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Department of Pharmacology and Toxicology, Michigan State University, East Lansing, Michigan 48824-1317
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ABSTRACT |
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 TOP
 ABSTRACT
 INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
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Frequency- and time-domain analyses were used to compare the effects of stimulation of the defense region of the midbrain periaqueductal gray (PAG) on the 10-Hz and cardiac-related discharges of sympathetic nerves with different cardiovascular targets. In baroreceptor-denervated cats anesthetized with urethan, PAG stimulation at frequencies equal to or higher (up to 25 Hz) than that of the free-running 10-Hz rhythm produced an immediate and sustained decrease in vertebral sympathetic nerve (VN) 10-Hz activity but increased the 10-Hz discharges of the inferior cardiac (CN) and renal (RN) nerves. In baroreceptor-innervated cats, VN cardiac-related activity was initially unchanged by high-frequency (25-Hz) PAG stimulation, or it increased along with that in the CN and RN. Later, during high-frequency PAG stimulation, when the rise in blood pressure approached its peak, VN cardiac-related activity usually was reduced below control level. At this time, the increases in CN and RN cardiac-related discharges were largely sustained. The cardiac-related discharges of the three nerves were unaffected by PAG stimulation at frequencies just below or just above that of the heartbeat. We conclude that the defenselike pattern of spinal sympathetic outflow involving the 10-Hz rhythm is different in mechanism and character from that involving the cardiac-related rhythm.
baroreceptor reflex; coupled oscillators; midbrain periaqueductal gray; sympathetic nerve discharge
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INTRODUCTION |
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TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
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WE HAVE OFFERED A NOVEL HYPOTHESIS on the mechanisms involved in formulating differential patterns of spinal sympathetic outflow in the baroreceptor-denervated cat that include reciprocal changes in the 10-Hz discharges of postganglionic nerves with different cardiovascular targets (15). Rather than viewing such patterns as arising from the activation of point-to-point hard-wired connections that excite some cell groups and inhibit others, our hypothesis is based on the principles of nonlinear dynamics and self-organization within large-scale neural networks. Specifically, we proposed that the reciprocal changes in spinal sympathetic outflow to the heart and forelimb vasculature induced by electrical activation of the defense region of the midbrain periaqueductal gray (PAG) arise as the consequence of reorganization of the coupling of multiple brain stem oscillators that generate a 10-Hz rhythm (14, 18). We found that the increase in the 10-Hz discharges of the inferior cardiac nerve (CN) and decrease in vertebral nerve (VN) 10-Hz activity produced by PAG stimulation were accompanied by lengthening of the phase lag of VN activity relative to CN activity. The change in phase angle was presumed to reflect reorganization of the coupling of the oscillators controlling the CN and VN, which innervate the heart and forelimb vasculature, respectively (20). The reciprocal changes in CN and VN 10-Hz activities and lengthening of the CN-VN phase angle were observed during high-frequency (25-Hz) PAG activation or when the rhythm was entrained 1:1 to frequencies of PAG stimulation equal to or just above that of the free-running rhythm. The magnitude of the change in CN-VN phase angle was directly related to the extent to which PAG activation reciprocally affected the 10-Hz discharges of the two nerves. The view that changes in the phase relations among coupled brain stem oscillators lead to differential changes in the 10-Hz discharges of sympathetic nerves with different targets was supported by the responses to lower frequencies of PAG stimulation. Quite remarkably, VN 10-Hz activity increased, rather than decreased, when the frequency of stimulation was reduced to just below that of the free-running rhythm. In cases when CN and VN 10-Hz discharges were uniformly increased by the lower frequencies of PAG activation, there was no change in the CN-VN phase angle. These results suggest that changes in the frequency of PAG stimulation lead a system of coupled brain stem 10-Hz oscillators with different peripheral targets through a repertoire of self-organized states, each of which is characterized by a different set of phase relations and, thus, a different pattern of spinal sympathetic outflow (15).
