scholarly journals Monosynaptic Excitatory Connection from the Rostral Ventrolateral Medulla to Sympathetic Preganglionic Neurons Revealed by Simultaneous Recordings

2008 ◽  
Vol 31 (7) ◽  
pp. 1445-1454 ◽  
Author(s):  
Naoki OSHIMA ◽  
Hiroo KUMAGAI ◽  
Hiroshi ONIMARU ◽  
Akira KAWAI ◽  
Paul M. PILOWSKY ◽  
...  
1997 ◽  
Vol 77 (1) ◽  
pp. 229-235 ◽  
Author(s):  
Susan A. Deuchars ◽  
K. Michael Spyer ◽  
Michael P. Gilbey

Deuchars, Susan A., K. Michael Spyer, and Michael P. Gilbey. Stimulation within the rostral ventrolateral medulla can evoke monosynaptic GABAergic IPSPs in sympathetic preganglionic neurons in vitro. J. Neurophysiol. 77: 229–235, 1997. The inhibitory responses of identified sympathetic preganglionic neurons (SPNs) to stimulation within the rostral ventrolateral medulla (RVLM) were studied to determine their nature and pharmacology. Whole cell patch-clamp recordings were made from 36 SPNs in the upper thoracic segments of the spinal cord in a neonatal rat brain stem-spinal cord preparation. Neurons were identified as SPNs on the basis of their antidromic activation after stimulation of the ipsilateral segmental ventral root and their morphology and location in the intermediolateral cell column and intercalated nucleus. In all SPNs, electrical stimulation of the RVLM evoked fast excitatory postsynaptic potentials (EPSPs) that were mediated by non- N-methyl-d-aspartate (NMDA) and NMDA receptors. These excitatory responses were the most prominent response in control artificial cerebrospinal fluid and have been studied previously. In 22 of the SPNs, RVLM stimulation also elicited fast inhibitory postsynaptic potentials (IPSPs), which increased in amplitude as the membrane was depolarized. Five of these neurons were not studied further as they responded occasionally with IPSPs that had highly variable onset latencies indicating the involvement of a polysynaptic pathway. In the remaining SPNs ( n = 17), the evoked IPSPs persisted in the presence of the excitatory amino acid antagonists 6-cyano-7-nitroquinoxaline-2,3,-dione and d,l-2-amino-5-phosphonopentanoic acid. In eight of these SPNs, it was necessary to block the EPSPs to reveal the IPSPs. In the 7 SPNs tested, the onset latencies of the IPSPs were not significantly different from the onset latencies of the fast EPSPs. The low sweep-to-sweep fluctuations in onset latency of individual IPSPs (absolute average deviation: 0.4 ms) indicated that the IPSPs were elicited by activation of a monosynaptic pathway. The amplitudes of the IPSPs decreased in amplitude as the membrane was hyperpolarized and reversed in polarity at −70.3 ± 1.7 mV (mean ± SD), which was close to the equilibrium potential for chloride ions. In addition, in seven SPNs, bath applications of 5 μM bicuculline, a γ-aminobuturic acid-A (GABAA) antagonist, abolished or reduced the evoked IPSPs. Five SPNs also were studied that displayed ongoing IPSPs. The amplitudes of these IPSPs increased with membrane depolarization and were blocked by bath applications of 5 μM bicuculline, suggesting that they also were mediated by activation of GABAA receptors. These results demonstrate the existence of a bulbospinal GABAergic pathway impinging directly onto SPNs. This pathway may be tonically active in the neonatal rat brain stem-spinal cord preparation.


