Selective modulation of cellular voltage-dependent calcium channels by hyperbaric pressureâ€”a suggested HPNS partial mechanism

Aviner, Ben; Gradwohl, Gérard; Aviner, Merav Mor; Levy, Shiri; Grossman, Yoram

doi:10.3389/fncel.2014.00136

Cited by 7 publications

(25 citation statements)

References 62 publications

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“…On the other hand, the increase in the currents' maximal amplitude in Ca V 2.2 channel at HP in this work is similar to HP effect found recently in Ca V 1.2 and reminiscent of the ‘delayed rectifier’ K + channels (another member of this protein superfamily) in which the non‐inactivating currents were greater at steady state during HP exposure in invertebrates such as squid , snail and lobster .…”

Section: Discussionsupporting

confidence: 89%

“…As demonstrated in our previous direct and indirect measurements of currents in VDCCs at HP, pressure effect can be selective. In this study, we report that currents through Ca V 2.2 are increased, whereas currents through the Ca V 2.1 channel are generally unaffected by HP.…”

Section: Discussionsupporting

confidence: 61%

“…In such a case, increased channel activity may augment synaptic release and contribute to ‘dendritic boosting’ (increased transfer function between synaptic inputs and somatic spike generation) previously reported by our laboratory . Such boosting, that conforms well to HPNS hyperexcitability, was attributed also to the Ca V 1.2 channel that is prevalent in the dendrites . This process is an example of HP influence on neuronal networks that does not act through synaptic transmission.…”

Section: Discussionsupporting

confidence: 58%

“…Further support to this notion was the observations that low [Ca 2+ ] o partially mimics the effects of HP and high [Ca 2+ ] o can antagonize to some extent HP depression of current amplitude . In fact, modulation of presynaptic Ca 2+ currents at HP has been already suggested . We, therefore, postulated that the major mechanism by which HP alters synaptic transmission is the modulation of Ca 2+ influx into the presynaptic terminals through voltage‐dependent Ca 2+ channels (VDCCs).…”

Section: Introductionmentioning

confidence: 89%

“…We have, therefore, embarked on a long‐term study that was aimed at overcoming these obstacles: direct measurement of VDCC currents by expressing the genetically identified cRNAs of the channels in frog oocytes under HP conditions. Recently, we have performed such a study for the first time on VDCCs currents of Ca V 1.2 and Ca V 3.2 , demonstrating selective and sometimes transient HP effects on the channels: Ca V 1.2 being potentiated, while the Ca V 3.2 is depressed.…”

Section: Introductionmentioning

confidence: 98%

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Selective pressure modulation of synaptic voltage‐dependent calcium channels—involvement in HPNS mechanism

Aviner

Gradwohl

Bliznyuk

et al. 2016

J Cellular Molecular Medi

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Exposure to hyperbaric pressure (HP) exceeding 100 msw (1.1 MPa) is known to cause a constellation of motor and cognitive impairments named high‐pressure neurological syndrome (HPNS), considered to be the result of synaptic transmission alteration. Long periods of repetitive HP exposure could be an occupational risk for professional deep‐sea divers. Previous studies have indicated the modulation of presynaptic Ca2+ currents based on synaptic activity modified by HP. We have recently demonstrated that currents in genetically identified cellular voltage‐dependent Ca2+ channels (VDCCs), CaV1.2 and CaV3.2 are selectively affected by HP. This work further elucidates the HPNS mechanism by examining HP effect on Ca2+ currents in neuronal VDCCs, CaV2.2 and CaV2.1, which are prevalent in presynaptic terminals, expressed in Xenopus oocytes. HP augmented the CaV2.2 current amplitude, much less so in a channel variation containing an additional modulatory subunit, and had almost no effect on the CaV2.1 currents. HP differentially affected the channels' kinetics. It is, therefore, suggested that HPNS signs and symptoms arise, at least in part, from pressure modulation of various VDCCs.

