ANALYSIS OF BRAIN-STEM A1 AND A2 NORADRENERGIC INPUTS TO THE PREOPTICAREA USING MICRODIALYSIS IN THE RAT

Citation
C. Fernandezgalaz et al., ANALYSIS OF BRAIN-STEM A1 AND A2 NORADRENERGIC INPUTS TO THE PREOPTICAREA USING MICRODIALYSIS IN THE RAT, Brain research, 636(2), 1994, pp. 227-232
Citations number
27
Categorie Soggetti
Neurosciences
Journal title
ISSN journal
00068993
Volume
636
Issue
2
Year of publication
1994
Pages
227 - 232
Database
ISI
SICI code
0006-8993(1994)636:2<227:AOBAAA>2.0.ZU;2-N
Abstract
Noradrenergic inputs to the preoptic area (POA) are involved in regula ting a variety of homeostatic functions. However, the accurate measure ment of endogenous noradrenaline (NA) release in the POA has been diff icult to achieve and consequently little has been done to characterise the different noradrenergic pathways. By combining the technique of i ntracranial microdialysis with tissue pre-loading of [H-3]NA we have d eveloped a sensitive index of NA release in the POA [8]. Using this me thod we have now examined and compared the effects of electrical stimu lation of the brainstem A1 and A2 cell groups on NA release in the POA . Anaesthetised proestrus rats were implanted with microdialysis probe s either unilaterally or bilaterally in the POA and stimulating electr odes positioned in either the A1 or A2 regions. Electrical stimulation (10 Hz, 10s on/off for 20 min) of the A1 region resulted in repeatabl e, calcium-dependent increases in radioactivity outflow from the ipsil ateral POA (P < 0.01). A1-evoked release was twice as large as that ob served after equivalent 10 Hz electrical stimulation of the A2 region (P < 0.05). In experiments using bilateral POA microdialysis and A1 st imulation, a significant increase in release from the contralateral PO A, amounting to approximately 80% of that observed in the ipsilateral POA, was observed. Experiments involving the blockade of A1-stimulated release in the ipsilateral POA by perfusion with a calcium-free mediu m demonstrated that increases in radioactivity measured in the contral ateral POA were not originating from the ipsilateral POA. These result s provide a functional evaluation of the A1 and A2 noradrenergic input s to the POA and provide evidence that (i) electrical activation of th e A2 cell group increases NA release in the POA, although stimulated r elease is less than that resulting from equivalent A1 stimulation, and that (ii) stimulation of the A1 group alters NA release bilaterally i n the POA.