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The Journal of Physiology

Cover image for Vol. 588 Issue 11

June 2010

Volume 588, Issue 11

Pages 1801–2010

  1. PERSPECTIVES

    1. Top of page
    2. PERSPECTIVES
    3. CLINICAL PERSPECTIVES
    4. JOURNAL CLUB
    5. SPECIAL SECTION REVIEWS: NEUROLOGICAL CHANNELOPATHIES
    6. SPECIAL SECTION RELATED PAPERS
    7. NEUROSCIENCE
    8. SKELETAL MUSCLE AND EXERCISE
    9. INTEGRATIVE
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      Single or double? Think zinc! (pages 1803–1804)

      Yasushi Okamura

      Article first published online: 28 MAY 2010 | DOI: 10.1113/jphysiol.2010.191122

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      A tale from the Crypt: splice variants of BK channels in colonic potassium secretion (pages 1807–1808)

      Carlos A. Flores, L. Pablo Cid and Francisco V. Sepúlveda

      Article first published online: 28 MAY 2010 | DOI: 10.1113/jphysiol.2010.191783

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  2. CLINICAL PERSPECTIVES

    1. Top of page
    2. PERSPECTIVES
    3. CLINICAL PERSPECTIVES
    4. JOURNAL CLUB
    5. SPECIAL SECTION REVIEWS: NEUROLOGICAL CHANNELOPATHIES
    6. SPECIAL SECTION RELATED PAPERS
    7. NEUROSCIENCE
    8. SKELETAL MUSCLE AND EXERCISE
    9. INTEGRATIVE
    1. You have free access to this content
    2. You have free access to this content
  3. JOURNAL CLUB

    1. Top of page
    2. PERSPECTIVES
    3. CLINICAL PERSPECTIVES
    4. JOURNAL CLUB
    5. SPECIAL SECTION REVIEWS: NEUROLOGICAL CHANNELOPATHIES
    6. SPECIAL SECTION RELATED PAPERS
    7. NEUROSCIENCE
    8. SKELETAL MUSCLE AND EXERCISE
    9. INTEGRATIVE
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    3. You have free access to this content
      Does obesity reduce load-induced muscle hypertrophy? (pages 1819–1820)

      Madhusudhan R. Papasani, Kara Thornton, Zhan Yinggian, Andreas Brezas, Cassie Welch, Guankui Wang, Alejandro Villasante, Deep Pokharel, Pallavi Cheguru, Swathi Kotla and Daniel C. Julien

      Article first published online: 28 MAY 2010 | DOI: 10.1113/jphysiol.2010.189357

  4. SPECIAL SECTION REVIEWS: NEUROLOGICAL CHANNELOPATHIES

    1. Top of page
    2. PERSPECTIVES
    3. CLINICAL PERSPECTIVES
    4. JOURNAL CLUB
    5. SPECIAL SECTION REVIEWS: NEUROLOGICAL CHANNELOPATHIES
    6. SPECIAL SECTION RELATED PAPERS
    7. NEUROSCIENCE
    8. SKELETAL MUSCLE AND EXERCISE
    9. INTEGRATIVE
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      Axon initial segment dysfunction in epilepsy (pages 1829–1840)

      Verena C. Wimmer, Christopher A. Reid, Eva Y.-W. So, Samuel F. Berkovic and Steven Petrou

      Article first published online: 28 MAY 2010 | DOI: 10.1113/jphysiol.2010.188417

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      Sodium channel gene family: epilepsy mutations, gene interactions and modifier effects (pages 1841–1848)

      Miriam H. Meisler, Janelle E. O’Brien and Lisa M. Sharkey

      Article first published online: 28 MAY 2010 | DOI: 10.1113/jphysiol.2010.188482

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      NaV1.1 channels and epilepsy (pages 1849–1859)

      William A. Catterall, Franck Kalume and John C. Oakley

      Article first published online: 28 MAY 2010 | DOI: 10.1113/jphysiol.2010.187484

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      Mutations in GABAA receptor subunits associated with genetic epilepsies (pages 1861–1869)

      Robert L. Macdonald, Jing-Qiong Kang and Martin J. Gallagher

      Article first published online: 28 MAY 2010 | DOI: 10.1113/jphysiol.2010.186999

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      Pain channelopathies (pages 1897–1904)