1993 ◽  
Vol 265 (1) ◽  
pp. R82-R89 ◽  
Author(s):  
S. F. Morrison

The responses of splanchnic sympathetic preganglionic neurons (SPNs) to stimulation in raphe pallidus and in rostral ventrolateral medulla (RVLM) were compared to determine the basis for the excitatory responses evoked in the whole splanchnic preganglionic nerve bundle. Most (88%) of the SPNs with a short-latency (32 ms) excitatory response to RVLM stimulation were unaffected by raphe pallidus stimulation, although 12% were excited at a long latency (123 ms). Each of the SPNs with long-latency (114 ms) excitatory responses to RVLM stimulation was also excited by raphe pallidus stimulation at latencies (106 ms) that were 7 ms (P < 0.01) shorter than those evoked from the RVLM. Antidromic activation of raphe pallidus neurons from both the T8 intermediolateral nucleus (98 ms) and from the RVLM (18 ms) indicated that their spinally projecting axons emit collaterals (mean conduction time: 12 ms) into the ventrolateral medulla. In conclusion, the short-latency (70 ms) splanchnic nerve excitation evoked by RVLM stimulation is mediated primarily by SPNs that do not respond to raphe pallidus stimulation. Similarly, the long-latency (162 ms) splanchnic excitation evoked from the raphe pallidus is mediated primarily by SPNs that do not respond to the rapidly conducting sympathoexcitatory pathway from the RVLM. The long-latency (169 ms), RVLM stimulus-evoked excitation of the splanchnic nerve may arise from action potentials conducted on the axonal branches of raphe spinal neurons.


1991 ◽  
Vol 261 (5) ◽  
pp. R1247-R1256 ◽  
Author(s):  
S. F. Morrison ◽  
D. J. Reis

Sympathoexcitatory pathways from the rostral ventrolateral medulla (RVL) play a significant role in maintaining the tonic discharge of sympathetic preganglionic neurons (SPNs) and, in turn, resting arterial pressure. We examined the responses of antidromically identified, splanchnic SPNs to single stimuli applied to the RVL. Four characteristic response patterns were observed. Forty-five percent (group 1) of responsive SPNs were excited with latencies between 15 and 41 ms (mean 27 ms). The spontaneous activity of these SPNs (mean 3.3 Hz) was strongly modulated by the baroreceptor reflex. Twenty-three percent (group 2) of SPNs were excited with a significantly longer latency (mean 108 ms) and frequently exhibited little spontaneous discharge. Twenty-one percent (group 3) were excited at both short (mean 29 ms) and long (mean 117 ms) latencies. Eleven percent (group 4) of responsive splanchnic SPNs had a biphasic response to RVL stimulation consisting of an early inhibition followed by a late, longer lasting increase in discharge probability. Spontaneous discharge of group 4 SPNs (mean 6.2 Hz) was significantly higher than other groups and was not related to the cardiac cycle (mean arterial pressure 105 mmHg). Microinjection of kainic acid into the RVL greatly reduced the short- and long-latency splanchnic nerve excitations evoked by RVL stimulation. The heterogeneity of the RVL stimulus-evoked responses in splanchnic SPNs may reflect specificity in the descending regulation of functionally distinct subsets of SPNs regulating the various tissues in the splanchnic distribution.


2000 ◽  
Vol 279 (5) ◽  
pp. R1763-R1775 ◽  
Author(s):  
Shaun F. Morrison ◽  
Wei-Hua Cao

Brain stimulation or activation of certain reflexes can result in differential activation of the two populations of adrenal medullary chromaffin cells: those secreting either epinephrine or norepinephrine, suggesting that they are controlled by different central sympathetic networks. In urethan-chloralose-anesthetized rats, we found that antidromically identified adrenal sympathetic preganglionic neurons (SPNs) were excited by stimulation of the rostral ventrolateral medulla (RVLM) with either a short (mean: 29 ms) or a long (mean: 129 ms) latency. The latter group of adrenal SPNs were remarkably insensitive to baroreceptor reflex activation but strongly activated by the glucopenic agent 2-deoxyglucose (2-DG), indicating their role in regulation of adrenal epinephrine release. In contrast, adrenal SPNs activated by RVLM stimulation at a short latency were completely inhibited by increases in arterial pressure or stimulation of the aortic depressor nerve, were unaffected by 2-DG administration, and are presumed to govern the discharge of adrenal norepinephrine-secreting chromaffin cells. These findings of a functionally distinct preganglionic innervation of epinephrine- and norepinephrine-releasing adrenal chromaffin cells provide a foundation for identifying the different sympathetic networks underlying the differential regulation of epinephrine and norepinephrine secretion from the adrenal medulla in response to physiological challenges and experimental stimuli.


Sign in / Sign up

Export Citation Format

Share Document