Lateral tegmental field neurons of cat medulla: a potential source of basal sympathetic nerve discharge

1985 ◽  
Vol 54 (6) ◽  
pp. 1498-1512 ◽  
Author(s):  
G. L. Gebber ◽  
S. M. Barman
Keyword(s):  
Slow Wave ◽  
Sympathetic Nerve ◽  
Baroreceptor Reflex ◽  
Raphe Nuclei ◽  
Ventrolateral Medulla ◽  
Related Activity ◽  
Medullary Raphe ◽  
Reflex Activation ◽  
Raphé Nuclei ◽  
Nerve Discharge

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)

Lateral tegmental field neurons of cat medulla: a source of basal activity of ventrolateral medullospinal sympathoexcitatory neurons

1987 ◽  
Vol 57 (5) ◽  
pp. 1410-1424 ◽  
Author(s):  
S. M. Barman ◽  
G. L. Gebber
Keyword(s):  
Firing Rate ◽  
Sympathetic Nerve ◽  
Threshold Current ◽  
Baroreceptor Reflex ◽  
Ventrolateral Medulla ◽  
Related Activity ◽  
Synaptic Excitation ◽  
Spike Triggered Averaging ◽  
Reflex Activation ◽  
The Difference

We tested the hypothesis that neurons of the lateral tegmental field (LTF) of the cat medulla exert their sympathoexcitatory actions over a pathway that includes rostral ventrolateral medullospinal neurons innervating the spinal intermediolateral nucleus (IML). Thirty-one LTF neurons with sympathetic nerve-related activity [as demonstrated with spike-triggered averaging of inferior cardiac postganglionic sympathetic nerve discharge (SND)] were antidromically activated by microstimulation of the rostral ventrolateral medulla (VLM). The threshold current required to elicit the longest latency antidromic response was increased when the stimulating microelectrode was moved to more dorsal or medial sites in the rostral medulla. This observation suggests that the axons of LTF neurons projected to the rostral VLM. The firing rate of LTF neurons with sympathetic nerve-related activity was decreased during baroreceptor reflex activation. This observation is consistent with the view that these neurons subserved a sympathoexcitatory function. Twenty-five VLM neurons with sympathetic nerve-related activity were synaptically activated by microstimulation of the LTF. The modal onset latency of synaptic excitation (25.6 +/- 2.6 ms) compared favorably with the difference (31 ms on the average) between the firing times of LTF and VLM neurons relative to the peak of the cardiac-related sympathetic nerve slow wave. The firing rate of these VLM neurons decreased during baroreceptor reflex activation. Of nine VLM neurons tested, seven were antidromically activated by microstimulation of the second thoracic (T2) IML. These data are consistent with the view that LTF neurons are a source of the basal discharge of VLM-spinal sympathoexcitatory neurons. Sixteen VLM neurons with sympathetic nerve-related activity were antidromically activated by microstimulation of both the LTF and the T2 IML. In some cases, LTF stimulation activated an axonal branch rather than the main axon. This was demonstrated using time-controlled collision of the VLM neuronal action potentials initiated by LTF and T2 IML stimulation. These data raise the possibility that individual VLM neurons influence SND by actions mediated at both spinal and supraspinal levels.

Powerful depressor and sympathoinhibitory effects evoked from neurons in the caudal raphe pallidus and obscurus

1995 ◽  
Vol 268 (5) ◽  
pp. R1295-R1302 ◽  
Author(s):  
M. J. Coleman ◽  
R. A. Dampney
Keyword(s):  
Arterial Pressure ◽  
Sympathetic Activity ◽  
Raphe Nuclei ◽  
Ventrolateral Medulla ◽  
Gamma Aminobutyric Acid ◽  
Medullary Raphe ◽  
Dose Dependent Decrease ◽  
Raphé Nuclei ◽  
Raphe Pallidus ◽  
Dose Dependent

Microinjection of glutamate into sites within the medullary raphe nuclei (pallidus and obscurus) at levels caudal to the obex resulted in a dose-dependent decrease in mean arterial pressure (MAP), renal sympathetic nerve activity (RSNA), and heart rate in anesthetized rabbits. The depressor and sympathoinhibitory responses were similar in magnitude to those elicited from the previously described depressor region in the caudal ventrolateral medulla (CVLM) but had a shorter duration, in both intact and barodenervated animals. The bradycardia was not altered by barodenervation but was reduced after administration of propranolol or atropine and abolished after administration of both drugs. The neuroinhibitory compounds gamma-aminobutyric acid or muscimol had no effect on MAP or RSNA when injected into the caudal medullary raphe nuclei but evoked a pressor and sympathoexcitatory response when injected into the CVLM. The results indicate that neurons within the caudal raphe pallidus and obscurus can powerfully inhibit sympathetic activity, but unlike sympathoinhibitory neurons in the CVLM, they are not tonically active and are not capable of producing sustained changes in arterial pressure and sympathetic activity.

