Selective modulation of cellular voltage-dependent calcium channels by hyperbaric pressure-a suggested HPNS partial mechanism.

Ben Aviner,Merav Mor Aviner,Shiri Levy,Gideon Gradwohl,Yoram Grossman

doi:10.3389/fncel.2014.00136

Ben Aviner, Merav Mor Aviner + Show 3 more

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https://doi.org/10.3389/fncel.2014.00136

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Abstract

Professional deep sea divers experience motor and cognitive impairment, known as High Pressure Neurological Syndrome (HPNS), when exposed to pressures of 100 msw (1.1 MPa) and above, considered to be the result of synaptic transmission alteration. Previous studies have indicated modulation of presynaptic Ca2+ currents at high pressure. We directly measured for the first time pressure effects on the currents of voltage dependent Ca2+ channels (VDCCs) expressed in Xenopus oocytes. Pressure selectivity augmented the current in CaV1.2 and depressed it in CaV3.2 channels. Pressure application also affected the channels' kinetics, such as ƮRise, ƮDecay. Pressure modulation of VDCCs seems to play an important role in generation of HPNS signs and symptoms.

Highlights

HPNS Every chemical reaction contributing to the continued existence of an organism is a potential target for pressure effects on biological processes
hyperbaric pressure (HP) affected the behavior of both CaV1.2
while other suggested that the HP effect can be reversible

Summary

Introduction

HPNS Every chemical reaction contributing to the continued existence of an organism is a potential target for pressure effects on biological processes. Various mechanisms for HP effects on synaptic transmission have been suggested over the past few decades, including modulation of ionotropic receptors activity (Heinemann et al, 1987; Shelton et al, 1993), decreased action potential (AP) amplitude (Aviner et al, 2013) and slowed kinetics (Grossman and Kendig, 1986; Etzion and Grossman, 1999), generally observed depression of neurotransmitter release (Parmentier et al, 1981; Ashford et al, 1982; Gilman et al, 1987; Etzion et al, 2008), decreased vesicle fusion (Ashford et al, 1982; Heinemann et al, 1987), and the reduction of Ca2+ currents (Talpalar and Grossman, 2003; Aviner et al, 2013). Grossman and his colleagues have presented indirect (Grossman and Kendig, 1990; Grossman et al, 1991; Etzion and Grossman, 2000) and semi-direct (Aviner et al, 2013) evidence for this HP effect on voltage-dependent Ca2+ currents

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