Tonic glutamate-mediated control of rostral ventrolateral medulla and sympathetic vasomotor tone.

Full cite: Ito S, Sved AF. 1997. Tonic glutamate-mediated control of rostral ventrolateral medulla and sympathetic vasomotor tone. Am J Physiol 273:R487-R494. Department of Neuroscience, University of Pittsburgh, Pennsylvania 15260, USA. This paper was one of the first that demonstrated that EAA is likely driving tonic GABAergic input by some indirect connection. It is either that EAA are driving GABAergic input, or that EAA input is only revealed following the removal of GABAergic inhibition. In this particular paper, they injected muscimol into CVLM to illicit a positive pressor response, similar to how we inject bicuculline into RVLM. In addition to this, they injected kynurenic acid into RVLM to decrease BP. It is important to note that they did not look at SNA, only BP in this paper. It believed that the BP decrease following injection of Kyn is due to the fact that glutamate is playing some kind of excitatory role only after removal of GABA. Something interesting out of this paper is that Sved suggests that the RVLM is feeding back to CVLM via some kind of interneuron. In addition to this, he suggests that the CVLM has some excitatory projections to RVLM and that they are not EAA-related. Something important to note is that they were not able to see any differences in responses due to the anesthetic used in the experiments (urethane v. chloralose). Similar to Nick’s 2012 paper, once the GABAergic input into RVLM is blocked, pressor responses to glutamate are increased, suggesting that GABA is limiting the amount of glutamate excitability under normotensive conditions. This paper is one of (if not the first) that demonstrates that injection of kyn alone has no particular effect on BP, suggesting that kyn under baseline conditions either has no effect, or that there are competing glutamatergic mechanisms that makes it seem like kyn as no effect. This paper is the primary pieces of background for my study looking at tonic glutamatergic/GABAergic input into RVLM and is one of the first that suggests that there may be some kind of interneuron activity in RVLM, whose activity is undetermined. -MTL