Korner P I, Head G A
J Auton Nerv Syst. 1981 Apr;3(2-4):511-23. doi: 10.1016/0165-1838(81)90084-9.
The acute and chronic effects of intracisternal (i.c.) 6-hydroxydopamine (6-OHDA) and 5,6-dihydroxytryptamine (5,6-DHT) on mean arterial pressure (MAP), heart rate, and baroreceptor-heart rate reflex properties were examined in conscious rabbits. The reflex was studied by deriving MAP-heart period (HP, pulse interval) curves. The acute effects occurring over the first few hours were due to release of transmitter (noradrenaline after 6-OHDA; serotonin after 5,6-DHT) from specific synaptic sites; the changes on day 14 were due to destruction of specific neurons. Noradrenergic bulbar neurons facilitate vagal heart rate motoneurons and serotonergic neurons have an inhibitory effect. Noradrenergic bulbospinal pathways have a depressor effect on MAP and serotonergic bulbospinal activity increases MAP. These effects on heart rate and MAP were mediated through independent parallel pathways. The acute circulatory changes due to each neurotoxin also included a long latency pressor component, which was mediated through a pathway where a serotonergic neuron was in series with a noradrenergic neuron which sends fibers to a suprapontine pressor site. There were no chronic changes in resting MAP or heart rate, but chronic changes in reflex HP range and gain were opposite to the acute effects of transmitter release. These findings indicate that noradrenergic and serotonergic neurons normally participate in the central baroreceptor-heart rate reflex pathways of the intact animal.
