Previous papers have shown that through the use of DBH-saporin, they were capable of depleting a significant number of C1 neurons within a given target area. In this paper, DBH was injected directly into RVLM and then the rats were given a period to recover and allow for the DBH to take effect. After this uptake period, the rats were exposed to several physiological conditions; particularly hypotension and glucoprivation. The authors were able to show that the C1 neurons were significantly responsible for the homeostatic response to both hypotension and glucoprivation, and drew suggestions that C1 neurons were responsible for other homeostatic responses as well. Two other important notes to make; they (once again) were able to show that basal blood pressure maintains near baseline w/ the knockout of C1 neurons and that C1 neurons must be highly depleted in order to see these results, a depletion under ~80% demonstrates similar results to control. Anyways, everyone should read this paper because I’m going to present it at journal club!
Posted by Max
This paper consists of a study quite similar to mine, however there are a few notable differences that I’m going to point out. This paper, of course, does not utilize our rat model. This paper does not keep into account the kyn+bic protocol that I have. They are recording from RSNA, not SSNA like we do. They also utilize a muscimol CVLM injection, which I don’t do. One thing that this paper does that I have is the bic+kyn protocol, which I’ve done extensively. A good judge of the success of my results is if they are at least somewhat similar to the bic+kyn results in our SED model. Another component that this paper does not have is the SNP injection and sciatic nerve stimulation that I do. I also inject gabazine+kyn, whereas this paper does not. Overall though, for a 2004 paper it really hits on the head what I’m trying to look at. This paper’s main finding is that during bic+kyn, the kyn injection attenuates (at least somewhat) the blood pressure increase following the injection of bic. Overall, I’m sure that I’ll have to cite this paper when I start writing because it is quite similar to mine and will add to the strength of my argument.
Posted by Max
This review covers all of the current knowledge about C1 neurons. C1 neurons are activated by any number of physiological conditions: hypoglycemia, infection or inflammation, hypoxia, nociception and hypotension and contribute to most glucoprivic responses. C1 cells also stimulate breathing and activate brainstem noradrenergic neurons including the locus coeruleus. C1 neurons seemed to be involved in glucose and cardiovascular homeostasis in the absence of such physical stresses and C1 cell hypersensitivity may contribute to the increases in SNA associated with diseases such as hypertension and physical inactivity. I guess it’s important to mention all of the things that C1 neurons are doing, which I don’t believe he mentions what C1 neurons are not doing: maintaining tonic sympathetic outflow to the heart. I think these C1 neurons are more involved in disease states and that non-C1 neurons are the neurons actually driving blood pressure at rest in the RVLM.
Posted by Max
Good summaries Max!! I think one think to keep in mind is that it is still fairly controversial how sympathetic activity to the heart (vs. the vasculature) is controlled. There is some extensive literature suggesting that SNS control of the heart (i.e. heart rate) may not be the entire responsibility of the RVLM and more midline structures like the raphe may be involved as well. Look forward to the journal club since that's also an interesting topic!
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