A STUDY OF THE EFFECTS OF NORADRENALINE IN THE RAT OLFACTORY-BULB USING EVOKED FIELD POTENTIAL RESPONSE

Citation
Am. Mouly et al., A STUDY OF THE EFFECTS OF NORADRENALINE IN THE RAT OLFACTORY-BULB USING EVOKED FIELD POTENTIAL RESPONSE, Brain research, 681(1-2), 1995, pp. 47-57
Citations number
38
Categorie Soggetti
Neurosciences
Journal title
ISSN journal
00068993
Volume
681
Issue
1-2
Year of publication
1995
Pages
47 - 57
Database
ISI
SICI code
0006-8993(1995)681:1-2<47:ASOTEO>2.0.ZU;2-P
Abstract
In the rat, the main olfactory bulb receives a strong noradrenergic (N A) input from the locus coeruleus which is critical for different type s of olfactory learning. However, the resulting effect of NA modulatio n on the olfactory bulb electrical activity and its pharmacology are n ot well understood. In this study, we investigated the action of NA on the bulbar neuronal population using evoked field potentials (EFP) el icited antidromically in the olfactory bulb of anesthetized rats, by s timulation of the lateral olfactory tract (LOT). EFPs in response to s ingle and paired-pulse stimulation of the LOT were collected before, d uring and until 2 h after a 10 min perfusion of pharmacological agents through a push-pull cannula. Four concentrations of NA were tested ra nging from 10(-5) M to 10(-2) M. NA induced a reversible dose-dependen t effect. The major effect was observed at 10(-3) M. It consisted of a n increase in Component 2 amplitude (depolarization of granules cell d endrites) and a decrease in Component 3 amplitude (depolarization of g ranule cell bodies). In parallel, paired-pulse inhibition of mitral ce lls by granule cells was increased. The alpha(1) agonist phenylephrine (10(-3) M) mimicked most of the effects of NA whereas the alpha(1) an tagonist prazosin (10(-3) M) blocked its main action. Isoproterenol (b eta agonist, 10(-3) M) and clonidine (alpha(2) agonist, 10(-3) M) coul d not reproduce the effects of NA. Thus mainly through the activation of alpha(1) receptors, NA enhances synaptic activation of granule cell s and increases feed-back inhibition of mitral cells. Consequences of such effects in the context of learning and memory are discussed.