Role of serotonergic input to the ventrolateral medulla in expression of the 10-Hz sympathetic nerve rhythm

2008 ◽  
Vol 294 (5) ◽  
pp. R1435-R1444 ◽  
Author(s):  
Hakan S. Orer ◽  
Gerard L. Gebber ◽  
Susan M. Barman
Keyword(s):  
Sympathetic Nerve ◽  
Receptor Agonist ◽  
Ventrolateral Medulla ◽  
Way 100635 ◽  
Aperiodic Component ◽  
Receptor Agonists And Antagonists ◽  
Ly 53857 ◽  
Stimulation Of ◽  
Nerve Discharge

We studied the changes in inferior cardiac sympathetic nerve discharge (SND) produced by unilateral microinjections of 5-hydroxytryptamine (5-HT) receptor agonists and antagonists into the ventrolateral medulla (VLM) of urethane-anesthetized, baroreceptor-denervated cats. Microinjection of the 5-HT2 receptor antagonist LY-53857 (10 mM) into either the rostral or caudal VLM significantly reduced ( P ≤ 0.05) the 10-Hz rhythmic component of basal SND without affecting its lower-frequency, aperiodic component. The selective depression of 10-Hz power was accompanied by a statistically significant decrease in mean arterial pressure (MAP). Microinjection of LY-53857 into the VLM also attenuated the increase in 10-Hz power that followed tetanic stimulation of depressor sites in the caudal medullary raphé nuclei. Microinjection of the 5-HT2 receptor agonist 1-(2,5-dimethoxy-4-iodophenyl)2-amino-propane (DOI; 10 μM) into the VLM selectively enhanced 10-Hz SND, and intravenous DOI (1 mg/kg) partially reversed the reduction in 10-Hz SND produced by 5-HT2 receptor blockade in the VLM. Microinjection of the 5-HT1A receptor agonist, 8-hydroxy-2-(di- n-propylamino)tetralin (8-OHDPAT; 10 mM), into either the rostral or caudal VLM also selectively attenuated 10-Hz SND and significantly reduced MAP. The reduction in 10-Hz SND produced by 8-OHDPAT was partially reversed by intravenous WAY-100635 (1 mg/kg), which selectively blocks 5-HT1A receptors. These results support the view that serotonergic inputs to the VLM play an important role in expression of the 10-Hz rhythm in SND.

Role of serotonergic neurons in the maintenance of the 10-Hz rhythm in sympathetic nerve discharge

1996 ◽  
Vol 270 (1) ◽  
pp. R174-R181 ◽  
Author(s):  
H. S. Orer ◽  
M. E. Clement ◽  
S. M. Barman ◽  
S. Zhong ◽  
G. L. Gebber ◽  
...  
Keyword(s):  
Sympathetic Nerve ◽  
Peak Frequency ◽  
Inhibitory Effects ◽  
Receptor Agonists ◽  
Naturally Occurring ◽  
Medullary Raphe ◽  
Receptor Agonists And Antagonists ◽  
Raphe Neurons ◽  
Nerve Discharge

We studied the effects of serotonin (5-HT)-receptor agonists and antagonists on the naturally occurring 10-Hz rhythm in sympathetic nerve discharge (SND) of urethan-anesthetized, baroreceptor-denervated cats. Intravenous doses of the 5-HT1A-receptor agonists 8-hydroxy-2(di-n-propylamino)-tetralin (8-OH-DPAT) and U-93385E, which inhibit the firing of serotonergic medullary raphe neurons, decreased the power in the 10-Hz band of SND without affecting the power at frequencies < or = 6 Hz. The inhibitory effects of 8-OH-DPAT and U-93385E were reversed by the 5-HT1A-receptor antagonists spiperone and WAY-100135. Microinjection of 8-OH-DPAT into medullary raphe nuclei also selectively eliminated the 10-Hz rhythm in SND. Intravenous administration of the 5-HT2-receptor antagonist methysergide blocked the 10-Hz rhythm in SND, whereas the 5-HT2-receptor agonist 1-(2,5-dimethoxy-4-iodophenyl)-2-amino-propane increased peak frequency and power in the 10-Hz band of SND. Microinjection of N-methyl-D-aspartic acid into the medullary raphe also enhanced the 10-Hz rhythm in SND. These data support the view that the naturally occurring discharges of serotonergic medullary raphe neurons preferentially enhance the 10-Hz rhythm in SND.