The primary goal of the present study was to compare the changes produced by PAG stimulation on the cardiac-related and 10-Hz discharges of sympathetic nerves with different targets. Because the cardiac-related and 10-Hz rhythms in sympathetic nerve discharge (SND) are generated independently by different groups of brain stem neurons (1, 4), we determined whether the pattern of spinal sympathetic outflow produced by activation of the defense region of the PAG is dependent on the preexisting rhythm in SND. This was shown to be the case. The results support the view that the mechanisms responsible for the patterns of spinal sympathetic outflow involving the 10-Hz and cardiac-related rhythms are different.
A second goal was to test the hypothesis (15) that the reciprocal changes in sympathetic outflow to the heart (CN) and forelimb vasculature (VN) induced by PAG stimulation represent an electrophysiological correlate of the defense reaction. Because sympathetic vasoconstrictor outflow to the kidney is increased during the defense reaction (17), we predicted that the 10-Hz discharges of the renal sympathetic nerve (RN) would be increased during the reciprocal changes in CN and VN activities induced by PAG stimulation. This was found to be the case.
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METHODS |
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TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
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Experimental animals and general procedures. The protocols used in the experiments on adult cats (2.2-3.8 kg) of either gender were approved by the All-University Committee on Animal Use and Care of Michigan State University. The cats were initially anesthetized with 2.5% isoflurane mixed with 100% oxygen. Urethan (1.2-1.8 g/kg iv) was then administered, and isoflurane inhalation was terminated. This dose range of urethan maintains a surgical level of anesthesia for a period (8-10 h) that exceeded the duration of our experiments (12).
Blood pressure was measured from a catheter inserted into the abdominal aorta via a femoral artery. In baroreceptor-innervated cats, an intravenous infusion of norepinephrine bitartrate (1-3 µg/min) in dextran (6% in saline) was used, when necessary, to maintain resting mean blood pressure at >100 mmHg. SND contained a strong cardiac-related rhythm under these conditions. Spontaneous respiration during urethan anesthesia was eupneic with end-tidal CO2 (Traverse Medial Monitors capnometer model 2200) in the normocapnic range. Subsequently, the animal was paralyzed with gallamine triethiodide (4 mg/kg iv initial dose) and artificially ventilated with room air, and a bilateral pneumothoracotomy was performed. End-tidal CO2 was kept between 4.0 and 4.5% by adjusting the parameters of artificial ventilation; rectal temperature was maintained near 38°C with a heat lamp. Baroreceptor denervation was performed by bilateral section of the carotid sinus, aortic depressor, and vagus nerves (3). The cardiac-related rhythm in SND was replaced by a variable mixture of the 10-Hz rhythm and irregular oscillations at frequencies
6 Hz after section of these nerves. Baroreceptor denervation eliminated the inhibition of SND induced by raising blood
pressure with a bolus injection of norepinephrine bitartrate (2 µg/kg iv).
Neural recordings and central stimulation. By using the methods described by Gebber et al. (14), potentials were recorded monophasically with bipolar platinum electrodes from the central ends of the cut left CN, VN, and RN. These nerves project to the heart and vasculature of the forelimb and kidney, respectively. Nerve recordings initially were made with the band pass of the preamplifiers (model 7P3, Grass) set at 1-1,000 Hz so that bursts of multiunit spikes appeared as slow waves (3, 8). The data were stored on magnetic tape and hard drive for off-line analysis.
