Sympathoexcitatory influence of a fast conducting raphe-spinal pathway in the rat

1995 ◽  
Vol 268 (5) ◽  
pp. R1230-R1235 ◽  
Author(s):  
S. Y. Zhou ◽  
M. P. Gilbey
Keyword(s):  
Blood Pressure ◽  
Electrical Stimulation ◽  
Sympathetic Neurons ◽  
Early Response ◽  
Gamma Aminobutyric Acid ◽  
Homocysteic Acid ◽  
Spinal Pathway ◽  
Pentobarbitone Sodium ◽  
Response Compatible ◽  
Excitatory Drive

Experiments were carried out on 20 pentobarbitone sodium (alpha-chloralose supplemented)-anesthetized, artificially ventilated, and paralyzed rats. The possibility was explored that raphe-spinal neurons with myelinated axons arising in the rostral part of raphe obscurus provide excitatory drive to sympathetic neurons. Electrical stimulation within obscurus was observed to evoke an “early” sympathoexcitatory response compatible with its conduction over such a pathway. The effect of the microinjection of excitatory and inhibitory amino acids [DL-homocysteic acid (DLH) and gamma-aminobutyric acid (GABA), respectively] on the evoked response was studied at the sites of electrical stimulation. The size of the early response was increased by 91.7 +/- 24.4% (n = 7) and depressed by -48 +/- 4.8% (n = 7) by DLH and GABA, respectively. Saline was without effect (-14.5 +/- 12.2%, n = 6). The evoked responses were decreased when blood pressure was raised by administration of phenylephrine (2-6 micrograms/kg iv) and totally suppressed by an increase in blood pressure of 19.3 +/- 4.3 mmHg (baseline 89.1 +/- 2.5 mmHg, n = 7). It is concluded that some cell bodies located in rostral raphe obscurus that project to the spinal cord relay excitatory drive to sympathetic neurons.

Midbrain vlPAG inhibits rVLM cardiovascular sympathoexcitatory responses during electroacupuncture

2006 ◽  
Vol 290 (6) ◽  
pp. H2543-H2553 ◽  
Author(s):  
Stephanie C. Tjen-A-Looi ◽  
Peng Li ◽  
John C. Longhurst
Keyword(s):  
Blood Pressure ◽  
Excitatory Amino Acid ◽  
Sympathetic Neurons ◽  
Cardiovascular Responses ◽  
Splanchnic Nerve ◽  
Ventrolateral Medulla ◽  
Inhibitory Influence ◽  
Afferent Stimulation ◽  
Homocysteic Acid ◽  
Blood Pressure Responses

The periaqueductal gray (PAG) is an important integrative region in the regulation of autonomic outflow and cardiovascular function and may serve as a regulatory center as part of a long-loop pathway during somatic afferent stimulation with acupuncture. Because the ventrolateral PAG (vlPAG) provides input to the rostral ventrolateral medulla (rVLM), an important area for electroacupuncture (EA) regulation of sympathetic outflow, we hypothesized that the vlPAG plays a role in the EA-related modulation of rVLM premotor sympathetic neurons activated during visceral afferent stimulation and autonomic excitatory reflexes. Cats were anesthetized and ventilated, and heart rate and mean blood pressure were monitored. Stimulation of the splanchnic nerve by a pledget of filter paper soaked in bradykinin (BK, 10 μg/ml) every 10 min on the gallbladder induced consistent cardiovascular reflex responses. Bilateral stimulation with EA at acupoints over the pericardial meridian (P5-6) situated over the median nerve reduced the increases in blood pressure from 34 ± 3 to 18 ± 5 mmHg for a period of time that lasted for 60 min or more. Unilateral inactivation of neuronal activity in the vlPAG with 50–75 nl of kainic acid (KA, 1 mM) restored the blood pressure responses from 18 ± 3 to 36 ± 5 mmHg during BK-induced gallbladder stimulation, an effect that lasted for 30 min. In the absence of EA, unilateral microinjection of the excitatory amino acid dl-homocysteic acid (DLH, 4 nM) in the vlPAG mimicked the effect of EA and reduced the reflex blood pressure responses from 35 ± 6 to 14 ± 5 mmHg. Responses of 21 cardiovascular sympathoexcitatory rVLM neurons, including 12 that were identified as premotor neurons, paralleled the cardiovascular responses. Thus splanchnic nerve-evoked neuronal discharge of 32 ± 4 spikes/30 stimuli in six neurons was reduced to 10 ± 2 spikes/30 stimuli by EA, which was restored rapidly to 28 ± 4 spikes/30 stimuli by unilateral injection of 50 nl KA into the vlPAG. Conversely, 50 nl of DLH in the vlPAG reduced the number of action potentials of 5 rVLM neurons from 30 ± 4 to 18 ± 4 spikes/30 stimuli. We conclude that the inhibitory influence of EA involves vlPAG stimulation, which, in turn, inhibits rVLM neurons in the EA-related attenuation of the cardiovascular excitatory response during visceral afferent stimulation.

