Woodruff M L, Baisden R H, Whittington D L
Brain Res. 1986 Jul 30;379(1):10-23. doi: 10.1016/0006-8993(86)90250-7.
The effects of electrical stimulation of the A5 noradrenergic cell group of the ventrolateral pons was assessed in rabbits. Stimulation administered through either concentric bipolar or monopolar electrodes produced current-intensity related increases in mean arterial pressure (MAP). Decreases in heart rate (HR) accompanied the increases in MAP, but were essentially eliminated by bilateral vagotomy or destruction of the nucleus and tractus solitarii (NTS), thereby indicating that the HR decelerations were secondary to activation of baroreceptor reflexes. Neither vagotomy nor midcollicular section of the brainstem altered the MAP response to A5 stimulation. Bilateral destruction of the NTS slightly enhanced the response. Several rabbits received microinjections of 6-hydroxydopamine (6-OHDA) into the A5 region 2 weeks before the experiment. Other rabbits received vehicle injections and served as control subjects for the non-specific effects of the 6-OHDA injections. 6-OHDA injections, but not vehicle injections, prevented the vasopressor effects of A5 stimulation. However, stimulation of the A1 noradrenergic nucleus of the ventrolateral medulla produced decreases in MAP in rabbits given prior microinjections of 6-OHDA into A5. These observations are interpreted to indicate that the 6-OHDA injections produced neurotoxic effects which were relatively restricted to the A5 region. Furthermore, the data from all of these experiments are interpreted as indicating that the vasopressor effects observed as a consequence of electrical stimulation of A5 are due to excitation of the noradrenaline-containing neuron cell bodies of this region and that this effect is mediated via pathways arising from this region and terminating in the intermediolateral cell column of the spinal cord.