Descending projections of hypothalamic neurons with sympathetic nerve-related activity

1990 ◽  
Vol 64 (3) ◽  
pp. 1019-1032 ◽  
Author(s):  
S. M. Barman
Keyword(s):  
Firing Rate ◽  
Lateral Hypothalamus ◽  
Sympathetic Nerve ◽  
Pressor Response ◽  
Baroreceptor Reflex ◽  
Onset Latency ◽  
Related Activity ◽  
Antidromic Activation ◽  
Reflex Activation ◽  
Aortic Obstruction

1. Spike-triggered averaging was used to identify 104 hypothalamic (HYP) neurons whose spontaneous or L-glutamate-induced action potentials were synchronized to inferior cardiac postganglionic-sympathetic nerve discharge (SND) in 39 pentobarbital sodium-anesthetized cats. Neurons were located primarily in the lateral hypothalamus but also in the posterior, dorsal, ventromedial, and anterior hypothalamus, as well as in the paraventricular region. Most neurons tested (41/60) were classified as sympathoexcitatory (SE) because their firing rate decreased during baroreceptor reflex activation. Because the firing rate of 15 neurons increased during the pressor response produced by aortic obstruction, they were classified as sympathoinhibitory (SI). The firing rate of the other four neurons tested was unaffected by baroreceptor reflex activation. 2. Microstimulation of the medullary lateral tegmental field (LTF; stereotaxic plane P10.5-P12, 2.3-3 mm lateral to the midline) antidromically activated 11 of 58 HYP neurons with sympathetic nerve-related activity, including seven SE neurons and one SI neuron. Antidromic mapping was used to trace the axonal trajectories of HYP neurons that were activated by LTF microstimulation. The results of these experiments suggested that the axons of eight of these neurons branched or terminated in the LTF. The data obtained from another series of experiments were consistent with the view that these HYP neurons excited LTF-SE neurons. LTF-SE neurons were synaptically activated by electrical stimulation of the posterior or lateral hypothalamus. This stimulus also increased SND. The modal onset latency (36 +/- 7.2 ms, mean +/- SE) of synaptic activation of LTF-SE neurons was similar to the onset latency (38 +/- 6.8 ms) of antidromic activation of HYP neurons by LTF microstimulation. These data support the view that LTF-SE neurons are involved in mediating HYP influences on SND. 3. Rostral ventrolateral medullary (RVLM)-SE neurons, including those whose axons projected to the thoracic intermediolateral nucleus (IML), also appear to be involved in mediating HYP-stimulus-induced increases in SND. HYP stimulation synaptically activated these neurons with a modal onset latency of 36 +/- 9.6 ms. Microstimulation of the region containing RVLM-SE neurons antidromically activated 16 of 60 HYP neurons with sympathetic nerve-related activity. The nine neurons tested were classified as SE. antidromic mapping revealed that RVLM microstimulation activated the main axon rather than an axonal branch or terminal of 9 of 12 of these HYP neurons. 4. Microstimulation of the mesencephalic periaqueductal gray (PAG) at stereotaxic planes A2-A3.5 antidromically activated 30 of 61 HYP neurons with sympathetic nerve-related activity, including 13 SE neurons and three SI neurons.(ABSTRACT TRUNCATED AT 400 WORDS)

Axonal projections of caudal ventrolateral medullary and medullary raphe neurons with activity correlated to the 10-Hz rhythm in sympathetic nerve discharge

1995 ◽  
Vol 74 (6) ◽  
pp. 2295-2308 ◽  
Author(s):  
S. M. Barman ◽  
H. S. Orer ◽  
G. L. Gebber
Keyword(s):  
Slow Wave ◽  
Sympathetic Nerve ◽  
Sympathetic Neurons ◽  
Onset Latency ◽  
Antidromic Activation ◽  
Axonal Projections ◽  
Spike Triggered Averaging ◽  
Medullary Raphe ◽  
Raphe Neurons ◽  
Nerve Discharge