A model of dynamic exercise: the decerebrate rat locomotor preparation

1992 ◽  
Vol 72 (1) ◽  
pp. 121-127 ◽  
Author(s):  
T. G. Bedford ◽  
P. K. Loi ◽  
C. C. Crandall
Keyword(s):  
Blood Pressure ◽  
Electrical Stimulation ◽  
Blood Pressure Response ◽  
Pressor Response ◽  
Dynamic Exercise ◽  
Pressure Response ◽  
Aminobutyric Acid ◽  
Gamma Aminobutyric Acid ◽  
Decerebrate Rat ◽  
Stimulation Of

The purpose of this study was to develop a dynamic exercise model in the rat that could be used to study central nervous system control of the cardiovascular system. Rats of both sexes were decerebrated under halothane anesthesia and prepared for induced locomotion on a freely turning wheel. Electrical stimulation of the mesencephalic locomotor region (MLR) elicited locomotion at different speeds and gait patterns and increased heart rate and blood pressure. Two maneuvers were performed to illustrate the potential use of the preparation. The first maneuver consisted of muscular paralysis, which prevents excitation of muscle mechanoreceptors and chemoreceptors resulting from exercise. MLR stimulation still increased blood pressure. The second maneuver was performed to determine whether the blood pressure response obtained during paralysis was an artifact of electrical stimulation of the MLR. After microinjection of gamma-aminobutyric acid into the MLR, electrical current thresholds for blood pressure and locomotion increased in parallel. gamma-Aminobutyric acid injection also reduced the pressor response to suprathreshold electrical stimulation by 76%. The injection results suggest that electrical stimulation of the MLR activates cells rather than fibers of passage. The blood pressure response of the exercise model is probably not an artifact of stimulation. The decerebrate rat locomotor preparation should offer another approach to investigate difficult problems in exercise physiology.

Evaluation of topical phenol as a means of producing autonomic denervation of the liver

1984 ◽  
Vol 62 (7) ◽  
pp. 849-853 ◽  
Author(s):  
W. Wayne Lautt ◽  
Anne M. Carroll
Keyword(s):  
Blood Pressure ◽  
Topical Application ◽  
Nerve Stimulation ◽  
Sympathetic Neurons ◽  
Portal Pressure ◽  
Nerve Degeneration ◽  
Hepatic Glycogen ◽  
Glucose Levels ◽  
Afferent Nerves ◽  
Chronic Denervation

Topical application of 90% phenol around the bile duct, portal vein, and hepatic artery, as well as along each of the three hepatic ligaments was tested for effectiveness of rapid and chronic denervation in cats. Because phenol produces nonselective nerve degeneration, it was assumed that proof of functional sympathectomy was adequate proof of disruption of parasympathetic and afferent nerves as well. Functional sympathetic neurons were evaluated by measuring physiological responses to direct electrical stimulation of the anterior hepatic plexus. Acute or rapid denervation was assessed by the degree of rise in portal blood pressure produced by nerve stimulation. Complete denervation appeared within 20 min and was still present by 80 min postapplication. Chronic denervation was tested by applying the phenol and recovering the cats for 6–14 days. An equal number (n = 6) of sham-denervated cats were compared. Phenol denervation did not alter basal glucose, insulin or glucagon levels, hematocrit, blood pressure, or hepatic glycogen levels. These variables are a good index of stress and metabolic status. Nerve stimulation in the chronic sham group raised portal pressure, arterial pressure, and blood glucose levels, whereas the chronic-denervated group showed no responses. The health of the two groups appeared normal with the sole difference being that the painted itssues were mildly discolored and more adhesions appeared in the phenol-denervated set. Thus phenol is a useful tool for producing hepatic denervation. It is less traumatic, faster, and more certain than surgical denervation. In addition, the hepatic lymphatics can be preserved using the topical application of phenol.

Interaction of aortic and carotid sinus baroreceptors: effect of activation times

1975 ◽  
Vol 228 (1) ◽  
pp. 238-243 ◽  
Author(s):  
PG Katona ◽  
KS Tan
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Electrical Stimulation ◽  
Pulse Wave Velocity ◽  
Wave Velocity ◽  
Pulse Wave ◽  
Carotid Sinus ◽  
Relative Timing ◽  
Relative Delay ◽  
Activation Times

Changes in pulse-wave velocity were simulated by changing the relative timing between aortic and carotid sinus barorecptor activity in anesthetized rabbits and dogs. In the rabbit, electrical stimulation was used to vary the timing; in the dog, it was also varied by perfusing the carotid sinuses with externally generated pressure pulses that could be triggered in any portion of the cardiac cycle. Changing the relative delay between aortic and carotid sinsus nerve stimulation did not result in variations of blood pressure or heart rate in the rabbit. Varing the time of electrical stimulation of the carotid sinus nerve caused at most 5 mmHg change of blood pressure in the dog. Delay-related heart-rate changes could be usually observed only when the stimulus consisted of short, high-intensity bursts. When the carotid sinus was externally perfused with pulses of pressure, only one out of five dogs showed delay-related variations in blood pressure (3mmHg) and heart rate (6 beats/min). It is concluded that variations in pulse-wave velocity are unlikely to play a significant role in acute cardiovascular control.

