The effect of complex double-axis rotation model on GABAergic neurons in caudal ventrolateral medulla of rats along the vestibulo-sympathetic reflex pathway.

INTRODUCTION: Motion sickness is a common physiological disorder induced by with unusual movement exposure, characterized by conflicting motion signals that trigger vestibulo-sympathetic reflexes (VSR). These reflexes mediate autonomic responses to motion-induced stress. Previous studies have implicated the vestibular nucleus complex and the caudal ventrolateral medulla (CVLM) in VSR modulation. GABA (γ-aminobutyric acid), the primary inhibitory neurotransmitter in the central nervous system (CNS), plays a key role in both cardiovascular regulation and vestibular function. However, the specific contribution of GABAergic structures to motion sickness-related cardiovascular responses remains unclear.

METHODS: In this study, we combined retrograde tracing and immunofluorescence labeling to investigate GABAergic pathways using complex double-axis rotation model. Fluoro-Gold (FG) was injected into the CVLM, while biotinylated dextran amine (BDA) was delivered to the medial vestibular nuclei (MVe).

RESULTS: Our results revealed a bilateral distribution of GABAergic neurons, predominantly within the caudal raphe nuclei. Notably, a subset of these neurons was activated (as indicated by Fos immunoreactivity) and projected to the CVLM (as shown by retrograde labeling with FG) under complex double-axis rotation model. Furthermore, these same neurons also received direct inputs from the MVe, as evidenced by their labeling with BDA.

DISCUSSION: Our findings offer morphological evidence that GABAergic neurons in the caudal raphe nuclei participate in the cardiovascular responses evoked by motion sickness in a complex double-axis rotation model.