After removal of medial portions of the occipital bone and cerebellum, bipolar stainless steel electrodes (model SNE-100, Rhodes) mounted on a DKI stereotaxic instrument were positioned into the PAG at a level caudal to the bony tentorium, with the inferior colliculi and cerebral aqueduct used as landmarks. A Grass S8800 quartz-timed digital stimulator and PSIU 6 constant-current unit were used to deliver 1-ms square-wave pulses of variable intensity and frequency through the electrodes that had 0.25-mm tip exposures separated by 0.75 mm. The histological methods used to identify sites of stimulation are described in an earlier report from this laboratory (15). Relative to the stereotaxic coordinates of Snider and Niemer (21), the sites of stimulation were P1-P2, L1-L2 (left), and H+3-H0. These sites are contained in the defense region of the caudal PAG, as defined by Carrive (6, 7).Data analysis. The frequency- and time-domain methods of analysis have been described previously (15). Briefly, spectral analysis was performed by fast Fourier transform (FFT) with use of a modified version (14) of the programs written by Cohen et al. (9) and Koscis et al. (20). FFT was performed after SND had been low-pass filtered at 50 Hz. The sampling rate of 200 Hz yielded a resolution of 0.2 Hz/bin. The resultant spectra usually were averages of 32 5-s data windows with 50% overlap for 80-s data blocks and 75% overlap for 40-s data blocks. In some instances, however, autospectra for consecutive 5-s data samples were displayed in an array (i.e., "waterfall"). FFT yielded autospectra of SND and the arterial pulse (AP). In addition, coherence functions (i.e., normalized cross spectra) and phase spectra relating pairs of signals were calculated from the same windows. The autospectrum of a signal shows how much power (voltage squared) is present at each frequency. The coherence function measures the strength of linear correlation (scale 0-1.0) of pairs of signals as a function of frequency. The phase spectrum provides a measure of the timing of the second signal in the pair relative to that of the first (scale ±180°). Although FFT was performed over a band of 0-100 Hz, the spectra are displayed on a scale of 0-20 Hz or 0-10 Hz to focus attention on the 10-Hz and cardiac-related rhythms in SND. The 0- to 20-Hz band contains >90% of the total power in SND (3).
A macro written in Microsoft Excel version 7.0 was used to measure power above background activity in the 10-Hz and cardiac-related bands of SND. A line was fitted to connect the left and right limits of the sharp peak near 10 Hz or at the frequency of the heartbeat in the autospectrum of SND. Power in these bands was calculated as the area above the line. Changes in power produced by PAG stimulation are expressed as a percentage of control. The Student's t-test (paired comparison) was used to test for significant changes (P 0.05) in power of SND, coherence values (after
z-transformation), and phase angles. Values are means ± SE.
Time-series analysis was performed using software written by Lewis and
used by Gebber et al. (15). The program was used to make cycle-by-cycle
measurements of peak systolic blood pressure (mmHg), peak-to-trough
sympathetic nerve slow-wave amplitude (normalized on a scale of
0-1.0), and phase angle (scale 0-360°) between pairs of
signals. Before these analyses, SND was digitally band-pass filtered
without phase distortion to extract the 10-Hz or cardiac-related band
of activity. The software for the digital filter (symmetrical, nonrecursive type with a Lanczos smoothing function) was obtained from
RC Electronics (Santa Barbara, CA). The width of the band pass was 4 Hz, with the center frequency matched to that of the sharp peak in the
autospectrum derived from the original recordings (low-pass filtered at
50 Hz). Power in the designated band pass was reduced by 10%, and
the digital filter had a roll-off slope of 39%/Hz outside the band
pass. The slow waves in SND extracted by digital filtering are smoother
and more sinusoid-like than the originals (see Fig. 1 in Ref. 15), thus
aiding in the accurate detection of peaks and troughs. Cycle-by-cycle
measurements of phase angle were derived from the interval between the
peaks of corresponding slow waves in two nerves (15). The resolution of
measurement of the phase angle for slow waves with a period of 333 ms
(heart rate, 3 Hz) was 5.4°/bin, and that for slow waves with a
period of 100 ms (10-Hz rhythm) was 7.2°/bin. The sampling period
(bin width) was 5 ms in the former case and 2 ms in the latter case.
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RESULTS |
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TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
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Effects of caudal PAG stimulation on 10-Hz SND in
baroreceptor-denervated cats.
