scholarly journals Role of 5‐hydroxytryptamine (5‐HT2) receptors in the ventrolateral medulla (VLM) in the expression of the 10‐Hz rhythm in sympathetic nerve discharge (SND)

2008 ◽  
Vol 22 (S1) ◽  
Author(s):  
Susan M Barman ◽  
Hakan S Orer ◽  
Gerard L Gebber
1993 ◽  
Vol 265 (5) ◽  
pp. R1026-R1035 ◽  
Author(s):  
S. Zhong ◽  
Z. S. Huang ◽  
G. L. Gebber ◽  
S. M. Barman

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.


1992 ◽  
Vol 262 (6) ◽  
pp. R1015-R1024 ◽  
Author(s):  
S. Zhong ◽  
S. M. Barman ◽  
G. L. Gebber

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.


2008 ◽  
Vol 294 (5) ◽  
pp. R1435-R1444 ◽  
Author(s):  
Hakan S. Orer ◽  
Gerard L. Gebber ◽  
Susan M. Barman

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.


1996 ◽  
Vol 270 (1) ◽  
pp. R174-R181 ◽  
Author(s):  
H. S. Orer ◽  
M. E. Clement ◽  
S. M. Barman ◽  
S. Zhong ◽  
G. L. Gebber ◽  
...  

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.


1985 ◽  
Vol 54 (6) ◽  
pp. 1498-1512 ◽  
Author(s):  
G. L. Gebber ◽  
S. M. Barman

A study was made of 170 neurons of the lateral tegmental field (LTF) of the cat medulla with spontaneous activity temporally related to the 2- to 6-Hz slow wave in inferior cardiac postganglionic sympathetic nerve discharge (as demonstrated with spike-triggered averaging). LTF neurons were excited by the iontophoresis of L-glutamate, and an inflection on the rising phase of their action potentials was observed. Thus, the site of extracellular unit recording presumably was in the region of the cell body. The lag between LTF unit spike occurrence and the peak of the 2- to 6-Hz slow wave in sympathetic nerve discharge (SND) was unchanged when blood pressure and, thus, baroreceptor nerve activity were lowered to a level at which the phase relationship between the slow wave and the cardiac cycle was disrupted. Thus, the discharges of LTF neurons apparently were more closely associated with those of elements of "efferent" brain stem networks controlling SND than with those of interneurons in the afferent limb of the baroreceptor reflex arc. LTF neurons with sympathetic nerve- and cardiac-related activity were classified into three types depending on their responses to elevated carotid sinus pressure (i.e., baroreceptor reflex activation). Of the 82 neurons tested, 33 were inhibited, 16 were excited, and 33 were unaffected by baroreceptor reflex activation. Using data collected in this and previous studies from our laboratory, we compared the firing times of neurons in the LTF, rostral ventrolateral medulla, and medullary raphe nuclei relative to the peak of the sympathetic nerve slow wave. LTF neurons that were inhibited by baroreceptor reflex activation are presumed to subserve a sympathoexcitatory function. These neurons fired significantly earlier during the sympathetic nerve slow wave than their counterparts in the rostral ventrolateral medulla and medullary raphe nuclei. LTF neurons classified as sympathoinhibitory (i.e., excited by baroreceptor reflex activation) fired significantly earlier than their counterparts in the medullary raphe nuclei. These data raise the possibility that LTF neurons are closer (at least in a temporal sense) to the region of origin of the 2- to 6-Hz component of SND than are ventrolateral medullary and raphe neurons. The firing times of sympathoexcitatory and sympathoinhibitory LTF neurons were not significantly different. These data are discussed relative to potential mechanisms involved in generating SND. Microstimulation of the second thoracic spinal segment was used to determine whether the axons of LTF neurons with sympathetic nerve-related activity projected to this level.(ABSTRACT TRUNCATED AT 400 WORDS)


2006 ◽  
Vol 95 (2) ◽  
pp. 1176-1184 ◽  
Author(s):  
Gerard L. Gebber ◽  
Hakan S. Orer ◽  
Susan M. Barman

We used Allan factor analysis to classify time series of the discharges of single presympathetic neurons in the cat medullary lateral tegmental field (LTF) and rostral ventrolateral medulla (RVLM) and of the postganglionic vertebral sympathetic nerve. These time series fell into two classes of fractal-based point processes characterized by statistically self-similar behavior reflecting long-range correlations among data points. Classification of a time series as either a fractional Gaussian noise (fGn)–or fractional Brownian motion (fBm)–based point process depended on the scaling exponent, α, of the power law in the Allan factor curve. fGn is defined as 0 < α < 1 and fBm as 1 < α < 3. The process responsible for the fractal spike trains of 11 of 12 classifiable LTF neurons with sympathetic nerve-related activity was fGn. In contrast, the process responsible for the fractal spike trains of eight of nine classifiable RVLM presympathetic neurons was fBm. The time series of simultaneously recorded vertebral sympathetic nerve discharge and the arterial pulse also were fBm-based signals. Because a fBm signal is the cumulative sum of the elements comprising the corresponding fGn signal, these results show smoothing of fractal time series in a feedforward direction from medullary presympathetic neurons to postganglionic sympathetic neurons. This may involve integration by RVLM neurons of their LTF inputs or independent fractal processes acting at different levels of the network controlling sympathetic nerve discharge. Whether feedforward smoothing of fractal signals is a feature in other neural systems is open to investigation.


1994 ◽  
Vol 661 (1-2) ◽  
pp. 283-288 ◽  
Author(s):  
Hakan S. Orer ◽  
Susan M. Barman ◽  
Sheng Zhong ◽  
Gerard L. Gebber

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