Oshima N, Kumagai H, Onimaru H, Kawai A, Pilowsky PM, Iigaya K, Takimoto C, Hayashi K, Saruta T, Itoh H.
Hypertens Res. 2008 Jul;31(7):1445-54
Before this paper, it was known that the rostral ventrolateral medulla (RVLM) projected to the intermediolateral cell column (IML), and it was known that changes in RVLM activity also corresponded to changes in the activity of sympathetic preganglionic neurons (SPNs) and those corresponded with postganglionic effects. Apparently nobody had been able to demonstrate that it was actually the RVLM neurons that drove the activation of SPNs through monosynaptic connections. It seems like a simple thing that should have been done early on, but after reading the paper, I can see how technically challenging it was to show that the two regions are functionally connected.
To show how the RVLM drives the sympathetic nervous system, they combined extracellular recording in the RVLM with whole cell recording of SPNs in the IML at the level of the second thoracic vertebra in a brainstem-spinal cord preparation. They verified SPNs by stimulating afferent preganglionic fiber bundles and observing induced antidromic action potentials. They experiment involved stimulating presympathetic neurons in the RVLM and also their afferent fibers in the cervical region and observing excitatory postsynaptic potentials (EPSPs) and action potentials.
Their results found 3 types of SPNs, one of which did not seem to respond to stimuli in the RVLM (which is interesting in that some area other than the RVLM must be driving them). They also found that application of antiotensin II (Ang II) to only the brainstem caused an increase in firing rate among PSNs. Through averaging 200 sweeps of paired neurons, they found that Ang II-induced spikes in the RVLM resulted in EPSPs in the SPNs with a latency similar to the known values for conduction velocity. So there you have it, the RVLM really does drive the activity of the sympathetic nervous system, and this paper shows that it is through monosynaptic connections to SPNs.
-DH
Friday, February 14, 2014
Monosynaptic excitatory connection from the rostral ventrolateral medulla to sympathetic preganglionic neurons revealed by simultaneous recordings.
Oshima N, Kumagai H, Onimaru H, Kawai A, Pilowsky PM, Iigaya K, Takimoto C, Hayashi K, Saruta T, Itoh H.
Hypertens Res. 2008 Jul;31(7):1445-54
Before this paper, it was known that the rostral ventrolateral medulla (RVLM) projected to the intermediolateral cell column (IML), and it was known that changes in RVLM activity also corresponded to changes in the activity of sympathetic preganglionic neurons (SPNs) and those corresponded with postganglionic effects. Apparently nobody had been able to demonstrate that it was actually the RVLM neurons that drove the activation of SPNs through monosynaptic connections. It seems like a simple thing that should have been done early on, but after reading the paper, I can see how technically challenging it was to show that the two regions are functionally connected.
To show how the RVLM drives the sympathetic nervous system, they combined extracellular recording in the RVLM with whole cell recording of SPNs in the IML at the level of the second thoracic vertebra in a brainstem-spinal cord preparation. They verified SPNs by stimulating afferent preganglionic fiber bundles and observing induced antidromic action potentials. They experiment involved stimulating presympathetic neurons in the RVLM and also their afferent fibers in the cervical region and observing excitatory postsynaptic potentials (EPSPs) and action potentials.
Their results found 3 types of SPNs, one of which did not seem to respond to stimuli in the RVLM (which is interesting in that some area other than the RVLM must be driving them). They also found that application of antiotensin II (Ang II) to only the brainstem caused an increase in firing rate among PSNs. Through averaging 200 sweeps of paired neurons, they found that Ang II-induced spikes in the RVLM resulted in EPSPs in the SPNs with a latency similar to the known values for conduction velocity. So there you have it, the RVLM really does drive the activity of the sympathetic nervous system, and this paper shows that it is through monosynaptic connections to SPNs.
-DH
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