Gaba Fails to regulate the release of ACh at efferent-cochlear hair cell synapse in GABAB-knock out mice.

CAROLINA WEDEMEYER; JAVIER ZORRILLA DE SAN MARTÍN; ANA VANESSA TORBIDONI; PAUL A. FUCHS; ANA BELÉN ELGOYHEN; ELEONORA KATZ

Huerta Grande, Córdoba, Argentina

Congreso; Segunda Reunión Conjunta de la Sociedad Argentina de Neurociencias (SAN) y el Taller Argentino de Neurociencias (TAN); 2010

During neonatal development inner hair cells (IHCs) of the mammalian cochlea are transiently innervated by medial olivocochlear (MOC) efferent fibers. Acetylcholine (ACh) is the main neurotransmitter released at this synapse but g-aminobutiric acid (GABA) is also present at MOC synaptic terminals. We have previously shown by electrophysiological and pharmacological methods that GABA modulates the cholinergic input at MOC-IHC synapses by acting on presynaptic GABAB receptors. To further evaluate the role of GABAB receptors in the modulation of ACh release, we recorded postsynaptic currents evoked by electrically stimulating the MOC efferent fibers contacting IHCs in acutely isolated mouse organs of Corti from GABAB-knockout mice. Application of the specific GABAB agonist, baclofen (1mM), caused a significant reduction in the quantal content of evoked release in wild-type mice (37.3±6.1% of control, n=4, p < 0.01) but did not affect this parameter in GABAB-knockout mice (103.1±1.6 % of control, n=2 p > 0.05). These preliminary results show that in the absence of GABAB receptors, GABA fails to regulate the release of ACh at MOC terminals. We are now evaluating whether P/Q or N-type Ca2+ channels, that support release at this synapse, are the targets of GABAB receptor activation.