Patterning of somatosympathetic reflexes reveals nonuniform organization of presympathetic drive from C1 and non-C1 RVLM neurons

Full cite: Burke, P. G. R., Neale, J. K. W. S., and McMullan, S. G. A. K. (2011). Patterning of somatosympathetic reflexes reveals nonuniform organization of presympathetic drive from C1 and non-C1 RVLM neurons. Am. J. Physiol. 301, R1112–R1122. doi: 10.1152/ajpregu.00131.2011 Peter G. R. Burke, Jemima Neale, Willian S. Korim, Simon McMullan, and Ann K. Goodchild Australian School of Advanced Medicine, Macquarie University, Sydney, Australia Submitted 16 March 2011; accepted in final form 20 July 2011 This paper is looking at the makeup/organization of C1 and non-C1 neurons within the RVLM. The method that was used to differentiate between these two subgroups was by recording sciatic nerve responses (SN) from several different afferent inputs. These inputs were activated at graded intensities by utilizing different intensities of SN they were able to excite different nerve fiber afferents specifically: A-fiber (low intensity), and A- and C- fiber (high intensity). In addition to this, they looked at low-intensity SN stimulation, they examined cervical somatosympathetic reflex (SSR) following RVLM microinjection of somatostatin. By using intraspinal injections of anti-dopamine-β-hydroxylase-saporin (anti-DβH-SAP) they were able to selectively lesion C1 neurons. As a result of the study, they determined that use of anti-DβH-SAP abolished the activity of RVLM neurons with slow conduction velocities and sparred RVLM neurons with fast velocities. They concluded that axons projecting from C1 neurons are likely unmylenated, whereas the axons from non-C1 neurons are likely mylenated, allowing for higher conduction velocities. If there was some means by which we could selectively lyse the non-C1 neurons in the RVLM, similar to how anti-DβH-SAP removes C1 neurons, by utilizing the fact that non-C1 neurons are myelinated, then we could prove whether or not non-C1 neurons are maintaining basal sympathetic outflow. In addition to this, I believe that looking at graded action potentials while pairing with immunohistochemistry may be the means by which we will be able to figure out where the excitation of RVLM neurons is coming from. If we are able to either expose some kind of excitatory projection to RVLM neurons that are not glutamatergic via immunohistochemistry, or characterize the neurons electrochemically to another similar known group of neurons, we might be able to determine the tonic excitatory drive. - MTL