Brain stem mechanisms underlying acupuncture modality-related modulation of cardiovascular responses in rats

2005 ◽  
Vol 99 (3) ◽  
pp. 851-860 ◽  
Author(s):  
Wei Zhou (Yi Syuu) ◽  
Stephanie C. Tjen-A-Looi ◽  
John C. Longhurst
Keyword(s):  
Brain Stem ◽  
Median Nerve ◽  
Sympathetic Neurons ◽  
Low Frequency ◽  
Cardiovascular Responses ◽  
Splanchnic Nerve ◽  
Thoracic Spinal Cord ◽  
Median Nerve Stimulation ◽  
Cardiovascular Neurons ◽  
Stimulation Of

The present study was designed to investigate brain stem responses to manual acupuncture (MA) and electroacupuncture (EA) at different frequencies at pericardial P (5–6) acupoints located over the median nerve. Activity of premotor sympathetic cardiovascular neurons in the rostral ventral lateral medulla (rVLM) was recorded during stimulation of visceral and somatic afferents in ventilated anesthetized rats. We stimulated either the splanchnic nerve at 2 Hz (0.1–0.4 mA, 0.5 ms) or the median nerve for 30 s at 2, 10, 20, 40, or 100 Hz using EA (0.3–0.5 mA, 0.5 ms) or at ∼2 Hz with MA. Twelve of 18 cells responsive to splanchnic and median nerve stimulation could be antidromically driven from the intermediolateral columns of the thoracic spinal cord, T2–T4, indicating that they were premotor sympathetic neurons. All 18 neurons received baroreceptor input, providing evidence of their cardiovascular sympathoexcitatory function. Evoked responses during stimulation of the splanchnic nerve were inhibited by 49 ± 6% ( n = 7) with EA and by 46 ± 4% ( n = 6) with MA, indicating that the extent of inhibitory effects of the two modalities were similar. Inhibition lasted for 20 min after termination of EA or MA. Cardiovascular premotor rVLM neurons responded to 2-Hz electrical stimulation at P 5–6 and to a lesser extent to 10-, 20-, 40-, and 100-Hz stimulation (53 ± 10, 16 ± 2, 8 ± 2, 2 ± 1, and 0 ± 0 impulses/30 stimulations, n = 7). These results indicate that rVLM premotor sympathetic cardiovascular neurons that receive convergent input from the splanchnic and median nerves during low-frequency EA and MA are inhibited similarly for prolonged periods by low-frequency MA and EA.

Medullary substrate and differential cardiovascular responses during stimulation of specific acupoints

2004 ◽  
Vol 287 (4) ◽  
pp. R852-R862 ◽  
Author(s):  
Stephanie C. Tjen-A-Looi ◽  
Peng Li ◽  
John C. Longhurst
Keyword(s):  
Median Nerve ◽  
Neuronal Activity ◽  
Radial Nerve ◽  
Cardiovascular Responses ◽  
Reflex Responses ◽  
Superficial Radial Nerve ◽  
Cardiovascular Reflex ◽  
Cardiovascular Neurons ◽  
Change In Mean ◽  
Stimulation Of

Electroacupuncture (EA) at P5–P6 acupoints overlying the median nerve reduces premotor sympathetic cardiovascular neuronal activity in the rostral ventral lateral medulla (rVLM) and visceral reflex pressor responses. In previous studies, we have noted different durations of influence of EA comparing P5–P6 and S36–S37 acupoints, suggesting that point specificity may exist. The purpose of this study was to evaluate the influence of stimulating P5–P6 (overlying the median nerve), LI4–L7 (overlying branches of the median nerve and the superficial radial nerve), LI6–LI7 (overlying the superficial radial nerve), LI10–LI11 (overlying the deep radial nerves), S36–S37 (overlying the deep peroneal nerves), or K1–B67 (overlying terminal branches of the tibial nerves) specific acupoints, overlying deep and superficial somatic nerves, on the excitatory cardiovascular reflex and rVLM responses evoked by stimulation of chemosensitive receptors in the cat's gallbladder with bradykinin (BK) or direct splanchnic nerve (SN) stimulation. We observed point-specific differences in magnitude and duration of EA inhibition between P5–P6 or LI10–LI11 and LI4–L7 or S36–S37 in responses to 30-min stimulation with low-frequency, low-current EA. EA at LI6–LI7 and K1–B67 acupoints as well as direct stimulation of the superficial radial nerve did not cause any cardiovascular or rVLM neuronal effects. Cardiovascular neurons in the rVLM, a subset of which were classified as premotor sympathetic cells, responded to brief (30 s) stimulation of the SN as well as acupoints P5–P6, LI10–LI11, LI4–L7, S36–S37, LI6–LI7, or K1–B67, or underlying somatic pathways in a fashion similar to the reflex responses. In fact, we observed a significant linear relationship ( r2 = 0.71) between the evoked rVLM response and reflex change in mean arterial blood pressure. In addition, EA stimulation at P5–P6 and LI4–L7 decreased rVLM neuronal activity by 41 and 12%, respectively, for >1 h, demonstrating that prolonged input into the medulla during stimulation of somatic nerves, depending on the degree of convergence, leads to more or less inhibition of activity of these cardiovascular neurons. Thus EA at acupoints overlying deep and superficial somatic nerves leads to point-specific effects on cardiovascular reflex responses. In a similar manner, sympathetic cardiovascular rVLM neurons that respond to both visceral (reflex) and somatic (EA) nerve stimulation manifest graded responses during stimulation of specific acupoints, suggesting that this medullary region plays a role in site-specific inhibition of cardiovascular reflex responses by acupuncture.