Role of the brain stem in generating the 2- to 6-Hz oscillation in sympathetic nerve discharge

1993 ◽  
Vol 265 (5) ◽  
pp. R1026-R1035 ◽  
Author(s):  
S. Zhong ◽  
Z. S. Huang ◽  
G. L. Gebber ◽  
S. M. Barman
Keyword(s):  
Brain Stem ◽  
Sympathetic Nerve ◽  
Cervical Spinal Cord ◽  
Ventrolateral Medulla ◽  
Population Activity ◽  
A Value ◽  
Decerebrate Cats ◽  
The Brain ◽  
Nerve Discharge

We tested the hypothesis that brain stem circuits normally generate a 2- to 6-Hz oscillation in sympathetic nerve discharge (SND). Experiments were performed on baroreceptor-denervated decerebrate cats and urethan-anesthetized rats in which renal or splanchnic SND was recorded along with field potentials (population activity) from sites in the rostral ventrolateral medulla, medullary raphe, or medullary lateral tegmental field. Our major findings were as follows. 1) Population activity recorded from the three medullary regions contained a 2- to 6-Hz oscillation. 2) The 2- to 6-Hz oscillation in population activity recorded from some medullary sites was correlated to that in SND. Peak coherence in the 2- to 6-Hz band approached a value of 1 in some cases. 3) Whereas cervical spinal cord transection abolished or markedly reduced SND, the 2- to 6-Hz oscillation in medullary activity was essentially unchanged. These results support the view that the 2- to 6-Hz oscillation in SND can be generated in the brain stem of cats and rats.

Effects of brain stem lesions on 10-Hz and 2- to 6-Hz rhythms in sympathetic nerve discharge

1992 ◽  
Vol 262 (6) ◽  
pp. R1015-R1024 ◽  
Author(s):  
S. Zhong ◽  
S. M. Barman ◽  
G. L. Gebber
Keyword(s):  
Brain Stem ◽  
Sympathetic Nerve ◽  
Sympathetic Nerves ◽  
Ventrolateral Medulla ◽  
Total Power ◽  
Field Potentials ◽  
Brain Stem Lesions ◽  
Stem Lesions ◽  
Nerve Discharge

We studied the effects of brain stem lesions or transection on the 10-Hz and 2- to 6-Hz rhythms in sympathetic nerve discharge (SND) in baroreceptor-denervated unanesthetized decerebrate cats. The results indicate that these two rhythms depend in part on different brain stem regions. The 10-Hz rhythm was eliminated by ablation of the rostral ventrolateral medulla (RVLM), medullary raphe complex, or pontine parabrachial and Kolliker-Fuse complex (PB/KF) or by pontomedullary border transection. Except for RVLM lesions, these procedures did not disrupt the 2- to 6-Hz rhythm in SND. In fact the power in SND at frequencies less than 6 Hz was increased by raphe or PB/KF lesions. Total power in SND was not significantly affected by raphe or PB/KF lesions, but mean arterial pressure was significantly reduced. Field potentials recorded from the RVLM (11 of 26 sites) and raphe (10 of 20 sites) were correlated to the 10-Hz rhythm in SND, further supporting a role of these areas in either generating or relaying this rhythm to sympathetic nerves. In contrast, field potentials recorded from the PB/KF were not correlated to the 10-Hz rhythm in SND. Thus this region may provide a tonic drive to the 10-Hz generator located elsewhere in the brain stem.

Sympathoinhibition from ventrolateral periaqueductal gray mediated by 5-HT1A receptors in the RVLM

2001 ◽  
Vol 280 (4) ◽  
pp. R976-R984 ◽  
Author(s):  
M. Bago ◽  
C. Dean
Keyword(s):  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Pressor Response ◽  
Periaqueductal Gray ◽  
Ventrolateral Medulla ◽  
Nerve Activity ◽  
Pentobarbital Sodium ◽  
Arterial Blood ◽  
Way 100635

The role of 5-hydroxytryptamine 1A (5-HT1A) receptors located in the rostral ventrolateral medulla (RVLM) in the mediation of a sympathoinhibitory and depressor response elicited from the ventrolateral periaqueductal gray (vlPAG) matter of the midbrain was examined in pentobarbital sodium-anesthetized rats. Activation of neurons in the vlPAG evoked a decrease in renal and lumbar sympathetic nerve activities and a decrease in arterial blood pressure. After microinjection of the specific 5-HT1A-receptor antagonist WAY-100635 into the pressor area of the RVLM, the vlPAG-evoked sympathoinhibition and hypotension was attenuated to control levels (7 of 15 animals) or converted into a sympathoexcitation and pressor response (8 of 15 animals). Baroreflex inhibition of sympathetic nerve activity was not impaired by microinjection of WAY into the sympathoexcitatory region of the RVLM. These data suggest that sympathoinhibition and hypotension elicited by activation of neurons in the vlPAG are mediated by 5-HT1A receptors in the RVLM.

Role of ventrolateral medulla in sympatholytic effect of 8-OHDPAT in rats

1991 ◽  
Vol 260 (3) ◽  
pp. R600-R609 ◽  
Author(s):  
A. Nosjean ◽  
P. G. Guyenet
Keyword(s):  
Adrenergic Receptors ◽  
Adrenergic Receptor ◽  
Receptor Agonist ◽  
Discharge Rate ◽  
Ventrolateral Medulla ◽  
Adrenergic Antagonists ◽  
Raphe Pallidus ◽  
Adrenergic Receptor Agonist ◽  
Nerve Discharge

