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. Author manuscript; available in PMC: 2016 Mar 16.
Published in final edited form as: Compr Physiol. 2014 Oct;4(4):1511–1562. doi: 10.1002/cphy.c140004

Figure 8.

Figure 8

Sympathetic nerve activation by carotid body stimulation: lower brainstem pathways. The four experiments depicted around the interpretative schematic (A–D, clockwise from top right) suggest that, in anesthetized rodents, carotid body stimulation increases sympathetic vasomotor tone via two pathways that converge on RVLM presympathetic neurons, only one of which depends on the respiratory pattern generator. (A) Microinjection of the GABA mimetic agonist muscimol into the commissural portion of the NTS abolishes the response to cyanide [adapted, with permission, from (294)]. (B) Injection of muscimol into the rVRG eliminates the phrenic nerve discharge but does not change the sympathetic response to carotid body activation (N2, 10 s nitrogen inhalation) [adapted, with permission, from (217)]. (C) Injection of muscimol into the pre-Bötzinger complex, eliminates the phrenic nerve discharge and eliminates the respiratory oscillations of the sympathetic nerve discharge elicited by carotid body stimulation. However, the sympathoexcitation produced by carotid body stimulation persists. The response of a simultaneously recorded single RVLM presympathetic neuron is also shown. Note that muscimol produces the same effect on the neuron as on SNA, that is, muscimol changes the response from respiratory synchronous oscillations to a tonic activation [adapted, with permission, from (216)]. (D) Administration of kynurenic acid into the RVLM dramatically reduces SNA activation caused by carotid body stimulation [after (294) reprinted with permission from the Society for Neuroscience]. The respiratory dependent pathway of the chemoreflex is considered in greater detail in Fig. 3).