Quantitative characterization and spinal pathway mediating inhibition of spinal nociceptive transmission from the lateral reticular nucleus in the rat

1988 ◽  
Vol 59 (1) ◽  
pp. 226-247 ◽  
Author(s):  
A. J. Janss ◽  
G. F. Gebhart
Keyword(s):  
Electrical Stimulation ◽  
Spontaneous Activity ◽  
Pulse Duration ◽  
Neuronal Response ◽  
Response Threshold ◽  
Reticular Nucleus ◽  
Lateral Reticular Nucleus ◽  
Descending Inhibition ◽  
Nociceptive Transmission ◽  
Spinal Pathway

1. The modulation of spinal nociceptive transmission from the lateral reticular nucleus (LRN) was characterized for 47 spinal dorsal horn neurons in pentobarbital-anesthetized, paralyzed rats. All 47 units studied had receptive fields confined to the glabrous skin of the plantar surface of the ipsilateral hind foot and responded to mechanical stimulation as well as noxious heating (50 degrees C). Rostral projections contained in the ventrolateral quadrant of the cervical spinal cord were demonstrated for 15 of the 47 units by antidromic invasion. Glutamate- and stimulation-produced descending inhibition, the spinal pathway, and tonic descending inhibition from the LRN were systematically examined. 2. Inhibition of unit responses to heating of the skin by electrical stimulation in the LRN varied with the intensity, pulse duration (100 or 400 microseconds), and frequency (25–100 Hz) of stimulation. Greater inhibition was produced at lower intensities of stimulation with the 400-microseconds pulse duration and a frequency of 100 Hz. The effects of stimulation on spontaneous activity and responses to heat were compared in 16 experiments; inhibition of spontaneous activity was intensity dependent and did not differ significantly in magnitude from stimulation-produced inhibition of responses to heating of the skin. 3. Tracking experiments established that stimulation in the ipsilateral and contralateral ventrolateral medulla reliably attenuated unit responses to noxious heating of the skin and that stimulation in the LRN produced maximal inhibition at a low intensity of stimulation. Descending inhibition was quantitatively characterized from sites within (n = 32) and outside (n = 30) the LRN. Both the extrapolated mean stimulation threshold for inhibition and mean intensity inhibiting unit responses to heat to 50% of control were significantly lower for sites in the LRN. 4. The responses of seven spinal units to graded noxious heating of the skin were studied; all exhibited linear monotonic stimulus-response functions (SRFs) throughout the temperature range examined (42–50 degrees C). Electrical stimulation in the LRN significantly decreased the slope (42 +/- 4% of control) of the SRFs and increased the neuronal response threshold (2.0 +/- 0.7 degrees C). 5. S-glutamate (50 nmol, 0.5 microliter) was microinjected into stimulation sites within (n = 15) and distant from (n = 6) the LRN. Glutamate produced a transient (less than 7 min) but significant attenuation of neuronal responses to heat to 35 +/- 6% of control only when microinjected into the LRN.(ABSTRACT TRUNCATED AT 400 WORDS)

Putative mechanisms involved in excitatory and inhibitory effects of somatostatin on intestinal motility

1989 ◽  
Vol 257 (4) ◽  
pp. G532-G538 ◽  
Author(s):  
T. Takeda ◽  
K. Taniyama ◽  
S. Baba ◽  
C. Tanaka
Keyword(s):  
Electrical Stimulation ◽  
Longitudinal Muscle ◽  
Cholinergic Neuron ◽  
Gamma Aminobutyric Acid ◽  
Inhibitory Effects ◽  
Guinea Pig Ileum ◽  
Excitatory Effect ◽  
Ergic Neuron ◽  
Gabaa Antagonist ◽  
Stimulation Of

