Vestibular Testing-New Physiological Results for the Optimization of Clinical VEMP Stimuli

by Selleckchem | Feb 12 2024

Both auditory and vestibular primary afferent neurons can be activated by sound and vibration. This review relates the differences between them to the different receptor/synaptic mechanisms of the two systems, as shown by indicators of peripheral function-cochlear and vestibular compound action potentials (cCAPs and vCAPs)-to click stimulation as recorded in animal studies. Sound- and vibration-sensitive type 1 receptors at the striola of the utricular macula are enveloped by the unique calyx afferent ending, which has three modes of synaptic transmission. Glutamate is the transmitter for both cochlear and vestibular primary afferents; however, blocking glutamate transmission has very little effect on vCAPs but greatly reduces cCAPs. We suggest that the ultrafast non-quantal synaptic mechanism called resistive coupling is the cause of the short latency vestibular afferent responses and related results-failure of transmitter blockade, masking, and temporal precision. This "ultrafast" non-quantal transmission is effectively electrical coupling that is dependent on the membrane potentials of the calyx and the type 1 receptor. The major clinical implication is that decreasing stimulus rise time increases vCAP response, corresponding to the increased VEMP response in human subjects. Short rise times are optimal in human clinical VEMP testing, whereas long rise times are mandatory for audiometric threshold testing.

Comments:

This review seems to delve deep into the intricate mechanisms of auditory and vestibular primary afferent neurons, particularly in relation to their response to sound and vibration. It's fascinating how the differences between these systems can be tied to receptor/synaptic mechanisms, as evidenced by indicators of peripheral function in animal studies.

The identification of unique calyx afferent endings enveloping sound- and vibration-sensitive type 1 receptors at the striola of the utricular macula is intriguing. The three modes of synaptic transmission associated with these calyx afferent endings further highlight the complexity of these neural pathways.

The observation that glutamate serves as the transmitter for both cochlear and vestibular primary afferents, yet exhibits differential effects when its transmission is blocked, is quite thought-provoking. The minimal impact on vCAPs compared to the significant reduction in cCAPs suggests a nuanced difference in the underlying mechanisms of these systems.

The proposal of an "ultrafast" non-quantal synaptic mechanism, referred to as resistive coupling, as the cause of short latency vestibular afferent responses is an interesting hypothesis. This mechanism, akin to electrical coupling, appears to be intricately linked to the membrane potentials of the calyx and the type 1 receptor, contributing to the rapid response and temporal precision observed in vestibular afferent reactions.

The clinical implications discussed, such as the effect of stimulus rise time on vCAP response and its correspondence to increased VEMP (vestibular-evoked myogenic potential) response in human subjects, underscore the relevance of these findings in diagnostic testing and potentially in understanding and treating vestibular disorders.

It's intriguing how varying stimulus rise times impact responses differently in clinical testing for VEMPs and audiometric threshold testing, emphasizing the need for a nuanced approach based on the system being evaluated.

The depth of this review sheds light on the intricate interplay of neural mechanisms in auditory and vestibular systems and their potential implications for both fundamental understanding and clinical applications.