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

Ben Aviner, Gideon Gradwohl, Alice Bliznyuk, Yoram Grossman

Research output: Contribution to journalArticlepeer-review

1 Scopus citations

Abstract

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.

Original languageEnglish
Pages (from-to)1872-1888
Number of pages17
JournalJournal of Cellular and Molecular Medicine
Volume20
Issue number10
DOIs
StatePublished - 1 Oct 2016

Keywords

  • high-pressure neurological syndrome
  • hyperbaric pressure
  • voltage-dependent calcium channel

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