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Related Experiment Video

Updated: Dec 7, 2025

Recording Spatially Restricted Oscillations in the Hippocampus of Behaving Mice

Recording Spatially Restricted Oscillations in the Hippocampus of Behaving Mice

Published on: July 1, 2018

TRICking SOCE into altered oscillations.

Barbara A Niemeyer¹

¹Molecular Biophysics, Center of Integrative Physiology and Molecular Medicine (CIPMM), Bld 48, Saarland University, 66421, Homburg, Germany.

|September 26, 2020

Summary

This summary is machine-generated.

Defective calcium (Ca²⁺) cycling in the endoplasmic reticulum (ER) and sarcoplasmic reticulum (SR) is linked to heart and muscle issues. New research reveals novel functions of trimeric intracellular cation (TRIC) channels in maintaining ER/SR balance.

Keywords:

I(CRAC)ORAI1 RyR SOCE STIM1 TRIC-A

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Area of Science:

Cellular Biology
Cardiovascular Physiology
Muscle Physiology

Background:

Defective endoplasmic reticulum (ER) and sarcoplasmic reticulum (SR) calcium (Ca²⁺) cycling is implicated in ER stress, heart disease, and muscle disorders.
Ryanodine receptor 2 (RyR2) plays a crucial role in excitation-contraction coupling within the SR.
Trimeric intracellular cation (TRIC) channels facilitate potassium (K⁺) influx, balancing Ca²⁺ release to maintain ER/SR membrane potential.

Purpose of the Study:

To investigate the role of TRIC channels in ER/SR Ca²⁺ homeostasis.
To explore newly discovered functions of TRIC channels.
To understand the implications of TRIC channel activity in cellular function and disease.

Main Methods:

Electrophysiological recordings of TRIC channel activity.
Ca²⁺ imaging in cells expressing TRIC channels.
Genetic manipulation of TRIC channel expression.

Main Results:

TRIC channels were found to be essential for counterbalancing Ca²⁺ release from the SR.
Evidence suggests TRIC channels actively regulate ER/SR polarity.
New functional roles for TRIC channels in cellular Ca²⁺ handling were identified.

Conclusions:

TRIC channels are critical components of ER/SR Ca²⁺ cycling.
Dysfunctional TRIC channels may contribute to pathological conditions associated with Ca²⁺ dysregulation.
Further research into TRIC channels could reveal new therapeutic targets for cardiovascular and muscular diseases.