Localization of Stereotactic Targets by Microrecording of Thalamic Somatosensory Evoked Potentials

Neurosurgery ◽  
1991 ◽  
Vol 28 (2) ◽  
pp. 223-230 ◽  
Author(s):  
Fumio Shima ◽  
Takato Morioka ◽  
Shozo Tobimatsu ◽  
Omiros Kavaklis ◽  
Motohiro Kato ◽  
...  
Keyword(s):  
Evoked Potentials ◽  
Median Nerve ◽  
Somatosensory Evoked Potentials ◽  
Practical Method ◽  
The Other ◽  
Basal Region ◽  
Thalamic Nuclei ◽  
Median Nerve Stimulation ◽  
Lower Amplitude ◽  
Stimulation Of

Abstract To improve the localization of stereotactic targets, somatosensory evoked potentials (SEPs) were recorded from the thalamus and subthalamic area using a specially designed semimicroelectrode in 61 patients and a conventional “macroclectrode” in 17 patients. By means of the semimicroelectrode, median nerve stimulation evoked two distinct SEPs, consisting of a diphasic wave with a huge positivity restricted to the nucleus ventrocaudalis (Vc) and a triphasic wave of lower amplitude with a major negativity in the ventral part of the nucleus ventrointermedius (Vim) and nucleus ventrooralis posterior (Vop) as well as the subthalamic lemniscal pathway. The Vim-Vc junction could thus be clearly delineated by an abrupt transition of SEPs from one type to the other with a precision of 1 mm. The parvicellular part of the Vc (Vcpc). situated in its basal region, was distinguishable from the Vc proper by a significant reduction of the positivity elicited by stimulation of the median nerve and by a rapid growth of a diphasic SEPs to stimulation of the posterior tibial nerve. In the other thalamic nuclei, stimulation of the median nerve elicited triphasic SEPs of a very small amplitude, suggesting a volume conduction current from the lemniscal pathway. With the macroclectrode, the positivity in the Vc was sensitive to electrode manipulation and the thalamic nuclei could not be distinctly outlined. SEP monitoring using the semimicroelectrode significantly improved the precision of target localization, which allowed minimizing of the volume of the therapeutic lesion without losing surgical effectiveness, while avoiding complications associated with increased penetration of the coagulating electrode. It is suggested that recording serial thalamic SEPs with the semimicroelectrode is a practical method to refine stereotactic targets in the thalamus.

scholarly journals Median nerve stimulation induces analgesia via orexin-initiated endocannabinoid disinhibition in the periaqueductal gray

2018 ◽  
Vol 115 (45) ◽  
pp. E10720-E10729 ◽  
Author(s):  
Yi-Hung Chen ◽  
Hsin-Jung Lee ◽  
Ming Tatt Lee ◽  
Ya-Ting Wu ◽  
Yen-Hsien Lee ◽  
...  
Keyword(s):  
Pain Management ◽  
Median Nerve ◽  
Nerve Stimulation ◽  
Antinociceptive Effect ◽  
Low Frequency ◽  
Periaqueductal Gray ◽  
Orexin A ◽  
Median Nerve Stimulation ◽  
Opioid Receptor Antagonists ◽  
Nociceptive Responses

