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Journal of Neuroscience, Vol 12, 3985-3991, Copyright © 1992 by Society for Neuroscience
Noradrenergic inhibition of synaptic transmission between mitral and granule cells in mammalian olfactory bulb cultures
PQ Trombley and GM Shepherd
Section of Neurobiology, Yale University Medical School, New Haven, Connecticut 06510.
Noradrenergic modulation of the glutamatergic-GABAergic synapses between
mitral/tufted (M/T) and granule cells has been implicated in some forms of
olfactory learning (Brennan et al., 1990). Norepinephrine (NE) has been
shown to disinhibit mitral cells (Jahr and Nicoll, 1982), but its site of
action is not well defined. The effects of NE on synaptic transmission
between monosynaptically coupled pairs of mitral and granule cells have
been examined using primary culture and whole- cell recording techniques.
Intracellular stimulation of M/T cells evoked dual-component EPSPs in
granule cells consisting of both NMDA and AMPA
(alpha-amino-3-hydroxy-5-methyl-4-isoxazoleproprionic acid)
receptor-mediated mechanisms. The EPSPs were reversibly inhibited by
approximately 50% during application of 30 microM NE. NE had no effect,
however, on the membrane current evoked by exogenous application of
glutamate, indicating a presynaptic site of action. The effect of NE on
EPSPs was mimicked by the alpha-adrenergic agonist clonidine but not by the
beta-adrenergic agonist isoproterenol. NE had no significant effect on
either accommodation or macroscopic currents in either M/T or granule
cells. NE also inhibited spontaneous GABAergic IPSPs recorded in M/T cells,
by a presynaptic alpha-adrenergic-mediated mechanism. These results support
previous results suggesting a disinhibitory role for NE in the olfactory
bulb. This action, however, is at least in part mediated by a reduction in
mitral cell-mediated granule cell excitation.
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