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Voltage-dependent calcium channel β subunit-derived peptides reduce excitatory neurotransmission and arterial blood

Haein Weon1, Jiyeon Jun2, Tae Wan Kim3

  • 1Department of Oral Physiology, School of Dentistry, Kyungpook National University, 2177, Dalgubeol-daero, Jung-gu, Daegu 41940, Republic of Korea.

Life Sciences
|November 1, 2020
PubMed
Abstract

Insights

Inhibiting voltage-dependent calcium channel (VDCC) α-β subunit interaction with peptides reduces channel activity. This interruption significantly impacts excitatory neurotransmission and arterial blood pressure, offering therapeutic insights.

Area of Science:

  • Neuroscience
  • Cardiovascular Physiology
  • Molecular Pharmacology

Background:

  • Voltage-dependent calcium channels (VDCCs) are crucial for nervous system and cardiovascular functions.
  • The β subunit modulates the α subunit, the pore-forming component of VDCCs, influencing membrane targeting and channel properties.
  • Understanding α-β subunit interactions is key to modulating VDCC activity.

Purpose of the Study:

  • To investigate the effects of inhibiting α-β subunit binding in VDCCs on channel activation and physiological functions.
  • To determine if disrupting the α-β subunit interaction impacts neurotransmission and blood pressure.

Main Methods:

  • Manufactured peptides targeting the α-β subunit interaction domain within the VDCC complex.
  • Tested peptide efficacy on voltage-activated Ca2+ currents in trigeminal ganglion neurons.
  • Assessed peptide effects on excitatory postsynaptic currents (EPSCs) in spinal dorsal horn neurons and arterial blood pressure in rats.

Main Results:

  • Intracellular peptide application reduced peak Ca2+ current amplitudes.
  • Extracellular application of TAT-fused peptides significantly decreased Ca2+ currents and EPSCs.
  • Intravenous administration of TAT-fused peptides dose-dependently lowered rat arterial blood pressure.

Conclusions:

  • Interruption of α-β subunit association in VDCCs inhibits channel activation.
  • This inhibition effectively reduces VDCC-mediated physiological functions, including excitatory neurotransmission and arterial blood pressure regulation.
Keywords:
Arterial blood pressureCa(2+) currentExcitatory postsynaptic currentSubunit interactionVoltage-dependent calcium channelβ subunit

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