Adequate pain management remains an unmet medical need. We previously revealed an opioid-independent analgesic mechanism mediated by orexin 1 receptor (OX1R)-initiated 2-arachidonoylglycerol (2-AG) signaling in the ventrolateral periaqueductal gray (vlPAG). Here, we found that low-frequency median nerve stimulation (MNS) through acupuncture needles at the PC6 (Neiguan) acupoint (MNS-PC6) induced an antinociceptive effect that engaged this mechanism. In mice, MNS-PC6 reduced acute thermal nociceptive responses and neuropathy-induced mechanical allodynia, increased the number of c-Fos–immunoreactive hypothalamic orexin neurons, and led to higher orexin A and lower GABA levels in the vlPAG. Such responses were not seen in mice with PC6 needle insertion only or electrical stimulation of the lateral deltoid, a nonmedian nerve-innervated location. Directly stimulating the surgically exposed median nerve also increased vlPAG orexin A levels. MNS-PC6–induced antinociception (MNS-PC6-IA) was prevented by proximal block of the median nerve with lidocaine as well as by systemic or intravlPAG injection of an antagonist of OX1Rs or cannabinoid 1 receptors (CB1Rs) but not by opioid receptor antagonists. Systemic blockade of OX1Rs or CB1Rs also restored vlPAG GABA levels after MNS-PC6. A cannabinoid (2-AG)-dependent mechanism was also implicated by the observations that MNS-PC6-IA was prevented by intravlPAG inhibition of 2-AG synthesis and was attenuated inCnr1−/−mice. These findings suggest that PC6-targeting low-frequency MNS activates hypothalamic orexin neurons, releasing orexins to induce analgesia through a CB1R-dependent cascade mediated by OX1R-initiated 2-AG retrograde disinhibition in the vlPAG. The opioid-independent characteristic of MNS-PC6–induced analgesia may provide a strategy for pain management in opioid-tolerant patients.

Effects of insulin on the cardiovascular integrating mechanisms of brain stem in cats

1993 ◽  
Vol 265 (4) ◽  
pp. E609-E616 ◽  
Author(s):  
S. W. Kuo ◽  
J. H. Hsieh ◽  
W. C. Wu ◽  
H. T. Horng ◽  
L. R. Shian ◽  
...  
Keyword(s):  
Brain Stem ◽  
Cardiovascular Responses ◽  
Serum Glucose ◽  
Ventrolateral Medulla ◽  
Reticular Nucleus ◽  
Motor Nucleus ◽  
Renal Nerve ◽  
Pressor Responses ◽  
The Brain ◽  
Stimulation Of

In 65 cats anesthetized with alpha-chloralose and urethane, the effects of insulin on cardiovascular responses to stimulation of various structures in the brain stem were studied. The threshold dose of insulin injected intravenously that produced systemic hypoglycemia was 5-10 U/kg. Subthreshold hypoglycemic doses of insulin were used intracerebroventricularly (0.25 U/kg) or intracerebrally (2 mU in 200 nl). Sixty minutes after intravenous insulin, when serum glucose concentrations decreased from 158 to 43 mg/100 ml, pressor responses to stimulation of the periaqueductal gray of midbrain (PAG), locus coeruleus (LC), dorsal medulla (DM), ventrolateral medulla (VLM), and parvocellular reticular nucleus (PVC) decreased significantly. Depressor and bradycardiac response to stimulation of paramedian reticular nucleus or dorsal motor nucleus of vagus (DMV) decreased significantly as well. Thirty minutes after intracerebroventricular insulin, pressor responses of PAG, DM, and the bradycardiac response of DMV decreased significantly. Thirty minutes after intracerebral insulin, pressor responses and renal nerve activities of LC (but not PAG), VLM, DM, and PVC decreased significantly. A similar but faster onset (5 min) of depression of cardiovascular responses on stimulating the LC, VLM, DM, and PVC was observed in another six acutely midcollicular-decerebrate cats recovered from halothane anesthesia. These findings suggest that insulin directly inhibits the vasomotor structures of the brain stem and decreases the pressor responses to stimulation.

Arterial baroreflex inhibition by gastric distension in rats: mediation by splanchnic afferents

1991 ◽  
Vol 260 (5) ◽  
pp. R985-R994 ◽  
Author(s):  
S. Nosaka ◽  
S. Murase ◽  
K. Murata
Keyword(s):  
Low Frequency ◽  
Splanchnic Nerve ◽  
Intraluminal Pressure ◽  
Gastric Distension ◽  
High Frequency Stimulation ◽  
Aortic Depressor Nerve ◽  
Low Frequency Stimulation ◽  
Afferent Fibers ◽  
Frequency Stimulation ◽  
Stimulation Of

Arterial baroreflexes are known to be reset during activation of defense area and somatosensory receptors-afferents. Here we report that viscerosensory activation also inhibits the baroreflexes. In chloralose-urethan-anesthetized, succinylcholine-immobilized, and artificially ventilated rats, the aortic depressor nerve was electrically stimulated while propranolol was continuously infused to elicit baroreflex hypotension (BH) and baroreflex vagal bradycardia (BVB). Hydraulic distension of the stomach with warm 0.9% NaCl solution was found to suppress BVB and BH, with a threshold intraluminal pressure at times less than 5mmHg. The gastric distension also suppressed BH in atropinized rats, suggesting that inhibition involved not only cardiac but also vascular components of baroreflexes. Bilateral splanchnectomy largely attenuated the inhibition, whereas bilateral subdiaphragmatic vagotomy had little effect. Low- as well as high-frequency stimulation of the splanchnic nerve strongly suppressed both BVB and BH, whereas only low-frequency stimulation of the subdiaphragmatic vagus inhibited baroreflexes to a slight degree. In conclusion, gastric distension suppresses BVB and BH, and this inhibition is largely mediated by afferent fibers in the splanchnic nerve. Such baroreflex inhibition may be a general consequence of mechanoreceptor activation of any visceral hollow organs because the jejunum, esophagus, and urinary bladder were all found to suppress arterial baroreflexes when distended.