1. This is the first study to map the axonal projections of medullary neurons that are elements of the network responsible for the 10-Hz rhythm in sympathetic nerve discharge (SND) of urethan-anesthetized cats. Spike-triggered averaging and coherence analysis were used to identify caudal ventrolateral medullary (CVLM) and medullary raphe neurons with activity correlated to this component of SND. Spike-triggered averaging showed that CVLM neurons fired significantly earlier (17 ms on the average) than raphe neurons during the 10-Hz slow wave in inferior cardiac postganglionic SND. This observation raised the possibility that CVLM neurons are a source of the discharges of raphe neurons that are correlated to SND. 2. Nineteen of 47 CVLM neurons with activity correlated to the 10-Hz rhythm in SND were antidromically activated by micro-stimulation of the raphe. The longest onset latency of antidromic activation was 19.9 +/- 2.8 (SE) ms, a value comparable with the difference in firing times of CVLM and raphe neurons during the naturally occurring 10-Hz slow wave in inferior cardiac SND. In most cases the response likely reflected activation of an axonal branch of the CVLM neuron, because the onset latency of antidromic activation could be changed dramatically by moving the stimulating microelectrode as little as 0.2 mm within the raphe. Also, the onset latency of antidromic activation of nine CVLM neurons was significantly shortened (25.0 +/- 2.5 vs. 16.7 +/- 2.7 ms) when the stimulus intensity was raised above threshold. 3. The hypothesis that the axons of CVLM neurons with activity correlated to the 10-Hz rhythm in SND terminated on and excited raphe neurons was supported by the following observations. First, CVLM neurons could not be antidromically activated by stimuli applied to sites in tracks located 1.5-2 mm lateral to the midline, contralateral to the neuronal recording site; thus their axons did not cross the midline. Second, some CVLM neurons could be antidromically activated by stimuli applied to sites in only one of the tracks through the midline; thus it is unlikely that their axons were destined for more rostral or caudal portions of the brain stem. Third, 37% of the raphe neurons with activity correlated to the 10-Hz rhythm were synaptically activated by microstimulation of the CVLM, with a minimum onset latency of 18.1 +/- 2.6 ms. This value was not significantly different than the longest onset latency of antidromic activation of CVLM neurons by raphe stimulation. 4. CVLM neurons with activity correlated to the 10-Hz rhythm in SND could not be antidromically activated by microstimulation of the rostral ventrolateral medulla (RVLM) or thoracic spinal cord. Thus CVLM neurons are not a direct source of the 10-Hz discharges of RVLM or preganglionic sympathetic neurons. 5. Eight of 41 raphe neurons with activity correlated to the 10-Hz rhythm in SND were antidromically activated by microstimulation of the CVLM. The latency of the antidromic response of six raphe neurons was shortened from 15.2 +/- 3.1 to 11.9 +/- 3.1 ms by raising stimulus current above threshold, implying the existence of local axonal branching. The onset latency of antidromic activation of five raphe neurons was changed by moving the stimulating microelectrode within the CVLM. 6. The axons of at least some of these raphe neurons likely terminated in the CVLM, because higher current was required to antidromically activate these neurons from sites in a track located 0.5 mm further laterally, and they were not antidromically activated by microstimulation of the RVLM. Also 32% of the CVLM neurons were either excited or inhibited by microstimulation of the raphe. The minimum onset latency of synaptic activation (18.3 +/- 4.2 ms) or inhibition (10-20 ms) of CVLM neurons by raphe stimulation was similar to the longest onset latency of antidromic activation of raphe neurons by CVLM microstimulation. 7. These data are consistent with the view

Rostral dorsolateral pontine neurons with sympathetic nerve-related activity

1999 ◽  
Vol 276 (2) ◽  
pp. H401-H412 ◽  
Author(s):  
Susan M. Barman ◽  
Gerard L. Gebber ◽  
Heather Kitchens
Keyword(s):  
Sympathetic Nerve ◽  
Baroreceptor Reflex ◽  
Related Activity ◽  
Thoracic Spinal Cord ◽  
Firing Rates ◽  
Naturally Occurring ◽  
Thoracic Spinal ◽  
Spike Triggered Averaging ◽  
Reflex Activation ◽  
Aortic Obstruction