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Section: Discussionsupporting

confidence: 89%

Section: Discussionsupporting

confidence: 61%

Section: Discussionsupporting

confidence: 58%

Section: Introductionmentioning

confidence: 89%

Section: Introductionmentioning

confidence: 98%

See 3 more Smart Citations

Selective pressure modulation of synaptic voltage‐dependent calcium channels—involvement in HPNS mechanism

Aviner

Gradwohl

Bliznyuk

et al. 2016

J Cellular Molecular Medi

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Modelling of noble anaesthetic gases and high hydrostatic pressure effects in lipid bilayers

Moskovitz

Yang

2015

Soft Matter

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Our objective was to study molecular processes that might be responsible for inert gas narcosis and high-pressure nervous syndrome. The classical molecular dynamics trajectories (200 ns) of dioleoylphosphatidylcholine (DOPC) bilayers simulated by the Berger force field were evaluated for water and the atomic distribution of noble gases around DOPC molecules in the pressure range of 1-1000 bar and at a temperature of 310 K. Xenon and argon have been tested as model gases for general anaesthetics, and neon has been investigated for distortions that are potentially responsible for neurological tremors in hyperbaric conditions. The analysis of stacked radial pair distribution functions of DOPC headgroup atoms revealed the explicit solvation potential of the gas molecules, which correlates with their dimensions. The orientational dynamics of water molecules at the biomolecular interface should be considered as an influential factor, while excessive solvation effects appearing in the lumen of membrane-embedded ion channels could be a possible cause of inert gas narcosis. All the noble gases tested exhibit similar order parameter patterns for both DOPC acyl chains, which are opposite of the patterns found for the order parameter curve at high hydrostatic pressures in intact bilayers. This finding supports the 'critical volume' hypothesis of anaesthesia pressure reversal. The irregular lipid headgroup-water boundary observed in DOPC bilayers saturated with neon in the pressure range of 1-100 bar could be associated with the possible manifestation of neurological tremors at the atomic scale. The non-immobiliser neon also demonstrated the highest momentum impact on the normal component of the DOPC diffusion coefficient representing the monolayer undulation rate, which indicates that enhanced diffusivity rather than atomic size is the key factor.

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Exocytosis from chromaffin cells: hydrostatic pressure slows vesicle fusion

Stühmer

2015

Phil. Trans. R. Soc. B

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One contribution of 16 to a discussion meeting issue 'Release of chemical transmitters from cell bodies and dendrites of nerve cells'. Pressure affects reaction kinetics because chemical transitions involve changes in volume, and therefore pressure is a standard thermodynamic parameter to measure these volume changes. Many organisms live in environments at external pressures other than one atmosphere (0.1 MPa). Marine animals have adapted to live at depths of over 7000 m (at pressures over 70 MPa), and microorganisms living in trenches at over 110 MPa have been retrieved. Here, kinetic changes in secretion from chromaffin cells, measured as capacitance changes using the patch-clamp technique at pressures of up to 20 MPa are presented. It is known that these high pressures drastically slow down physiological functions. High hydrostatic pressure also affects the kinetics of ion channel gating and the amount of current carried by them, and it drastically slows down synaptic transmission. The results presented here indicate a similar change in volume (activation volume) of 390 + 57 Å 3 for large dense-core vesicles undergoing fusion in chromaffin cells and for degranulation of mast cells. It is significantly larger than activation volumes of voltage-gated ion channels in chromaffin cells. This information will be useful in finding possible protein conformational changes during the reactions involved in vesicle fusion and in testing possible molecular dynamic models of secretory processes.

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Selective modulation of cellular voltage-dependent calcium channels by hyperbaric pressureâ€”a suggested HPNS partial mechanism

Cited by 7 publications

References 62 publications

Selective pressure modulation of synaptic voltage‐dependent calcium channels—involvement in HPNS mechanism

Selective pressure modulation of synaptic voltage‐dependent calcium channels—involvement in HPNS mechanism

Modelling of noble anaesthetic gases and high hydrostatic pressure effects in lipid bilayers

Exocytosis from chromaffin cells: hydrostatic pressure slows vesicle fusion

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