Figure 1 shows typical responses of the CN,
VN, and RN produced by electrical activation of the caudal PAG in
baroreceptor-denervated cats. Figure 1 shows the original records
(low-pass filtered at 50 Hz) of SND from three different cats. PAG
stimulation at frequencies equal to or higher than that of the
free-running rhythm almost immediately increased the amplitudes of the
10-Hz slow waves in CN and RN discharges but decreased VN slow-wave
amplitude. In Fig. 1A, the frequency of PAG stimulation was
equal to that (8 Hz) of the free-running rhythm in SND. The vertical
line running through the records of CN, VN, and RN discharges marks the
first stimulus. Although only the first 4 s of PAG activation are
shown, such responses were sustained throughout the 40-s period of
stimulation (see Figs. 3 and 10 in Ref. 15). The example in Fig.
1B shows the effects produced by high-frequency (25-Hz) PAG
stimulation. As was the case for stimulus frequencies equal to or
slightly higher than that of the free-running rhythm, the 10-Hz
discharges of the VN were decreased whereas the 10-Hz discharges of the
other nerves were increased. High-frequency PAG stimulation did not change the frequency of the free-running rhythm, which was 9.6 Hz in
the case shown in Fig. 1B. In contrast to the patterns elicited by PAG stimulation at frequencies equal to or higher than that of the
free-running rhythm, frequencies of stimulation 0.5-2.0 Hz lower
than that of the free-running rhythm increased the 10-Hz discharges of
all three postganglionic nerves. In the example shown in Fig.
1C, the frequency of the free-running rhythm was 9.2 Hz and the
PAG stimulus frequency was 8.2 Hz.
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6 Hz was not
significantly affected by PAG stimulation. The superposed coherence
functions in Fig. 3B show that the strength of linear correlation of the 10-Hz discharges of the nerve pairs (CN-VN, CN-RN,
and VN-RN) was not markedly affected during PAG stimulation. Peak
coherence values in the 10-Hz band were >0.8 in all cases. A
coherence value 
0.1 reflects a statistically significant correlation when 32 data windows are averaged (5). Although there was little change
in coherence values, PAG stimulation markedly affected the phase angles
relating the 10-Hz discharges of the CN-VN and VN-RN pairs. As shown in
Fig. 3C, top, the CN-VN phase angle at the frequency of
peak coherence in the 10-Hz band was changed from 
93° in
control (trace 1) to +106° during PAG stimulation (trace 2). In trace 2 there is an abrupt shift in the
phase angle to more negative values as the band of coherent 10-Hz
activity is entered, and the downward shift continues after the
crossover to positive values. We interpret the downward shift as
indicating that the phase lag of VN 10-Hz activity relative to CN
activity was increased during PAG stimulation from 93° to 254°
(i.e., the difference between 360° and the reading of +106° in
the phase spectrum at the frequency of peak coherence in the 10-Hz
band).
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31° in
control (trace 1) to +100° during PAG stimulation
(trace 2). The shift in phase angle (trace 2) is in the
upward direction crossing 0° from negative to positive values. We
interpret the upward shift as indicating that RN 10-Hz activity lagged
VN activity by 31° in control and led VN activity by 100°
during PAG stimulation. PAG stimulation had little effect on the CN-RN
phase angle (10-Hz band) in this experiment (Fig. 3C, middle).
Tables 1 and 2 summarize the changes
produced by PAG stimulation in 28 cases (21 baroreceptor-denervated
cats) in which CN and RN 10-Hz activities were increased and VN 10-Hz
activity was decreased. The frequency of PAG stimulation was equal to
or just above that of the free-running rhythm in 19 cases and at 25 Hz
in the other 9 cases. The increases in CN and RN 10-Hz band power and
the decrease in VN 10-Hz band power produced by PAG stimulation were
statistically significant (Table 1). The peak coherence values relating
VN 10-Hz activity to CN and RN 10-Hz discharges were significantly
reduced, albeit modestly, during PAG stimulation (Table 2). The
coherence value relating the 10-Hz discharges of the CN and RN was not
changed. PAG stimulation significantly increased the phase lags of VN
and RN 10-Hz discharges relative to CN 10-Hz activity (Table 2). On the
average, RN 10-Hz activity lagged VN 10-Hz activity in control but led
VN activity during PAG stimulation. This change was also statistically
significant and can be accounted for by the fact that the increase in
the CN-VN phase angle was greater than that of the CN-RN phase angle. Corresponding changes in intervals (ms), derived from the phase angles,
are included in Table 2.
