Evidence for cholinergic regulation of basal norepinephrine release in the rat olfactory bulb
Section snippets
Materials
Soman (pinacolyl methylphosphonofluoridate) was supplied by the U.S. Army Institute for Chemical Defense (Aberdeen Proving Ground, Maryland). Acetylcholine (ACh) hydrochloride, pilocarpine hydrochloride, desipramine hydrochloride, (−)-nicotine, monochloroacetic acid, octyl sodium sulfate, NE bitartrate and ascorbate oxidase (EC 1.10.3.3) were obtained from Sigma Chemical Co. (St Louis, MO).
Microdialysis probe implantation
Experimental procedures were conducted so as to minimize animal suffering and the number of animals used.
Basal and locus coeruleus-evoked norepinephrine levels in the olfactory bulb
The basal level of NE in the olfactory bulb of anesthetized rats recovered by in vivo microdialysis was 0.55±0.11 pg/10 μl dialysate (n=21). In the first set of experiments, we determined if extracellular NE levels were modified by stimuli known to increase transmitter release. First, NE levels were measured before, during and after local depolarization by infusing a high K+ ACSF solution through the microdialysis probe. As shown in Fig. 1A, infusion of ACSF (pH 7.4) containing 30 mM K+ for 10 min
Discussion
The major finding of this study is that ACh regulates extracellular NE levels in the olfactory bulb via actions on nicotinic and muscarinic receptors. Nicotinic and muscarinic receptors in the olfactory bulb appear to exert opposing actions, as local perfusion of the nicotinic receptor agonist nicotine increased, and the muscarinic receptor agonist pilocarpine decreased, NE levels. Local infusion of ACh or the AChE inhibitor soman increased NE levels, suggesting that the action of increased ACh
Acknowledgements
We thank Mrs Mingxin Song for technical assistance. This work was supported by U.S. Army Contract DAMD-17-95-C-5031, and PHS grants DC02588 and NS24698.
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