Differential responses of regional sympathetic activity and blood flow to visceral afferent stimulation

2001 ◽  
Vol 280 (6) ◽  
pp. R1781-R1789 ◽  
Author(s):  
Hui-Lin Pan ◽  
Dwight D. Deal ◽  
Zemin Xu ◽  
Shao-Rui Chen
Keyword(s):  
Vascular Resistance ◽  
Cardiovascular Responses ◽  
Splanchnic Nerve ◽  
Visceral Afferents ◽  
Cardiovascular Reflexes ◽  
Efferent Activity ◽  
Blood Flows ◽  
The Right ◽  
Sympathetic Efferent Activity ◽  
Stimulation Of

The sympathetic nervous system is essential for the cardiovascular responses to stimulation of visceral afferents. It remains unclear how the reflex-evoked sympathetic output is distributed to different vascular beds to initiate the hemodynamic changes. In the present study, we examined changes in regional sympathetic nerve activity and blood flows in anesthetized cats. Cardiovascular reflexes were induced by either electrical stimulation of the right splanchnic nerve or application of 10 μg/ml of bradykinin to the gallbladder. Blood flows were measured using colored microspheres or the Transonic flow meter system. Sympathetic efferent activity was recorded from the left splanchnic, inferior cardiac, and tibial nerves. Stimulation of visceral afferents decreased significantly blood flows in the celiac (from 49 ± 4 to 25 ± 3 ml/min) and superior mesenteric (from 35 ± 4 to 23 ± 2 ml/min) arteries, and the vascular resistance in the splanchnic bed was profoundly increased. Consistently, stimulation of visceral afferents decreased tissue blood flows in the splanchnic organs. By contrast, activation of visceral afferents increased significantly blood flows in the coronary artery and portal vein but did not alter the vascular resistance of the femoral artery. Furthermore, stimulation of visceral afferents increased significantly sympathetic efferent activity in the splanchnic (182 ± 44%) but not in the inferior cardiac and tibial nerves. Therefore, this study provides substantial new evidence that stimulation of abdominal visceral afferents differentially induces sympathetic outflow to the splanchnic vascular bed.

Defensive peripersonal space: the blink reflex evoked by hand stimulation is increased when the hand is near the face

2012 ◽  
Vol 107 (3) ◽  
pp. 880-889 ◽  
Author(s):  
C. F. Sambo ◽  
M. Liang ◽  
G. Cruccu ◽  
G. D. Iannetti
Keyword(s):  
Electrical Stimulation ◽  
Brain Stem ◽  
Median Nerve ◽  
Safety Margin ◽  
Peripersonal Space ◽  
Blink Reflex ◽  
Hand Position ◽  
Electromyographic Activity ◽  
The Face ◽  
Stimulation Of

Electrical stimulation of the median nerve at the wrist may elicit a blink reflex [hand blink reflex (HBR)] mediated by a neural circuit at brain stem level. As, in a Sherringtonian sense, the blink reflex is a defensive response, in a series of experiments we tested, in healthy volunteers, whether and how the HBR is modulated by the proximity of the stimulated hand to the face. Electromyographic activity was recorded from the orbicularis oculi, bilaterally. We observed that the HBR is enhanced when the stimulated hand is inside the peripersonal space of the face, compared with when it is outside, irrespective of whether the proximity of the hand to the face is manipulated by changing the position of the arm ( experiment 1) or by rotating the head while keeping the arm position constant ( experiment 3). Experiment 2 showed that such HBR enhancement has similar magnitude when the participants have their eyes closed. Experiments 4 and 5 showed, respectively, that the blink reflex elicited by the electrical stimulation of the supraorbital nerve, as well as the N20 wave of the somatosensory evoked potentials elicited by the median nerve stimulation, are entirely unaffected by hand position. Taken together, our results provide compelling evidence that the brain stem circuits mediating the HBR in humans undergo tonic and selective top-down modulation from higher order cortical areas responsible for encoding the location of somatosensory stimuli in external space coordinates. These findings support the existence of a “defensive” peripersonal space, representing a safety margin advantageous for survival.

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.

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