      Roman Cregg, Aliakmal Momin, Francois Rugiero, John N. Wood and Jing Zhao

      Article first published online: 28 MAY 2010 | DOI: 10.1113/jphysiol.2010.187807

  5. SPECIAL SECTION RELATED PAPERS

    1. Top of page
    2. PERSPECTIVES
    3. CLINICAL PERSPECTIVES
    4. JOURNAL CLUB
    5. SPECIAL SECTION REVIEWS: NEUROLOGICAL CHANNELOPATHIES
    6. SPECIAL SECTION RELATED PAPERS
    7. NEUROSCIENCE
    8. SKELETAL MUSCLE AND EXERCISE
    9. INTEGRATIVE
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      Genetic and functional characterisation of the P/Q calcium channel in episodic ataxia with epilepsy (pages 1905–1913)

      Sanjeev Rajakulendran, Tracey D. Graves, Robyn W. Labrum, Dimitrios Kotzadimitriou, Louise Eunson, Mary B. Davis, Rosalyn Davies, Nicholas W. Wood, Dimitri M. Kullmann, Michael G. Hanna and Stephanie Schorge

      Article first published online: 28 MAY 2010 | DOI: 10.1113/jphysiol.2009.186437

      Rare inherited mutations of the CACNA1A gene cause bouts of incoordination (episodic ataxia), and sometimes epilepsy. CACNA1A encodes a protein that allows calcium ions to travel through the membranes of neurons. We have studied the sequence of CACNA1A in people with episodic ataxia and epilepsy. We found that, in addition to rare mutations, genetic changes that are present in the general population (polymorphisms) occur in these patients. A common feature of the over-represented polymorphisms is that they subtly reduce the flow of calcium ions through the membrane. Our results show that by carefully measuring the effects of common polymorphisms, it is possible to detect genetic factors that contribute to the susceptibility to neurological diseases characterised by altered neuronal excitability.

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      Can robots patch-clamp as well as humans? Characterization of a novel sodium channel mutation (pages 1915–1927)

      M. Estacion, J. S. Choi, E. M. Eastman, Z. Lin, Y. Li, L. Tyrrell, Y. Yang, S. D. Dib-Hajj and S. G. Waxman

      Article first published online: 28 MAY 2010 | DOI: 10.1113/jphysiol.2009.186114

      As hundreds of mutations in genes encoding ion channels have been linked to neurological disorders or produced by mutagenesis in the laboratory, the need for functional analysis by patch-clamp has increased. We compared an automated technique for electrophysiological characterization of mutant channels with analysis by human physiologists, in functional assessment of a Nav1.7 sodium channel mutation which causes erythromelalgia. Robotic patch-clamping, which can increase throughput (number of cells analysed per day) 3- to 10-fold, has strengths and limitations. If robotic profiling is used to screen ion channel mutations, each protocol should be validated by initial comparison to manual recording. With this caveat, if results are interpreted cautiously, robotic patch-clamp can facilitate the electrophysiological profiling of ion channel mutations.

  6. NEUROSCIENCE

    1. Top of page
    2. PERSPECTIVES
    3. CLINICAL PERSPECTIVES
    4. JOURNAL CLUB
    5. SPECIAL SECTION REVIEWS: NEUROLOGICAL CHANNELOPATHIES
    6. SPECIAL SECTION RELATED PAPERS
    7. NEUROSCIENCE
    8. SKELETAL MUSCLE AND EXERCISE
    9. INTEGRATIVE
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      AMPA receptor subunits define properties of state-dependent synaptic plasticity (pages 1929–1946)

      Michelle R. Emond, Johanna M. Montgomery, Matthew L. Huggins, Jesse E. Hanson, Lifang Mao, Richard L. Huganir and Daniel V. Madison

      Article first published online: 28 MAY 2010 | DOI: 10.1113/jphysiol.2010.187229

      The most widely accepted model for the neuronal substrate of learning is the activity-dependent strengthening of synapses known as long-term potentiation, or LTP. LTP occurs when the receiving nerve cell (the postsynaptic cell) becomes more sensitive to the signal sent by the transmitting nerve cell (the presynaptic cell). This increase in sensitivity happens because the receptor proteins that detect synaptic signals are added to the membrane of the postsynaptic nerve cell. We have found that different compositions of these receptors can put the synapse into different ‘states’, in addition to making them more sensitive. This has the result of providing to the synapse information about its history. As a result, the information carrying capacity of synapses is increased. These results contribute to our understanding of how memories are formed, and thus bring us closer to designing interventions to correct disabilities of learning and memory.