Spike-triggered averaging, arterial pulse-triggered analysis, and coherence analysis were used to classify rostral dorsolateral pontine (RDLP) neurons into groups whose naturally occurring discharges were correlated to only the 10-Hz rhythm ( n = 29), to only the cardiac-related rhythm ( n = 15), and to both rhythms ( n = 15) in inferior cardiac sympathetic nerve discharge (SND) of urethan-anesthetized cats. Most of the neurons with activity correlated to only the cardiac-related rhythm were located medial to the other two groups of neurons. The firing rates of most RDLP neurons with activity correlated to only the 10-Hz rhythm (9 of 12) or both rhythms (7 of 8) were decreased during baroreceptor reflex-induced inhibition of SND produced by aortic obstruction; thus, they are presumed to be sympathoexcitatory. The firing rates of four of seven RDLP neurons with activity correlated to only the cardiac-related rhythm increased during baroreceptor reflex activation; thus, they may be sympathoinhibitory. We conclude that the RDLP contains a functionally heterogeneous population of neurons with sympathetic nerve-related activity. These neurons could not be antidromically activated by stimulation of the thoracic spinal cord.

Rostral ventrolateral medullary and caudal medullary raphe neurons with activity correlated to the 10-Hz rhythm in sympathetic nerve discharge

1992 ◽  
Vol 68 (5) ◽  
pp. 1535-1547 ◽  
Author(s):  
S. M. Barman ◽  
G. L. Gebber
Keyword(s):  
Slow Wave ◽  
Sympathetic Nerve ◽  
Frequency Domain Analysis ◽  
Firing Rates ◽  
Medullary Raphe ◽  
The Mean ◽  
The Relationship ◽  
Medullary Neurons ◽  
Raphe Neurons ◽  
Nerve Discharge

1. The current study is the first to identify medullary neurons whose naturally occurring discharges were correlated to the 10-Hz rhythm in sympathetic nerve discharge (SND). Spike-triggered averaging showed that 44 of 164 rostral ventrolateral medullary (RVLM) and 44 of 174 caudal medullary raphe neurons had activity correlated to the 10-Hz rhythm in inferior cardiac postganglionic SND of 23 baroreceptor-denervated, decerebrate cats. 2. When the frequency of the rhythm in SND was decreased by lowering body temperature, the discharges of the 10 neurons tested (6 RVLM and 4 raphe) remained locked to the peak of the next 10-Hz sympathetic nerve slow wave rather than to the peak of the preceding slow wave. This observation supports the contention that the 10-Hz rhythm in basal SND was generated in the brain stem rather than in the spinal cord. 3. Frequency-domain analysis was used to characterize further the relationship between the 10-Hz rhythm in SND and the discharges of 30 RVLM and 24 raphe neurons. The autospectra of the discharges of eight RVLM and four raphe neurons contained a sharp peak near 10 Hz, although the mean firing rates of these neurons were lower than the frequency of the rhythm in SND. Coherence values as high as 0.76 characterized the relationship between the discharges of these "rhythmically firing neurons" and the 10-Hz rhythm in SND. A coherence value of 1.0 indicates a perfect correlation. The autospectra of the discharges of the 22 RVLM and 20 raphe neurons did not contain a peak near 10 Hz. The mean firing rates and coherence values relating the discharges of these "nonrhythmically firing neurons" and the 10-Hz rhythm in SND were significantly lower than those for the rhythmically firing neurons. Because the frequency of the population rhythm recorded from the inferior cardiac nerve was higher than the firing rates of individual medullary neurons, the 10-Hz rhythm in SND appears to be an emergent property of a network of neurons whose discharges are probabilistically related to the population rhythm. 4. In addition to the peak near 10-Hz, the autospectrum of SND often contained considerable power at frequencies < 6 Hz. This component of SND is called the 2- to 6-Hz rhythm.(ABSTRACT TRUNCATED AT 400 WORDS)

GABA-mediated inhibition of sympathoexcitatory neurons by midline medullary stimulation

1988 ◽  
Vol 255 (4) ◽  
pp. R605-R615 ◽  
Author(s):  
R. B. McCall
Keyword(s):  
Electrical Stimulation ◽  
Rostral Ventrolateral Medulla ◽  
Raphe Nuclei ◽  
Ventrolateral Medulla ◽  
Conduction Time ◽  
Gamma Aminobutyric Acid ◽  
Medullary Raphe ◽  
Raphé Nuclei ◽  
Inferior Cardiac Nerve ◽  
Stimulation Of

