Differentiation of two cardiovascular regions within caudal ventrolateral medulla.

Cravo SL, Morrison SF, Reis DJ.
Am J Physiol. 1991 Oct;261(4 Pt 2):R985-94.

   Leading up to this paper, there had been some disagreement over the role of CVLM neurons in regulating SNA via inhibition of the RVLM. Some groups had seen barorecepter-dependent inhibition, while others had seen baroreceptor-INdependent inhibition. This paper examined the possiblity that there were 2 different subpopulations of CVLM neurons, rostral and caudal, that had different functions in regulating RVLM activity. They used kainic acid (KA) as an excitotoxic agent to inactivate subregions of the CVLM and examined what happened to splanchnic sympathetic nerve activity (SSNA) when they "activated the baroreceptor" by electrically stimulating the aortic depressor nerve (ADN).
   In control rats, baseline SSNA showed bursts tied to the pulse (frequency analysis of SSNA showed the most power at ~6Hz), and stimulation of the ADN caused inhibition of SSNA, as expected. However, after bilateral injections of KA into the rostral CVLM, they found that ADN stimulation no longer caused inhibition of SSNA and the power at 6Hz was almost completely eliminated. The arterial pressure and SSNA were both greatly increased following KA injection (after a brief decrease in both), consistent with excitotoxic lesioning of neurons that would normally inhibit the RVLM. This effect required bilateral lesioning of the rostral CVLM. Unilateral lesioning only abolished ADN-dependent inhibtion of SSNA when the ipsilateral ADN was stimulated.
   When the caudal CVLM was lesioned by KA, an increase in arterial pressure and SSNA were seen, similar to what happened when the rostral CVLM was lesioned.  However, with the caudal CVLM lesioned, stimulation of the ADN was still capable of causing an inhibition of SSNA and a drop in blood pressure. It also cause a huge increase in the relative power of the 6Hz SSNA frequency (or a huge decrease in all other frequencies, depending on how you look at it). The proposed reason for this is that with the baroreceptor-independent inhibition abolished, the increased arterial pressure caused a greater activation of baroreceptors, resulting in a greater coherence between SSNA and the frequency of the heart.  The final "trick" they did in this paper was to take the same rats that had caudal CVLM lesions, and then give them lesions in the rostral CVLM. This was then able to wipe out the effect of ADN stimulation on SSNA and arterial pressure, showing that the baroreceptor-dependent inhibition of SSNA is tied to the rostral but not the caudal CVLM. -dh