INVESTIGADORES
PIREZ Nicolas
congresos y reuniones científicas
Título:
Modulation of odorant representations by feedback versus lateral presynaptic inhibition of receptor neuron input to the olfactory bulb
Autor/es:
MCGANN, J.P.; PÍREZ, N.; MURATORE, C.; ELIAS, A.S.; GAINEY, M.A.; WACHOWIAK, M.
Lugar:
Washington DC, Estados Unidos
Reunión:
Conferencia; Reunion Anual de Society for Neuroscience; 2005
Institución organizadora:
Society for Neuroscience
Resumen:
In the mammalian olfactory bulb, homotypic olfactory receptor neurons (ORNs) converge onto individual glomeruli. ORN input to a glomerulus can be modualed by presynaptic inhibition mediated, at least in part, by GABAB receptors. We investigated the functional organization of this presynaptic inhibition using optical imaging with synaptopHluorin, a genetically encoded indicator of transmitter release from ORNs, in mouse olfactory bulb slices and in vivo. In slices, single olfactory nerve shocks strongly supressed subsequent transmitter release for up to several seconds. Stimulation of one axon bundle innervating a glomerulus could suppress release from other axons in the same glomerulus. This intraglomerular feedback inhibition was long-lasting and reduced by glutamate receptor blockers and by GABAB antagonists. We also found GABAB-mediated lateral inhibition of transmitter release between neighboring glomeruli in slices, but this inhibition was sparse and was much weaker than feedback inhibition. We asked how these different forms of presynaptic inhibition modulate odorant representations in vivo. Co-activation of neighboring glomeruli with odorant mixtures did not suppress odorant responses relative to the corresponding single-odorant presentations, suggesting that lateral inhibition of ORN input plays little or no role in vivo. However, blocking GABAB receptors in vivo greatly increased the amplitude of odorant-evoked input to a glomerulus. GABAB receptor blockade did not change the spatial map of activated glomeruli. We conclude that intraglomerular inhibition of transmitter release from ORNs strongly modulates the magnitude of sensory input to the bulb, but that lateral presynaptic inhibition plays a relatively small role.