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This Article Full Text Full Text (PDF) All Versions of this Article: 102/2/1103    most recent 91093.2008v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Google Scholar Articles by Smith, R. S. Articles by Araneda, R. C. PubMed PubMed Citation Articles by Smith, R. S. Articles by Araneda, R. C.

Excitatory Actions of Noradrenaline and Metabotropic Glutamate Receptor Activation in Granule Cells of the Accessory Olfactory Bulb

Department of Biology, University of Maryland, College Park, Maryland

Submitted 30 September 2008; accepted in final form 21 May 2009

Modulation of dendrodendritic synapses by the noradrenergic system in the accessory olfactory bulb (AOB) plays a key role in the formation of memory in olfactory-mediated behaviors. We have recently shown that noradrenaline (NA) inhibits mitral cells by increasing -aminobutyric acid inhibitory input onto mitral cells in the AOB, suggesting an excitatory action of NA on granule cells (GCs). Here, we show that NA (10 µM) elicits a long-lasting depolarization of GCs. This effect is mediated by activation of ₁-adrenergic receptors as the depolarization is mimicked by phenylephrine (PE, 30 µM) and completely blocked by the ₁-adrenergic receptor antagonist prazosin (300 nM). In addition to this depolarization, application of NA induced the appearance of a slow afterdepolarization (sADP) following a stimulus-elicited train of action potentials. Similarly, the group I metabotropic glutamate receptor (mGluR1) agonist DHPG (10–30 µM) also produced a depolarization of GCs and the appearance of a stimulus-induced sADP. The ionic and voltage dependence and sensitivity to blockers of the sADP suggest that it is mediated by the nonselective cationic conductance I_CAN. Thus the excitatory action resulting from the activation of these receptors could be mediated by a common transduction target. Surprisingly, the excitatory effect of PE on GCs was completely blocked by the mGluR1 antagonist LY367385 (100 µM). Conversely, the effect of DHPG was not antagonized by the ₁-adrenergic receptor antagonist prazosin (300 nM). These results suggest that most of the noradrenergic effect on GCs in the AOB is mediated by potentiation of a basal activity of mGluR1s.