Attenuated baroreflex control of sympathetic nerve activity in obese Zucker rats by central mechanisms

Full cite: Huber DA & Schreihofer AM (2010). Attenuated baroreflex control of sympathetic nerve activity in obese Zucker rats by central mechanisms. J Physiol 588, 1515–1525.

Attenuated baroreflex control of sympathetic nerve activity in obese Zucker rats by central mechanisms

Domitila A. Huber and Ann M. Schreihofer

Department of Physiology, Medical College of Georgia, Augusta, GA, USA

This study is looking at how reflex control of the vasculature is affected by obesity; the main technique they are using in this paper is electrophysiology. It is widely known that obesity is a risk factor for the development of hypertension, in addition to this; obesity has been shown to be an independent contributor to the elevation of sympathetic nerve activity (SNA). The goal of this paper is to illuminate how obesity alters sympathoregulation, in an attempt to tie the condition to other disease states. The main component of sympathetic control examined is the sympathetic baroreflex responses, with an attempt to see if it is altered due to altered sensory or central mechanisms. It has been a long while since I’ve read a Zucker rat paper, adult obese Zucker rats (OZRs) vs. lean Zucker rats (LZRs) were the rats used in this study. The OZRs weighed about 600g and the LZRs weighed about 400g on average. The OZRs had significantly higher resting sympathetic nerve activities and blood press, interestingly enough they did not have significantly different heart rate. Stimulation of the aortic depressor nerve (ADN) elicited blunted responses in the OZRs, whereas the net responses in the LZRs were significantly greater. This result suggests that OZRs are less sensitive to stimulation of the ADN. In addition, stimulation of the vagal afferent nerve brought about significantly greater responses in the LZR when compared to the OZR. These results suggest that the vagal afferents have inherently less sensitive in the OZR rats. This reduction in baroreflex sensitivity in the OZRs may contribute to the likelihood of cardiovascular diseases in overweight individuals. -MTL

Tonic glutamatergic input in the rostral ventrolateral medulla is increased in rats with chronic heart failure

Full cite: Wang WZ, Gao L, Wang HJ, Zucker IH, Wang W. 2009. Tonic glutamatergic input in the rostral ventrolateral medulla is increased in rats with chronic heart failure. Hypertension 53:370–374.

Wang WZ, Gao L, Wang HJ, Zucker IH, Wang W.

Department of Cellular and Integrative Physiology (W.-Z.W., L.G., H.-J.W., I.H.Z., W.W.), University of Nebraska Medical Center, Omaha; and the Department of Physiology (W.-Z.W.), Second Military Medical University, Shanghai, China.

The headline of this paper essentially sums up the message of this paper; chronic heart failure animals have heightened glutamatergic tone. While the finding of this paper is pretty straightforward, what I thought was particularly cool was how they used triple barrel pipettes and paired it when electrophysiology. They used kynurenic acid, an NMDA/non-NMDA receptor antagonist, non-NMDA antagonist 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX), and NMDA antagonist D-2-amino-5-phosphonopentanoate (D-AP5) to block glutamate reception and recorded the responses via single-unit electrophysiology. In addition to the triple barrel pipette they used, they had a 5-barrel micropipette containing an electrode. Using a penta barrel pipette sounds like a huge technical difficulty, that being said, if we could get some way for it to work, we could easily test the responsiveness of neurons to various direct stimuli, something we’ve never done before. With a 5-barrel micropipette, it might actually be possible to record in one piece of the pipette, have neurobiotin in another, and maybe some kind of antagonists, say bicuculline, xanthurenic acid, and kynurenic acid. I could imagine that it would be really difficult to ensure that the pipette is successfully able to inject out of each portion, but the ability to sit on a neuron and inject a slew of drugs would be incredibly powerful. It would be cool to do a similar study in runners & seds in order to get some definitive proof onto the tonic input of glutamate in seds. I believe though, we would likely see a prevalence of glutamatergic tone in the sedentary animals; it just would not be as distinct as that of the heart failure animals. -MTL