The amino acid taurine is abundant in the olfactory bulb (OB), exceeding glutamate and GABA in concentration. In whole-cell patch-clamp recordings in slices of rat OB, we studied the actions of taurine on the principal neurons (PNs), mitral and tufted cells, and the local interneurons, periglomerular (PG) cells. Taurine decreased, in a dose-dependent manner (EC50 = 2.2 mM), the input resistance of PNs and shifted membrane potential towards ECl. The GABAA receptor antagonists, bicuculline and picrotoxin, but not GABAB receptor antagonists, CGP 35348 and CGP 55845A, blocked the taurine effects. This implies that taurine inhibits PNs by increasing GABAA receptor Cl– conductance. PG cells, which also express GABAA receptors, were insensitive to taurine. Olfactory nerve stimulation evoked monosynaptic excitatory responses in PNs and PG cells voltage clamped at ECl or treated with picrotoxin. Taurine (5 mM) and the GABAB receptor agonist baclofen suppressed PNs responses. CGP 55845A, but not bicuculline and the postsynaptic GABAB receptor antagonist CGP 35348, abolished this suppression. The taurine action most likely was due to GABAB receptor-mediated inhibition of presynaptic glutamate release. Neither taurine nor baclofen affected PG cell responses. The results suggest that taurine reduces the excitability of PNs and their sensory input without influencing PG cells. Selective inhibitory actions of taurine in the OB may represent a physiologic mechanism protecting PNs from hyperexcitation. Supported by NIH grant DC04083 (I.K.) and Fondazione Caricento (O.B.).
Neuroinhibitory actions of taurine in the main olfactory bulb
BENEDUSI, Mascia;BELLUZZI, Ottorino
2003
Abstract
The amino acid taurine is abundant in the olfactory bulb (OB), exceeding glutamate and GABA in concentration. In whole-cell patch-clamp recordings in slices of rat OB, we studied the actions of taurine on the principal neurons (PNs), mitral and tufted cells, and the local interneurons, periglomerular (PG) cells. Taurine decreased, in a dose-dependent manner (EC50 = 2.2 mM), the input resistance of PNs and shifted membrane potential towards ECl. The GABAA receptor antagonists, bicuculline and picrotoxin, but not GABAB receptor antagonists, CGP 35348 and CGP 55845A, blocked the taurine effects. This implies that taurine inhibits PNs by increasing GABAA receptor Cl– conductance. PG cells, which also express GABAA receptors, were insensitive to taurine. Olfactory nerve stimulation evoked monosynaptic excitatory responses in PNs and PG cells voltage clamped at ECl or treated with picrotoxin. Taurine (5 mM) and the GABAB receptor agonist baclofen suppressed PNs responses. CGP 55845A, but not bicuculline and the postsynaptic GABAB receptor antagonist CGP 35348, abolished this suppression. The taurine action most likely was due to GABAB receptor-mediated inhibition of presynaptic glutamate release. Neither taurine nor baclofen affected PG cell responses. The results suggest that taurine reduces the excitability of PNs and their sensory input without influencing PG cells. Selective inhibitory actions of taurine in the OB may represent a physiologic mechanism protecting PNs from hyperexcitation. Supported by NIH grant DC04083 (I.K.) and Fondazione Caricento (O.B.).I documenti in SFERA sono protetti da copyright e tutti i diritti sono riservati, salvo diversa indicazione.
