Hot off the press! Patterning of somatosympathetic reflexes reveals non-uniform organization of presympathetic drive from C1 and non-C1 RVLM neurons

It is well known that activation of muscle afferents by contracting muscle causes an increase in blood pressure. This is known as the somatopressor reflex. The reflex is driven by the SNS, and neurons in the RVLM mediate it. Some differential patterning of responses between different sympathetic nerves has been observed before, but not thoroughly investigated. This study investigates differential sympathetic nerve responses to graded activation of the afferent arm of the sciatic nerve, a.k.a. the somatosympathetic reflex. Furthermore, the relative contributions of C1 to non-C1 neurons in this response were examined.
Briefly, anesthetized rats were instrumeted to record arterial pressure and sympathetic activity from four nerves, cervical, splanchnic, lumbar, and renal. Stimulating electrodes were implanted on the left or right sciatic nerve. They performed sciatic nerve stimulation (ScNS) at varying intensities and amplitudes in normal rats. An additional set of experiments was performed in C1 neuron-depleted rats in which only splanchnic SNA was recorded.
Under normal conditions, ScNS produced double-peak responses in all but the cervical nerve. The peaks in the lumbar and renal nerves had slightly longer latency than splanchnic and cervical. In addition, the first peak of the splanchnic nerve was of larger amplitude than the second, but the opposite was seen in renal and lumbar nerves. In rats which had about 60% depletion of C1 neurons, the second peak in splanchnic SNA was abolished, but the first peak was only slightly attenuated.
These results suggest that, indeed, different sympathetic nerves have specific roles in the SNS response to muscle contraction. Moreover, C1 and non-C1 neurons are both involved in the response, each producing distinct peaks in splanchnic SNA, possibly according to the conduction velocity of their axons (C1 fast, non-C1 slow). This study provides even more evidence that SNA to specific vascular beds may be differentially controlled. It also highlights the importance of recording from multiple versus a single sympathetic output(s) in a single animal when performing in vivo experiments.
-Nick