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      Optimal processing of photoreceptor signals is required to maximize behavioural sensitivity (pages 1947–1960)

      Haruhisa Okawa, K. Joshua Miyagishima, A. Cyrus Arman, James B. Hurley, Greg D. Field and Alapakkam P. Sampath

      Article first published online: 28 MAY 2010 | DOI: 10.1113/jphysiol.2010.188573

      A dark-adapted observer can detect flashes of light that activate few retinal rod photoreceptors. This exquisite sensitivity depends on rods signalling single-photon absorptions, but relatively little is understood about how the visual system processes these signals. We studied how the rod single-photon response and noise impact light detection using transgenic mice with more discernible rod photoresponses. Surprisingly, behavioural threshold was elevated in these mice. Electrophysiological recordings from the retina reveal that poor synaptic tuning of rod bipolar cells to the single-photon response and dark noise of rods could explain the impaired behaviour. We find that the optimal readout of rod photoresponses in the retina is critical for maximizing the fidelity of downstream signals and in maximizing visual sensitivity.

  7. SKELETAL MUSCLE AND EXERCISE

    1. Top of page
    2. PERSPECTIVES
    3. CLINICAL PERSPECTIVES
    4. JOURNAL CLUB
    5. SPECIAL SECTION REVIEWS: NEUROLOGICAL CHANNELOPATHIES
    6. SPECIAL SECTION RELATED PAPERS
    7. NEUROSCIENCE
    8. SKELETAL MUSCLE AND EXERCISE
    9. INTEGRATIVE
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      Common phenotype of resting mouse extensor digitorum longus and soleus muscles: equal ATPase and glycolytic flux during transient anoxia (pages 1961–1983)

      Kalyan C. Vinnakota, Joshua Rusk, Lauren Palmer, Eric Shankland and Martin J. Kushmerick

      Article first published online: 28 MAY 2010 | DOI: 10.1113/jphysiol.2009.185934

      Some muscles contract more rapidly with higher rates of lactate formation than others that are slower with greater oxygen uptake, and have corresponding differences in enzyme contents. We studied both types of muscle, experimentally and by mathematical modelling. Our results show the rates of ATP utilization and lactate production in each type are not distinguishable at rest. Thus the two muscle types are closely similar when inactive. A mathematical model of the reactions simulates the experimental data and reveals details of the mechanisms of regulation involved. These results expand our understanding of the different muscle types by defining a novel baseline state for both muscle types at rest but leave unanswered the mechanisms by which their properties differ during exercise.

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      Reduced muscle activation during exercise related to brain oxygenation and metabolism in humans (pages 1985–1995)

      P. Rasmussen, J. Nielsen, M. Overgaard, R. Krogh-Madsen, A. Gjedde, N. H. Secher and N. C. Petersen

      Article first published online: 28 MAY 2010 | DOI: 10.1113/jphysiol.2009.186767

      Maximal exercise may be limited not only by the muscles but also by fatigue occurring within the brain. It is not clear what causes the brain to fatigue, but here we show that the brain cannot fully activate the muscles during exercise when the oxygen supply to the brain is reduced. These results show that to understand why human exercise performance is limited, the role of the brain needs to be considered and that the metabolism of the brain may play an important role in determining the end-point of exercise.

  8. INTEGRATIVE

    1. Top of page
    2. PERSPECTIVES
    3. CLINICAL PERSPECTIVES
    4. JOURNAL CLUB
    5. SPECIAL SECTION REVIEWS: NEUROLOGICAL CHANNELOPATHIES
    6. SPECIAL SECTION RELATED PAPERS
    7. NEUROSCIENCE
    8. SKELETAL MUSCLE AND EXERCISE
    9. INTEGRATIVE
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      Uteroplacental insufficiency programs regional vascular dysfunction and alters arterial stiffness in female offspring (pages 1997–2010)

      Marc Q. Mazzuca, Mary E. Wlodek, Nicoleta M. Dragomir, Helena C. Parkington and Marianne Tare

      Article first published online: 28 MAY 2010 | DOI: 10.1113/jphysiol.2010.187849

      An adverse environment during early life in the fetus can increase risk of cardiovascular disease in adulthood. This study shows that adult female rat offspring exposed to a poor environment as fetuses, created by reduced uteroplacental blood flow (oxygen and nutrients), have impaired function of their blood vessels, particularly those supplying the uterus. The wall of the uterine artery is stiffer, caused by changes in structural proteins. The ability of the uterine artery to relax is impaired by a deficiency in the actions of endothelium-derived hyperpolarizing factor, which is important in small blood vessel relaxation. The uterine artery-specific pathophysiology in females exposed to adverse early life environments has important implications for understanding pregnancy complications in females born small.

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