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TREK CHANNELS CONTROL EXCITABILITY IN INTRACARDIAC PARASYMPATHETIC NEURONS

Manuela Rodríguez Castañedaand 3 co-authors

CINBIO

FENS Forum 2026 (2026)

Barcelona, Spain

Board PS05-09AM-437

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Date TBA

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Board: PS05-09AM-437

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PS05-09AM-437

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Abstract

The intrinsic activity of the intracardiac nervous system is governed by cardiac pacemakers and strongly modulated by the sympathetic and parasympathetic branches of the autonomic nervous system. While the general mechanisms controlling cardiac function have been extensively studied, the electrophysiological properties and functional role of parasympathetic neurons within the intracardiac ganglia (ICG) remain poorly understood.

TREK channels, a subfamily of two-pore domain potassium (K2P) channels, play a key role in setting the resting membrane potential and regulating neuronal excitability. However, their contribution to ICG physiology is still unclear. In this study, we explored the presence and functional role of TREK channels in cultured mouse ICG neurons and examined how physiological stimuli known to activate these channels, such as increased temperature, intracellular acidification and mechanical distension, modulate neuronal behaviour.
Our results show that different physiological stimuli modulate neuronal excitability, producing membrane hyperpolarization, decreased firing activity and increased outward K⁺ currents. Altogether, these findings demonstrate that TREK channels are key regulators of ICG neuronal excitability at physiological conditions and support their role as neuroprotective channels within the cardiac parasympathetic network.

TREK CHANNELS CONTROL EXCITABILITY IN INTRACARDIAC PARASYMPATHETIC NEURONS

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