In halothane-anesthetized, paralyzed, and artificially ventilated rats, the putative 5-hydroxytryptamine1A receptor agonist 8-OHDPAT (13.1 micrograms/kg iv) produced hypotension (-14.6 +/- 1.3 mmHg, n = 35), reduced lumbar sympathetic nerve discharge (SND, -17.8%, n = 35), and slowed the discharge rate of sympathoexcitatory neurons recorded in the rostroventrolateral medulla (RVLM, -17.6%, n = 20). The gain of the baroreflex was unaffected by the drug, but SND and RVLM unit discharges were silenced at significantly reduced levels of mean arterial pressure (MAP; 153 vs. 171 mmHg for SND, 155 vs. 172 mmHg for RVLM cells). Subsequent intravenous administration of the alpha 2-adrenergic receptor agonist clonidine (5.3 micrograms/kg) produced an additional decrease in MAP (-21.2 +/- 1.9 mmHg, n = 24) and SND (-24%, n = 24), Bilateral microinjections of 8-OHDPAT into the RVLM (1 nmol/side, n = 9) or into the raphe pallidus-obscurus (2 injections of 1 nmol each, n = 7) also produced hypotension (-22.9 +/- 3.2 and -14.4 +/- 2.8 mmHg, respectively) and sympathoinhibition (-39.1 and -24.6%, respectively). Bilateral microinjection into RVLM of the alpha 2-adrenergic antagonists idazoxan (16 nmol/side, n = 6) or rauwolscine (2 nmol/side, n = 6) attenuated the sympatholytic effect of both 8-OHDPAT (13.1 micrograms/kg, iv) and clonidine (5.3 micrograms/kg iv). These results suggest that 8-OHDPAT may exert a portion of its central sympatholytic effect by activating alpha 2-adrenergic receptors in the rostroventral medulla.

Medullary sympathoexcitatory neurons are inhibited by activation of the medial prefrontal cortex in the rat

1996 ◽  
Vol 270 (4) ◽  
pp. R713-R719 ◽  
Author(s):  
A. J. Verberne
Keyword(s):  
Blood Pressure ◽  
Electrical Stimulation ◽  
Prefrontal Cortex ◽  
Arterial Blood Pressure ◽  
Medial Prefrontal Cortex ◽  
Sympathetic Nerve ◽  
Ventrolateral Medulla ◽  
Arterial Blood ◽  
Stimulation Of ◽  
Nerve Discharge

Electrical stimulation of the medial prefrontal cortex (MPFC) reduces arterial blood pressure. To investigate the mechanism of this response, the effects of electrical and chemical stimulation of the MPFC on splanchnic and lumbar sympathetic nerve discharge and on the discharges of barosensitive neurons of the rostral ventrolateral medulla (RVLM) were studied in halothane-anesthetized rats. Electrical stimulation (20 Hz, 1 ms, 100 and sympathoinhibitory responses (reduced discharge of the splanchnic sympathetic nerve). Microinjection of glutamate (10 nmol/100 nl) into the MPFC also reduced arterial blood pressure and sympathetic discharge. Electrical stimulation (0.5 Hz, 1-ms pulse pairs, 3-ms interval, 150-300 microA) produced distinct patterns of splanchnic and lumbar sympathetic nerve discharge. A clear sympathoinhibitory phase with an onset latency of 146 +/- 14 ms was observed only in the case of the splanchnic sympathetic nerve activity. Electrical stimulation at depressor sites within the MPFC also inhibited the discharge of 10 of 21 RVLM barosensitive neurons tested. RVLM neurons were never excited by MPFC stimulation. These results indicate that the MPFC contains neurons that form part of a central sympathoinhibitory pathway.

GABAA and GABAC Receptors Have Contrasting Effects on Excitability in Superior Colliculus

1999 ◽  
Vol 82 (4) ◽  
pp. 2020-2023 ◽  
Author(s):  
Michael Pasternack ◽  
Mathias Boller ◽  
Belinda Pau ◽  
Matthias Schmidt
Keyword(s):  
Superior Colliculus ◽  
Receptor Agonist ◽  
Brain Slices ◽  
Superficial Layer ◽  
Field Potentials ◽  
Competitive Antagonist ◽  
Postsynaptic Potential ◽  
Late Potential ◽  
Receptor Agonists And Antagonists

We have recently found that GABAC receptor subunit transcripts are expressed in the superficial layers of rat superior colliculus (SC). In the present study we used immunocytochemistry to demonstrate the presence of GABAC receptors in rat SC at protein level. We also investigated in acute rat brain slices the effect of GABAA and GABAC receptor agonists and antagonists on stimulus-evoked extracellular field potentials in SC. Electrical stimulation of the SC optic layer induced a biphasic, early and late, potential in the adjacent superficial layer. The late component was completely inhibited by 6-cyano-7-nitroquinoxaline-2,3-dione or CoCl2, indicating that it was generated by postsynaptic activation. Muscimol, a potent GABAA and GABAC receptor agonist, strongly attenuated this postsynaptic potential at concentrations >10 μM. In contrast, the GABAC receptor agonist cis-aminocrotonic acid, as well as muscimol at lower concentrations (0.1–1 μM) increased the postsynaptic potential. This increase was blocked by (1,2,5,6-tetrahydropyridine-4-yl)methylphosphinic acid, a novel competitive antagonist of GABAC receptors. Our findings demonstrate the presence of functional GABAC receptors in SC and suggest a disinhibitory role of these receptors in SC neuronal circuitry.

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