NDLI: Potentiation of barbiturate-induced alterations in presynaptic noradrenergic function in rat frontal cortex by imidazol(in)e α 2-adrenoceptor agonists

Content Provider	PubMed Central
Author	Dalley, J. W. Parker, C. A. Wülfert, E. Hudson, A. L. Nutt, D. J.
Copyright Year	1998
Abstract	In order to resolve the extent to which presynaptic noradrenergic mechanisms contribute to the anaesthetic-sparing effects of α2-adrenoceptor agonists in vivo microdialysis was used to investigate the combined effects of sodium pentobarbitone and imidazol(in)e α2-adrenoceptor agonists on extracellular levels of noradrenaline (NA) in the rat frontal cortex. Dialysate levels of NA were markedly reduced by the addition of TTX (2 μM) or by the removal of calcium in the perfusate. These data imply that dialysate NA levels are ultimately dependent on exocytotic release mechanisms from afferent coeruleo-cortical neurones. Systemic administration of sodium pentobarbitone (85 mg kg−1, i.p.) induced general anaesthesia and reduced NA levels by 92% after 30 min. The restoration of basal levels 90 min later was closely associated with a return of the corneal blink reflex. Basal NA levels in conscious animals were not affected by an intravenous infusion of equally radioactive solutions of either imidazoline (clonidine) or imidazole (mivazerol) α2-adrenoceptor agonists. The dose rate employed for each compound was 2 μg kg−1 h−1 over 2 h. The co-administration of intravenous clonidine or mivazerol, each at 2 μg kg−1 h−1 for 2 h, with sodium pentobarbitone (85 mg kg−1, i.p.), produced a marked and prolonged reduction in NA efflux. After 2 h, NA levels remained suppressed by 95% (clonidine) and 80% (mivazerol) and animals remained deeply anaesthetized. The accumulation of tritium in brain tissue was 42–73% lower across all brain regions examined after [3H]-mivazerol administration than after [3H]-clonidine administration. Sodium pentobarbitone did not alter the accumulation of tritium in brain tissue after the administration of either α2-adrenoceptor agonist. These data demonstrate that α2-adrenoceptor agonists potentiate the inhibitory effects of sodium pentobarbitone on extracellular levels of NA in the frontal cortex. Further studies will be necessary to establish a causal role of noradrenergic mechanisms in the potentiation of anaesthesia by selective α2-adrenoceptor agonists.
Related Links	http://dx.doi.org/10.1038/sj.bjp.0702091
Ending Page	446
Page Count	6
Starting Page	441
File Format	PDF
ISSN	00071188
Journal	British Journal of Pharmacology
Issue Number	3
Volume Number	125
Language	English
Publisher Date	1998-10-01
Access Restriction	Open
Subject Keyword	Pharmacology Research in Higher Education
Content Type	Text
Resource Type	Article
Subject	Pharmacology

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