PRESYNAPTIC CONTROL OF NORADRENALINE RELEASE FROM SYMPATHETIC-NERVES IN HUMAN DENTAL-PULP

Citation
Das. Parker et al., PRESYNAPTIC CONTROL OF NORADRENALINE RELEASE FROM SYMPATHETIC-NERVES IN HUMAN DENTAL-PULP, Archives of oral biology, 39(1), 1994, pp. 35-41
Citations number
30
Categorie Soggetti
Dentistry,Oral Surgery & Medicine
Journal title
ISSN journal
00039969
Volume
39
Issue
1
Year of publication
1994
Pages
35 - 41
Database
ISI
SICI code
0003-9969(1994)39:1<35:PCONRF>2.0.ZU;2-8
Abstract
This study was undertaken to determine whether release of noradrenalin e from sympathetic nerves in human dental pulp in vitro was modulated by presynaptic adrenoceptors and by dopamine receptors. Pulp was incub ated for 30 min with H-3-noradrenaline (0.6 mu mol/l) and then perfuse d continuously with Krebs solution. Field stimulation of the sympathet ic nerves at 5 Hz increased the overflow of H-3 into the perfusate thr ee-to fourfold. The stimulation-induced overflow of H-3 was abolished by tetrodotoxin (0.1 mu mol/l) and under Ca2+-free conditions, indicat ing that the increased H-3 was derived from nerves. The stimulation-in duced overflow was inhibited by noradrenaline (0.1 and 1.0 mu mol/l), the alpha(2)-adrenoceptor agonist UK14,304 (0.1 mu mol/l), dopamine (1 .0 mu mol/l) and the dopamine receptor agonist, apomorphine (1.0 mu mo l/l). When the receptor agonists were noradrenaline or dopamine, desip ramine (0.3 or 3.0 mu mol/l) was present to prevent their uptake by th e sympathetic nerves. Clonidine (1.0 mu mol/l; tested at 2 Hz as well as 5 Hz) and the alpha(1)-receptor agonist methoxamine (1.0 mu mol/l) were without effect. The alpha(2)-receptor antagonist/rauwolscine (0.1 mu mol/l) prevented the inhibitory effects of noradrenaline and UK14, 304, but had little effect on the inhibition produced by dopamine. Inh ibition of the stimulation-induced overflow by apomorphine was prevent ed by the dopamine receptor antagonist haloperidol(0.1 mu mol/l). The resting overflow of H-3 was unaffected by any of the above agents exce pt dopamine, which caused a small increase. It is concluded that the s ympathetic nerves in human dental pulp possess inhibitory presynaptic alpha(2)-adrenoceptors and dopamine receptors. As the stimulation-indu ced overflow was increased by rauwolscine, but not by haloperidol, it is suggested that the alpha(2)-adrenoceptor plays a physiological role in modulating sympathetic transmission, but this may not apply to the dopamine receptor.