Control of sympathetic vasomotor tone by catecholaminergic C1 neurons of the rostral ventrolateral medulla oblongata

Marina, Nephtali, et al. "Control of sympathetic vasomotor tone by catecholaminergic C1 neurones of the rostral ventrolateral medulla oblongata." Cardiovascular research 91.4 (2011): 703-710. Obstructive sleep apnoea is a common sleep disorder that leads to many cardiovascular dysfunctions such as hypertension, coronary artery disease, and cerebrovascular disease. Symptoms of obstructive sleep apnoea usually include an increase in pCO2 levels and a decrease in pO2 levels (hypercapnia and hypoxia respectively). Many of these cardio pathologies are believe to come from chronic occurrences of hypercapnia and hypoxia increasing levels of sympathetic tone. However, little is known about how central chemoreceptors affect catecholaminergic neurons in the rostral ventrolateral medulla that control modulation of tonic sympathetic output. In this experiment rats were transfected with a lenivirus to express a drosophila allostatin receptor so that the administration of allostatin would cause reversible inhibition of selective CNS neurons. The drosophila allostatin receptor, upon activation has the ability to open potassium channels within the expressing neuron causing hyperpolarization. After verifying the transfection was successful in C1 neurons within the RVLM, allostatin was administered and the inhibition of these neurons produced a decrease in RSNA, ABP, and HR (not seen in control animals). Following, the transfected rats were then introduced to hypercapnia and at the peak of CO2, allostatin was applied and significant reductions were again seen in RSNA, ABP, and HR. In vitro allostatin applied to transfected rats lowered perfusion pressure and reduce the amplitude of respiratory tSNA bursts. With these data the authors were able to conclude that C1 neurons located in the RVLM are important for the modulation of resting sympathetic tone. However, they do not believe that these C1 neurons play an important role in increasing sympathetic tone via the stimulation of central chemoreceptors induced by hypercapnia. They were also able to observe that blockade of chemo-sensitive projections from the RTN had no effect on resting SNA. Conclusively, increase in SNA due to hypercapnia is not modulated by C1 RVLM neurons and may either be a product of non-C1 neurons within the RVLM or C1 neurons located in other regions of the brain. ~JI