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Journal of Neuroscience, Vol 12, 3992-3998, Copyright © 1992 by Society for Neuroscience
Norepinephrine inhibits calcium currents and EPSPs via a G-protein- coupled mechanism in olfactory bulb neurons
PQ Trombley
Section of Neurobiology, Yale University Medical School, New Haven, Connecticut 06510.
The most pronounced effect of norepinephrine (NE) in the olfactory bulb is
disinhibition of mitral/tufted (M/T) cells. Although it has been previously
proposed that the effects of NE are mediated by a direct inhibitory action
on granule cells, we have demonstrated that NE could exert it effects
through inhibition of excitatory synaptic transmission from M/T cells to
granule cells (Trombley and Shepherd, 1992). In order to define further the
mechanism underlying NE-mediated inhibition of synaptic transmission, the
effects of NE on calcium channel currents were examined using whole-cell
recording techniques on bulb neurons in primary culture. NE inhibited
high-threshold calcium currents at concentrations that were effective in
reducing synaptic transmission. Clonidine, but not isoproterenol, mimicked
the effects of NE on calcium currents, suggesting that the effects were
mediated through activation of presynaptic alpha-adrenergic receptors. The
effects of NE on calcium currents were irreversible in the presence of
internal GTP-gamma S and prevented by preincubation with pertussis toxin,
results that are consistent with a G-protein-coupled mechanism.
Preincubation with pertussis toxin also prevented the effects of NE on
synaptic transmission, suggesting that a similar G-protein couple mechanism
mediates both effects. Intracellular dialysis with staurosporin or calcium
buffering with EGTA did not prevent the effects of NE, suggesting that
neither protein phosphorylation nor elevated intracellular calcium were
required. These results suggest that NE may inhibit synaptic transmission
in the olfactory bulb by reducing calcium currents via a G-protein-coupled
alpha-adrenergic receptor.
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