Contribution to sympathetic vasomotor tone of tonic glutamatergic inputs to neurons in the RVLM

Horiuchi J, Killinger S, Dampney RA.
Dept. of Physiology and Institute of Biomedical Research, The University of Sydney, New South Wales, Australia.  Am J Physiol Regul Integr Comp Physiol. 2004 Dec;287(6):R1335-43. Epub 2004 Jul 22.
    
        In my previous post I have discussed about Ito and Sved's paper which showed that if the CVLM is inhibited first, then blocking the glutamate receptors in the RVLM reduced the arterial pressure. The idea was that RVLM balances its glutamatergic inputs (which have direct excitatory action on the pre-sympathetic neurons) and GABAergic inputs (which have inhibitory action) resulting in no changes in arterial pressure. This idea was challenged by Dampney's group. In this article the authors tested the hypothesis that the inhibition of presympathetic neurons of the RVLM is a balancing act that occurs when excitatory amino acids (EAA) in the RVLM is involved in mediating the excitatory inputs to both the presympathetic neurons and the interneurons in the CVLM.

         In order to test this hypothesis the authors inhibited the CVLM neurons and measured the effects of EAA receptors blockade on mean arterial pressure (MAP), heart rate (HR) and renal sympathetic nerve activity (RSNA). Similar to the previous study the male SD rats were bilaterally injected with muscimol in the CVLM, which increased MAP and HR. In addition to that the authors also tested the RSNA which is also increased. Subsequently when kynurenic acid was injected in the RVLM it decreased the MAP significantly compared to vehicle injection but there were no changes in the HR and RSNA. After 50 minutes of injection all three parameters returned to the baseline level with MAP just below it and HR and RSNA above it. The results show that inhibition of tonic glutamatergic inputs to the neurons in the RVLM has minimal effect on the activity of RVLM presympathetic neurons. These results were quite contradictory to what was reported previously by Ito and Sved. 


Tonic glutamatergic drive of RVLM vasomotor neurons?
Alan F. Sved
Dept. of Neuroscience, Univ. of Pittsburgh, Pennsylvania.  Am J Physiol Regul Integr Comp Physiol 287: R1301–R1303, 2004;                                                                                                                                                                    
      
          Dr. Sved gave an editorial comment on the above article, in which he have reports that the decrease in MAP in the above study was not associated with a decrease in RSNA. He also points out a number of differences between the two studies. The anesthetic usage was different (Ito and Sved used intravenous chloralose or urethane  after induction of anesthesia with halothane, where as Horiuchi et al. used intraperitoneal urethane, which could increase the plasma osmolality and may cause an effect on the central neural vasomotor control).  The timing and speed of injections are not reported but may play a role in the difference seen between the two experiments. Most importantly the exact sites of injections, even though the center is identical, the angle of the head, pipette or design of pipette tip may produce differences.