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Effects of caudal PAG stimulation on cardiac-related SND in
baroreceptor-innervated cats.
In place of the 10-Hz rhythm, SND contains a strong cardiac-related
rhythm in baroreceptor-innervated cats anesthetized with urethan (2).
That is, bursts of SND are locked in a 1:1 relationship to the cardiac
cycle. Under this condition, we monitored the changes in left CN, VN,
and RN discharges produced by PAG stimulation. Unlike the situation for
the 10-Hz rhythm, high-frequency (25-Hz) PAG stimulation did not
produce an immediate and sustained decrease in VN cardiac-related
activity (16 episodes in 10 cats). Rather, during the first 15-20
s of stimulation, cardiac-related slow waves in the VN were essentially
unchanged, or they were increased in amplitude along with those in the
CN and RN. An example is shown in Fig. 4.
High-frequency PAG stimulation was begun at the vertical line, and the
responses of the CN, VN, and RN during the first 15 s of stimulation
are shown. After a brief period of reduced activity in all three
nerves, the cardiac-related rhythm again became predominant. The
amplitudes of the cardiac-related slow waves in CN and VN discharges
were not much changed from control at this time, whereas the amplitude
of the slow waves in RN activity was dramatically increased. Mean blood
pressure increased from 143 mmHg before stimulation to 171 mmHg at the end of the trace.
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9° in the case shown in Fig. 8B.
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DISCUSSION |
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TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
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In an earlier report (15) we argued that the reciprocal changes in CN and VN 10-Hz discharges produced by electrical stimulation of the defense region of the PAG do not arise simply from the activation of point-to-point hard-wired connections that excite some brain stem and/or spinal cell groups and inhibit others. Rather, we proposed that this pattern arises as the consequence of reorganization of the coupling of multiple 10-Hz brain stem oscillators, each with a different peripheral target. Changes in the phase angle between the 10-Hz discharges of the CN and VN were presumed to reflect the reorganization. The results of the present study provide new evidence in support of this proposal and, in addition, provide a more complete picture of the differential patterns of spinal sympathetic outflow produced by caudal PAG stimulation.
Although the 10-Hz and cardiac-related rhythms in SND are generated independently by different pools of brain stem neurons (1, 4), they are carried to sympathetic nerves by the same bulbospinal neurons (2). On this basis, we reasoned that the changes in the cardiac-related discharges of the CN, VN, and RN of baroreceptor-innervated cats would be similar to those of their 10-Hz discharges in baroreceptor-denervated cats if PAG activation simply exerts opposing actions on populations of bulbospinal and/or spinal neurons with different targets. Contrary to this prediction, the patterns of spinal sympathetic outflow induced by PAG stimulation in baroreceptor-innervated cats were markedly different from those in baroreceptor-denervated cats. As illustrated in Figs. 1B and 2, the increases in CN and RN 10-Hz discharges and decrease in VN 10-Hz activity produced by high-frequency (25-Hz) PAG stimulation in baroreceptor-denervated cats were immediate in onset and sustained throughout the period of activation. Moreover, high-frequency PAG stimulation significantly changed the phase relations between the 10-Hz discharges of the CN-VN, CN-RN, and VN-RN pairs (Fig. 2, Table 2). In contrast, VN cardiac-related activity was unchanged or increased during the first 15-20 s of high-frequency PAG stimulation in baroreceptor-innervated cats (Figs. 4-6). Later during the 40-s period of PAG stimulation, as blood pressure continued to rise, VN cardiac-related activity was decreased below control level in most cases (Figs. 5 and 7). At this time, the increase in CN cardiac-related activity was largely maintained, whereas that in the RN was blunted but not completely reversed. Also, in contrast to the patterns involving the 10-Hz rhythm, high-frequency PAG stimulation had little effect on the phase relations between the cardiac-related discharges of the three nerve pairs. Because the increases in cardiac-related activity during the first 20 s of PAG stimulation were greater in the CN and RN than VN, it appears that high-frequency PAG stimulation initially exerted differential excitatory effects on the circuits responsible for this component of the discharges of the three postganglionic nerves. Subsequently, these changes apparently were buffered to different degrees by increased baroreceptor afferent nerve activity attendant to the rise in blood pressure. We conclude that the mechanisms responsible for the differential patterns of spinal sympathetic outflow involving the cardiac-related rhythm are distinct from those responsible for the differential patterns involving the 10-Hz rhythm.
