Role of serotonergic input to the ventrolateral medulla in expression of the 10-Hz sympathetic nerve rhythm

Full cite: Orer HS, Gebber GL, Barman SM. Role of serotonergic input to the ventrolateral medulla in expression of the 10-Hz sympathetic nerve rhythm. Am J Physiol ReguI Integr Comp Physiol 2008;294:R1435-44.

Hakan S. Orer, Gerard L. Gebber, and Susan M. Barman

Department of Pharmacology and Toxicology, Michigan State University, East Lansing, Michigan; and

Department of Pharmacology, Faculty of Medicine, Hacettepe University, Ankara, Turkey

Submitted 7 January 2008; accepted in final form 10 March 2008

A majority of Dr. Barman’s research seems to involve the study of the 10 Hz rhythm in sympathetic neurons. In this particular study she is looking at the role of serotonin in the maintenance of this rhythm. The 10 Hz rhythm is correlated to sympathetic nerve discharge (SND) which raises blood pressure and is one of the main properties examined in sympathetic tone. Dr. Barman demonstrated in a previous study that the 10 Hz rhythm was GABA-mediated, as such; the rhythm was abolished with injection of a GABA antagonist into the ventrolateral medulla. Interestingly enough, it seemed that both the rostral and caudal portions of the VLM were contributing to the 10 Hz rhythm, which seemed weird to me because the rostral and caudal VLMs have entirely different functional roles – based on what I have gathered from prior reading. The caudal medullary raphe seems to play a modulatory role in the 10 Hz rhythm presumably by serotonergic neurons to the VLM. By injecting serotonin antagonists in to VLM, they found that the 10 Hz rhythm was significantly reduced, while the lower frequency bursts were maintained. It was also demonstrated that the decrease in 10 Hz was paired with a significant fall in MAP. By stimulating the caudal raphe, they were able to demonstrate an increase in the 10 Hz rhythm and blood pressure. It would be interesting to look at the input of serotonin within our model (presuming we haven’t done it before). In addition it would be interesting to look at 5-HT2 receptors and see if they are changing following physical (in)activity. It is strange—in my opinion— that blocking serotonin in both RVLM and CVLM decreases blood pressure. Of course, this suggests that the relationship between RVLM and CVLM are EVEN more complicated that what we had originally thought, much less the implications on physical activity dependent changes. The RVLM has such complex relationships with its inputs that it seems nearly impossible to illuminate the web of communication between RVLM and other brain regions based off of the current methods at our disposal, adding any physiological state such as heart failure, hypertension, high-salt, obesity, (in)activity, makes it seemingly impossible for us to come up with any conclusive and overarching understandings about any of the more intricate functions of RVLM. - MTL