The present investigation determined whether the effects of electrical stimulation of depressor sites in midline medullary raphe nuclei were a result of inhibition of sympathoexcitatory medullospinal neurons in the rostral ventrolateral medulla of anesthetized cats. Electrical stimulation of the raphe inhibited inferior cardiac sympathetic activity. Microinjections of glutamate mimicked the effects of electrical stimulation. Electrical stimulation inhibited sympathoexcitatory neurons in the rostral ventrolateral medulla. The onset of the sympathoinhibition recorded from the inferior cardiac nerve (72 ms) was equal to the sum of the onset latency of the sympathoexcitatory response elicited from the rostral ventrolateral medulla (49 ms) plus the conduction time in the raphe to rostral ventrolateral sympathoinhibitory pathway (23 ms). Raphe stimulation excited a second set of neurons in the rostral ventrolateral medulla with an onset of 21 ms. Microiontophoretically applied bicuculline increased the discharge of sympathoexcitatory neurons and blocked the raphe-evoked inhibition. Iontophoretic glutamate excited sympathoexcitatory neurons but failed to antagonize raphe-elicited inhibition. These data suggest that neuronal elements in medullary raphe nuclei tonically inhibit sympathoexcitatory medullospinal neurons in the rostral ventrolateral medulla by activating closely adjacent gamma-aminobutyric acid (GABA) interneurons.

Lateral tegmental field neurons of cat medulla: a source of basal activity of raphespinal sympathoinhibitory neurons

1989 ◽  
Vol 61 (5) ◽  
pp. 1011-1024 ◽  
Author(s):  
S. M. Barman ◽  
G. L. Gebber
Keyword(s):  
Firing Rate ◽  
Sympathetic Nerve ◽  
Dorsal Surface ◽  
Baroreceptor Reflex ◽  
Related Activity ◽  
Unit Recording ◽  
Antidromic Responses ◽  
Reflex Activation ◽  
Raphe Neurons ◽  
Stimulation Of

1. We tested the hypothesis that sympathoinhibitory (SI) neurons in the lateral tegmental field (LTF) of the cat medulla exert their actions over a pathway that includes raphe neurons whose axons innervate the thoracic intermediolateral nucleus (IML). 2. We recorded from 32 LTF neurons with sympathetic nerve-related activity [as demonstrated with spike-triggered averaging of inferior cardiac sympathetic nerve discharge (SND)] whose firing rate increased during the inhibition of SND produced by baroreceptor reflex activation. These neurons were classified as SI in function. 3. Twenty-three of these 32 LTF-SI neurons were antidromically activated by microstimulation of the raphe nuclei, 2-4 mm rostral to the obex and 3-4.5 mm below the dorsal surface of the medulla. The threshold current for eliciting the longest-latency antidromic responses [18.9 +/- 2.4 (SE) ms] was increased when the stimulating microelectrode was moved more dorsally in the midline. With one exception, these neurons could not be antidromically activated by stimulation of sites either 1.5-2.0 mm lateral to the midline, contralateral to the site of unit recording or raphe sites caudal to the obex. Threshold stimuli applied 2-4 mm rostral to the obex and 1 mm lateral to the midline, ipsilateral to the site of unit recording, elicited antidromic responses whose onset latencies were shorter than those produced by raphe stimulation. These data support the view that the axons of LTF-SI neurons terminated in the region of the raphe that contains SI neurons whose axons innervate the IML. 4. We recorded from 32 raphe neurons with sympathetic nerve-related activity whose firing rate increased during baroreceptor reflex activation. These neurons were classified as SI in function. Twenty-five of the 32 raphe-SI neurons were antidromically activated by microstimulation of the third thoracic (T3) IML. Seven (including 5 with spinal axons) of 24 raphe-SI neurons tested were synaptically activated by microstimulation of the region of the LTF containing SI neurons. The modal onset latency of synaptic activation was 22.8 +/- 8.4 ms. This value is close to the difference in spontaneous firing times (26 ms on the average) of LTF-SI and raphe-SI neurons, relative to the peak of the cardiac-related burst of SND. 5. Taken together, these data are consistent with the hypothesis that LTF-SI neurons are a source of the background discharges of raphespinal-SI neurons. 6. Thirteen raphe-SI neurons were antidromically activated by stimulation of both the medulla and T3 IML.(ABSTRACT TRUNCATED AT 400 WORDS)

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