As was the case for high-frequency PAG stimulation, the patterns produced by low-frequency stimulation were dependent on the preexisting rhythm in SND. First, whereas the 10-Hz rhythm was entrained to frequencies of PAG stimulation near that of the free-running rhythm (Fig. 3), entrainment of the cardiac-related rhythm to frequencies of PAG stimulation just below or above that of the heartbeat could not be demonstrated (Fig. 8). Second, the decrease in VN 10-Hz activity was changed to an increase when the frequency of PAG stimulation was reduced to just below that of the free-running rhythm (Fig. 1C). In contrast, PAG stimulation at frequencies just below, equal to, or just above that of the free-running cardiac-related rhythm elicited excitatory responses in the VN as well as CN and RN that were simply added to ongoing cardiac-related activity (Fig. 8). These observations further support the view that the changes in cardiac-related and 10-Hz SND induced by PAG stimulation cannot be attributed to a common mechanism. Regarding the mechanism responsible for the patterns elicited in baroreceptor-denervated cats, we (15) proposed that changes in the frequency of PAG stimulation lead a system of coupled 10-Hz oscillators through a repertoire of internally self-organized states, each of which is characterized by a different set of phase relations and, thus, a different pattern of spinal sympathetic outflow.
In an earlier report (15) we suggested that the reciprocal changes in CN and VN 10-Hz discharges produced by PAG stimulation represent an electrophysiological correlate of the defense reaction. Regarding this point, chemical or electrical activation of the defense regions of the PAG or hypothalamus increases heart rate and blood flow to skeletal muscle of the limbs (7, 11, 13, 17). Importantly, in cats, full expression of the increase in limb blood flow requires not only the activation of sympathetic cholinergic vasodilator fibers but also the selective inhibition of vasoconstrictor outflow to skeletal muscle (10). The cardiovascular component of the defense reaction also includes a decrease in renal blood flow due to increased sympathetic vasoconstrictor outflow to that organ (17). Thus the increase in RN 10-Hz activity observed in the present study lends further support to the idea that the differential pattern of changes in 10-Hz SND elicited by frequencies of PAG stimulation equal to or above that of the free-running rhythm was defenselike in character.
The fact remains that the pattern of changes in the cardiac-related discharges of the CN, VN, and RN produced by high-frequency PAG stimulation in baroreceptor-innervated cats also was defenselike. Although delayed in onset, the change in VN cardiac-related activity occurred in a direction (decrease) opposite that of the changes in CN and RN cardiac-related activities. Whether the changes in cardiac function and regional blood flows that accompany the naturally occurring defense reaction in behaving animals are based on the mechanisms proposed here to explain the differential changes in cardiac-related and 10-Hz SND deserves further attention. It would be particularly interesting to compare the changes in skeletal muscle blood flow that accompany decreases versus increases in VN 10-Hz activity produced by different frequencies of PAG stimulation.
