:12724135

 

Activity-dependent and -independent nuclear fluxes of HDAC4 mediated by different kinases in adult skeletal muscle.

Liu Y, Randall WR, Schneider MF.

The Journal of cell biology. 2005; 168(6):887-97.PMID:15767461; PMCID: PMC2171787

 

Parallel mechanisms for resting nucleo-cytoplasmic shuttling and activity dependent translocation provide dual control of transcriptional regulators HDAC and NFAT in skeletal muscle fiber type plasticity.

Shen T, Liu Y, Randall WR, Schneider MF.

Journal of muscle research and cell motility. 2006; 27(5-7):405-11.  PMID:16874450

 

Ca2+ sparks and T tubule reorganization in dedifferentiating adult mouse skeletal muscle fibers.

Brown LD, Rodney GG, Hernández-Ochoa E, Ward CW, Schneider MF.

American journal of physiology. Cell physiology. 2007; 292(3):C1156-66. NIHMSID: NIHMS93257.  PMID:17065203; PMCID: PMC2654399

 

Ca2+ signal summation and NFATc1 nuclear translocation in sympathetic ganglion neurons during repetitive action potentials.

Hernández-Ochoa EO, Contreras M, Cseresnyés Z, Schneider MF.

Cell calcium. 2007; 41(6):559-71. NIHMSID: NIHMS23810  PMID:17125834; PMCID: PMC3164312

 

S100A1 binds to the calmodulin-binding site of ryanodine receptor and modulates skeletal muscle excitation-contraction coupling.

Prosser BL, Wright NT, Hernãndez-Ochoa EO, Varney KM, Liu Y, Olojo RO, Zimmer DB, Weber DJ, Schneider MF.

The Journal of biological chemistry. 2008; 283(8):5046-57. NIHMSID: NIHMS765845.  PMID:18089560; PMCID: PMC4821168

 

Alpha-adrenergic signalling activates protein kinase D and causes nuclear efflux of the transcriptional repressor HDAC5 in cultured adult mouse soleus skeletal muscle fibres.

Liu Y, Contreras M, Shen T, Randall WR, Schneider MF.

The Journal of physiology. 2009; 587(Pt 5):1101-15.  PMID:19124542;  PMCID: PMC2673778

 

The Qgamma component of intra-membrane charge movement is present in mammalian muscle fibres, but suppressed in the absence of S100A1.

Prosser BL, Hernández-Ochoa EO, Zimmer DB, Schneider MF.

The Journal of physiology. 2009; 587(Pt 18):4523-41.  PMID:19651767; PMCID: PMC2766655

 

Simultaneous recording of intramembrane charge movement components and calcium release in wild-type and S100A1-/- muscle fibres.

Prosser BL, Hernández-Ochoa EO, Zimmer DB, Schneider MF.

The Journal of physiology. 2009; 587(Pt 18):4543-59.  PMID:19651766; PMCID:PMC2766656

 

NOX2-dependent ROS is required for HDAC5 nuclear efflux and contributes to HDAC4 nuclear efflux during intense repetitive activity of fast skeletal muscle fibers.

Liu Y, Hernández-Ochoa EO, Randall WR, Schneider MF.

American journal of physiology. Cell physiology. 2012; 303(3):C334-47. PMID:22648949; PMCID:PMC3423023

Research Interests

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Clinical Specialty Details

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Awards and Affiliations

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