Phenotypic identification of rat rostroventrolateral medullary presympathetic vasomotor neurons inhibited by exogenous cholecystokinin.

J Comp Neurol. 2003 Oct 27;465(4):467-79.
Sartor DM, Verberne AJ.
I guess I'm having a "reading Sartor and Verberne week" in honor of the assistance and advice coming from their way. And their stuff is highly related to my stuff, so I like trying to steal tips where I can. This paper sort of addressed the idea of differential control by looking at how cholecystokinin (CCK), a peptide released by the gut, can inhibit the activity of presympathetic neurons that may control splanchnic nerve activity. They examined RVLM neurons, verified them to be spinally projecting by antidromic action potentials, verified them to be presympathetic by seeing them decrease firing while they raised blood pressure via aortic occlusion, re-verified them to be presympathetic by seeing them decrease firing during i.v. administration of phenylbiguanide (PBG) aka the bezold-jarisch reflex, and then tested them with i.v. CCK to see if they would be activated or inhibited. Neurons were either inhibited, activated, or not affected by CCK administration. Conduction velocities were slow and similar between not-affected and activated groups, so these two populations were pooled in to one. In general, neurons that had slow conduction rates also had a low firing frequency. On the other hand, they also found neurons with high firing frequencies had faster conduction rates. The neurons that were inhibited by CCK fell into this group.
So far, the experiments were pretty indirect and unable to say that any particular neuron controlled the splanchnic nerve. Directly testing this would be extremely difficult and a technical nightmare... so they did the next best thing, which was to electrically stimulate the region of the periaquaductal gray which is responsible for activating RVLM neurons to cause mesenteric vasoconstriction. They found that 79% of the neurons that were inhibited by CCK were activated by PAG stimulations. Only 50% of the neurons not inhibited by CCK were activated by PAG stimulation. The conclusion from this experiment was that stimulation of the PAG was more likely to activate neurons that get inhibited by CCK than it is to activate non-CCK sensitive neurons. They also did juxtacellular labeling but did not find any correlation between phenotype and response to PAG stimulus. However, they did find that the fast-firing, fast-conducting, CCK-sensitive cells were more likely to be non-C1 (but only at 59%) Cells not inhibited by CCK were more likely to be slow firing and conducting C1 cells (79%).
What I did find very interesting is that they said in this paper that "All medullospinal (presympathetic) C1- and non-C1 neurons are inhibited by elevation of arterial blood pressure..." which is in contrast to what was said in the other paper from them that I blogged this week, which was that some presympathetic neurons are NOT barosensitve, but are sensitive to neuroglucoprivation.  However, there's about 7 years in between these two papers, with this one being the early one - so I guess that just shows that I have to keep track of publication dates and learn the timeline of discoveries. -DH