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Control of sympathetic activity by A5 noradrenergic neurons in the in situ rat preparations

Zoccal DB, Taxini CL, Gargaglioni LH (2015) Control of sympathetic activity by A5 noradrenergic neurons in the in situ rat preparations. Neuroscience 2015 Abstracts 432.16/X11. Society for Neuroscience, Chicago IL.

Summary: The A5 area represents an important noradrenergic neuronal group located in the ventral pons that receives and sends projections to various medullary areas involved in the cardiorespiratory control. Its involvement in the chemoreflex control was previously studied in anesthetized conditions. In the present study, we explored the contribution of A5 noradrenergic neurons in the processing of sympathetic responses to central and peripheral chemoreceptors stimulation using the in situ working heart-brainstem rat preparation. Juvenile male Holztman rats received bilateral microinjections of either IgG-SAP (50nl, n=7) or toxin anti-dopamine beta-hydroxylase-saporin (anti-DβH-SAP, 4.2 ng/50 nl, n=6) in the A5. One week later, in situ preparations were obtained to record the thoracic sympathetic (tSN) and phrenic nerve (PN) activities; and stimulation of peripheral (KCN, 0.05%, 50nL) and central chemoreceptors (7 and 10% CO2 in the perfusate, 5 min) were performed. Baseline tSN activity (12.5±2.0 vs 12.6±2.4 μV), PN burst amplitude (40.7±9.7 vs 44.8 ±19.9 μV) and frequency (13±1 vs 15±2 bpm) and the respiratory-sympathetic coupling pattern were similar between control and A5-lesioned rats. The sympathetic ([[unable to display character: ∆]]tSN: 110±12 vs 58±8 %, P<0.05), but not the phrenic response to peripheral chemoreflex stimulation was marked attenuated in animals with lesion of A5 noradrenergic neurons. As to the central chemoreflex, the tSN response to 7% CO2 tSN: 9.5±1.4 vs 3.9±1.7%, P<0.05), but not to 10% CO2 (16.4±2.9 vs 10.9±1.6%) was lower in A5-lesioned rats in comparison to controls. On the other hand, the PN response to 7 and 10% CO2 were similar between control and A5-lesioned rats. Our data show that the A5 noradrenergic neurons are critical for the full expression of the sympathetic chemoreflex responses, possibly by providing an excitatory drive to the neurons generating sympathetic activity.

Related Products: Anti-DBH-SAP (Cat. #IT-03), Mouse IgG-SAP (Cat. #IT-18)