Perspectives
Although it is well established that the brain can formulate differential patterns of spinal sympathetic outflow leading to cardiovascular responses that support such behavioral states as the defense reaction, the underlying mechanisms for these patterns remain under active investigation. Most models that try to explain reciprocal changes in sympathetic outflows to different peripheral targets presuppose coordination of the activity of different cell groups by shared inputs from central "command" centers and/or peripheral afferent nerves. The implication drawn from these models is that the shared inputs excite some cell groups and inhibit others. As pointed out by Gebber et al. (15), models of this type need not include the direct interconnection of cell groups with different targets. One such model combining differential excitation from the PAG and differential inhibition of baroreceptor reflex origin could explain the reciprocal changes in VN and CN (or RN) cardiac-related discharges observed in the present study. However, the reciprocal changes of the 10-Hz discharges of the same nerves produced by PAG stimulation in baroreceptor-denervated cats appear to be dependent on an entirely different mechanism, i.e., abrupt changes in the state of coupling of multiple nonlinear brain stem oscillators, as reflected by alterations in the phase angles between the 10-Hz discharges of the postganglionic nerves that they target. Models based on the principles of nonlinear dynamics and self-organization within large-scale neural networks have been proposed to explain how the pattern of locomotion might be changed from one characterized by in-phase movements of the limbs to another characterized by out-of-phase movements (16, 19). To our knowledge, however, the present study and an earlier report from our laboratory (15) are the first to apply such principles to central autonomic networks.| |
ACKNOWLEDGEMENTS |
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The authors thank Shannon Sykes for typing the manuscript.
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FOOTNOTES |
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This study was supported by National Heart, Lung, and Blood Institute Grant HL-13187.
The costs of publication of this article were defrayed in part by the payment of page charges. The article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. §1734 solely to indicate this fact.
Address for reprint requests and other correspondence: G. L. Gebber, Dept. of Pharmacology and Toxicology, Michigan State University, East Lansing, MI 48824-1317 (E-mail: gebber{at}msu.edu).
Received 15 September 1999; accepted in final form 21 December 1999.
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TOP
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INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
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  H. S. Orer, G. L. Gebber, and S. M. Barman Role of serotonergic input to the ventrolateral medulla in expression of the 10-Hz sympathetic nerve rhythm Am J Physiol Regulatory Integrative Comp Physiol, May 1, 2008; 294(5): R1435 - R1444. [Abstract] [Full Text] [PDF]
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S. M. Barman and G. L. Gebber Role of ventrolateral medulla in generating the 10-Hz rhythm in sympathetic nerve discharge Am J Physiol Regulatory Integrative Comp Physiol, July 1, 2007; 293(1): R223 - R233. [Abstract] [Full Text] [PDF]
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H. M. Stauss Baroreceptor reflex function Am J Physiol Regulatory Integrative Comp Physiol, August 1, 2002; 283(2): R284 - R286. [Full Text] [PDF]
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S. F. Morrison Differential control of sympathetic outflow Am J Physiol Regulatory Integrative Comp Physiol, September 1, 2001; 281(3): R683 - R698. [Abstract] [Full Text] [PDF]
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P. D. Larsen, S. Zhong, G. L. Gebber, and S. M. Barman Sympathetic nerve and cardiovascular responses to chemical activation of the midbrain defense region Am J Physiol Regulatory Integrative Comp Physiol, June 1, 2001; 280(6): R1704 - R1712. [Abstract] [Full Text] [PDF]
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P. D. Larsen, S. Zhong, G. L. Gebber, and S. M. Barman Differential pattern of spinal sympathetic outflow in response to stimulation of the caudal medullary raphe Am J Physiol Regulatory Integrative Comp Physiol, July 1, 2000; 279(1): R210 - R221. [Abstract] [Full Text] [PDF]
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,
Frequency of PAG stimulation. A: PAG stimulation at 2.8 Hz;
free-running cardiac-related rhythm was 3.8 Hz. B: PAG
stimulation at 4.0 Hz; free-running cardiac-related rhythm was 4.0 Hz.
C: PAG stimulation at 4.8 Hz; free-running cardiac-related
rhythm was 3.6 Hz. Each spectrum is average of 32 5-s windows with 75%
overlap. Frequency resolution is 0.2 Hz/bin. Insets: PAG
stimulus-triggered averages (200 sweeps) of CN, VN, and RN responses.
Negative potentials (upward deflection) denote stimulus-locked
excitatory responses. Stimulus was applied at beginning of trace.
Vertical calibration is 100 µV and refers to all insets.
Horizontal calibration is 100 ms.