LAUSR

Previous studies have found GABA in vestibular end organs. However, existence of GABA receptors or possible GABAergic effects on vestibular nerve afferents has not been investigated. The current study was conducted to determine whether activation of GABA-B receptors affects calyx afferent terminals in the central region of the cristae of semicircular canals. We used patch clamp recording in P13 - P18 Sprague-Dawley rats of either sex. Application of GABA-B receptor agonist baclofen inhibited voltage-sensitive potassium currents. This effect was blocked by selective GABA-B receptor antagonist CGP 35348. Application of antagonists of small (SK) and large (BK) conductance potassium channels almost completely blocked the effects of baclofen. The remaining baclofen effect was blocked by cadmium chloride, suggesting that it could be due to inhibition of voltage gated calcium channels. Furthermore, baclofen had no effect in the absence of calcium in the extracellular fluid. Inhibition of potassium currents by GABA-B activation resulted in an excitatory effect on calyx terminal action potential firing. While in the control condition calyces could only fire a single action potential during step depolarizations, in the presence of baclofen they fired continuously during steps and a few even showed repetitive discharge. We also found a decrease in threshold for action potential generation and a decrease in first spike latency during step depolarization. These results provide the first evidence for the presence of GABA-B receptors on calyx terminals, show that their activation results in an excitatory effect and that GABA inputs could be used to modulate calyx response properties.