The mechanism of action of somatostatin on the motility of intestine was examined in the entire preparation and the longitudinal muscle attached with Auerbach's plexus (LA) preparation of guinea pig ileum, in relation to the cholinergic neuron and gamma-aminobutyric acid (GABA)ergic neuron. Somatostatin produced a transient potentiation of electrical stimulation-induced twitch contractions followed by an inhibition. The excitatory effect of somatostatin was associated with an increase in the release of [3H]acetylcholine (ACh) from the preparations preloaded with [3H]choline. Bicuculline, a GABAA antagonist, inhibited the somatostatin-induced excitatory effect. Somatostatin inhibited the electrical stimulation-induced twitch contraction and release of [3H]ACh, and the inhibition was greater in the entire preparation than in the LA. Phaclofen, a GABAB antagonist, prevented the inhibitory effects of somatostatin. Somatostatin induced a Ca2+ -dependent, tetrodotoxin-sensitive release of [3H]GABA from the preparations preloaded with [3H]GABA. Therefore somatostatin exerts excitatory and inhibitory effects on the cholinergic neuron due to the stimulation of the GABAergic neuron, and the motility of the intestine is regulated.

Stimulation of the caudal ventrolateral medulla decreases total lung resistance in dogs

1987 ◽  
Vol 63 (3) ◽  
pp. 912-917 ◽  
Author(s):  
J. C. Connelly ◽  
L. W. McCallister ◽  
M. P. Kaufman
Keyword(s):  
Electrical Stimulation ◽  
Nucleus Ambiguus ◽  
Ventrolateral Medulla ◽  
Adrenergic Blockade ◽  
Homocysteic Acid ◽  
Caudal Ventrolateral Medulla ◽  
Airway Caliber ◽  
Lung Resistance ◽  
Total Lung Resistance ◽  
Stimulation Of

Although the role played by the caudal ventrolateral medulla in the regulation of the cardiovascular system has been extensively investigated, little is known about the role played by this area in the regulation of airway caliber. Therefore, in alpha-chloralose-anesthetized dogs, we used both electrical and chemical means to stimulate the caudal ventrolateral medulla while we monitored changes in total lung resistance breath by breath. We found that electrical stimulation (25 microA) of 26 sites in this area significantly decreased total lung resistance from 7.1 +/- 0.4 to 5.7 +/- 0.3 cmH2O.1'1.s (P less than 0.001). The bronchodilation evoked by electrical stimulation was unaffected by beta-adrenergic blockade but was abolished by cholinergic blockade. In addition, chemical stimulation of seven sites in the caudal ventrolateral medulla with microinjections of DL-homocysteic acid (0.2 M; 66 nl), which stimulates cell bodies but not fibers of passage, also decreased total lung resistance from 8.3 +/- 1.1 to 6.5 +/- 0.8 cmH2O.l'1.s (P less than 0.01). In contrast, microinjections of DL-homocysteic acid into the nucleus ambiguus (n = 6) increased total lung resistance from 7.5 +/- 0.5 to 9.2 +/- 0.4 cmH2O.l'1.s (P less than 0.05). We conclude that the caudal ventrolateral medulla contains a pool of cell bodies whose excitation causes bronchodilation by withdrawing cholinergic input to airway smooth muscle.

Neurogenically derived nitrosyl factors mediate sympathetic vasodilation in the hindlimb of the rat

1997 ◽  
Vol 272 (5) ◽  
pp. H2369-H2376 ◽  
Author(s):  
R. L. Davisson ◽  
O. S. Possas ◽  
S. P. Murphy ◽  
S. J. Lewis
Keyword(s):  
Nitric Oxide ◽  
Skeletal Muscle ◽  
Electrical Stimulation ◽  
Sympathetic Neurons ◽  
Specific Inhibitor ◽  
No Synthase ◽  
Systemic Administration ◽  
Sympathetic Chain ◽  
Low Intensity ◽  
Stimulation Of

Skeletal muscle vasculature of the hindlimb is innervated by a sympathetic noncholinergic vasodilator system. The aim of this study was to determine whether this vasodilator system may represent postganglionic lumbar sympathetic neurons that synthesize and release nitric oxide (NO) or related NO-containing factors. We examined whether NO synthase (NOS)-positive postganglionic lumbar nerves innervate the hindlimb vasculature of the rat and whether the hindlimb vasodilation produced by electrical stimulation of the lumbar sympathetic chain of anesthetized rats is reduced after the systemic administration of the specific inhibitor of neuronal NOS 7-nitroindazole (7-NI). Subpopulations of lumbar sympathetic cell bodies stained intensely for NOS. Postganglionic fibers and varicosities within the iliac and femoral arteries also stained for NOS. Double ligation of the lumbar chain demonstrated that NOS was transported from the cell bodies toward the peripheral terminals. Low-intensity electrical stimulation of the lumbar chain produced a pronounced hindlimb vasodilation that was markedly diminished by pretreatment with 7-NI (45 mg/kg i.v.). In contrast, the vasodilator potency of acetylcholine and S-nitrosocysteine were augmented by 7-NI. These results suggest that postganglionic lumbar sympathetic neurons may synthesize and release NO-containing factors.

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