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Using Unidirectional Rotations to Improve Vestibular System Asymmetry in Patients with Vestibular Dysfunction

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Presynaptic GABA(B) receptors decrease neurotransmitter release in vestibular nuclei neurons during vestibular

M Shao¹, R Reddaway, J C Hirsch

¹Department of Anatomy and Regenerative Biology, George Washington University School of Medicine, Washington, DC 20037, United States.

|August 9, 2012

Summary

This summary is machine-generated.

This study reveals how GABA(B) receptors on nerve terminals, not cell surfaces, aid vestibular compensation after injury. Differences in receptor function were observed between compensating and uncompensated chickens.

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Area of Science:

Neuroscience
Vestibular System Research
Receptor Pharmacology

Background:

Unilateral vestibular damage causes balance and eye movement deficits.
Vestibular compensation mechanisms are not fully understood.
GABA(B) receptor activation is implicated in recovery, but its precise action site is unknown.

Purpose of the Study:

To investigate the presynaptic and postsynaptic roles of GABA(B) receptors in vestibular nuclei neurons after unilateral vestibular ganglionectomy (UVG).
To correlate GABA(B) receptor subunit-2 (GABA(B)R2) expression with receptor function in different stages of vestibular compensation.

Main Methods:

Patch-clamp recordings were used to measure postsynaptic currents and miniature events in principal cells of the tangential nucleus in control and UVG-operated chickens.
Immunolabeling and confocal imaging identified GABA(B)R2 localization in relation to synaptic markers.
Baclofen, a GABA(B) agonist, was applied to assess receptor activity.

Main Results:

Baclofen did not induce postsynaptic currents, indicating minimal postsynaptic GABA(B) receptor activity.
Baclofen reduced miniature excitatory and inhibitory postsynaptic currents, confirming functional presynaptic GABA(B) receptors.
Changes in GABA(B)R2 expression and localization in presynaptic terminals were observed, differing between compensating and uncompensated states.

Conclusions:

Presynaptic GABA(B) receptors play a crucial role in vestibular compensation following UVG.
GABA(B) autoreceptors on vestibular nuclei neurons and GABA(B) heteroreceptors on glutamatergic terminals are involved in early compensation and recovery failure, respectively.