scholarly journals Electroacupuncture Improved the Function of Myocardial Ischemia Involved in the Hippocampus-Paraventricular Nucleus-Sympathetic Nerve Pathway

2018 ◽  
Vol 2018 ◽  
pp. 1-13 ◽  
Author(s):  
Shuai Cui ◽  
Yiping Zhou ◽  
Shengbing Wu ◽  
Jian Cao ◽  
Guoqi Zhu ◽  
...  
Keyword(s):  
Myocardial Ischemia ◽  
Paraventricular Nucleus ◽  
Sympathetic Nerve ◽  
Discharge Frequency ◽  
Rate Pressure Product ◽  
Sprague Dawley ◽  
Heart Meridian ◽  
Lower Discharge ◽  
Total Discharge ◽  
Nerve Discharge

We investigated the hippocampus-paraventricular nucleus- (PVN-) sympathetic nerve pathway in electroacupuncture (EA) at the heart meridian for the treatment of myocardial ischemia by observing PVN neuronal discharge, sympathetic nerve discharge, and hemodynamics parameters. Sprague Dawley (SD) rats were equally divided into four groups: Sham, Model, Model + EA, and Model + EA + Lesion. The model rat was established by ligating the left anterior descending branch of the coronary artery. Changes in the sympathetic nerve discharge and hemodynamic parameters were observed. The Model + EA exhibited a significantly lower discharge frequency of PVN neurons compared with the Model. The Model + EA + Lesion had a significantly higher discharge frequency compared with the Model + EA. The total discharge frequency of PVN neurons and interneurons were positively correlated with the sympathetic nerve discharge. The total discharge frequency of PVN neurons was positively correlated with heart rate (HR) and negatively correlated with mean arterial pressure (MAP) and rate pressure product (RPP). The discharge frequency of interneurons was positively correlated with HR and negatively correlated with MAP and RPP. The hippocampus-PVN-sympathetic nerve pathway is involved in electroacupuncture at the heart meridian and interneurons are the key neurons in PVNs.

Paraventricular nucleus bicuculline alters frequency components of sympathetic nerve discharge bursts

2001 ◽  
Vol 281 (3) ◽  
pp. H1233-H1241 ◽  
Author(s):  
Michael J. Kenney ◽  
Mark L. Weiss ◽  
Kaushik P. Patel ◽  
Yan Wang ◽  
Richard J. Fels
Keyword(s):  
Paraventricular Nucleus ◽  
Sympathetic Nerve ◽  
Cardiac Cycle ◽  
Low Frequency ◽  
Sympathetic Nerves ◽  
Receptor Antagonism ◽  
Gaba Agonist ◽  
Frequency Components ◽  
Induced Changes ◽  
Nerve Discharge

Autospectral and coherence analyses were used to determine the effect of paraventricular nucleus (PVN) GABAA receptor antagonism [microinfusion or microinjections of bicuculline methiodide (BMI) 100 pmoles] on sympathetic nerve discharge (SND) frequency components (bursting pattern and relationships between discharges in regionally selective nerves) in α-chloralose-anesthetized rats. SND was recorded from the renal, splenic, and lumbar nerves. The following observations were made. First, PVN BMI microinjections, but not PVN saline or cortical BMI microinjections, transformed the cardiac-related SND bursting pattern in baroreceptor-innervated rats to one characterized by the presence of low-frequency bursts not synchronized to the cardiac cycle or phrenic nerve discharge bursts. Second, SND pattern changes were similar in the renal, splenic, and lumbar nerves, and peak coherence values relating low-frequency bursts in sympathetic nerve pairs (renal-splenic, renal-lumbar, and splenic-lumbar) were significantly increased from preinjection control after PVN BMI microinjection. Third, PVN BMI microinjections significantly increased the coupling between low-frequency SND bursts in baroreceptor-denervated rats. Finally, PVN BMI-induced changes in the SND bursting pattern were not observed after PVN pretreatment with muscimol (GABA agonist, 1 nmole). We conclude that PVN GABAA receptor antagonism profoundly alters the frequency components in sympathetic nerves.

The sympathoinhibitory effects of systemic cholecystokinin are dependent on neurons in the caudal ventrolateral medulla in the rat

2006 ◽  
Vol 291 (5) ◽  
pp. R1390-R1398 ◽  
Author(s):  
D. M. Sartor ◽  
A. J. M. Verberne
Keyword(s):  
Sympathetic Nerve ◽  
Excitatory Amino Acid ◽  
Inhibitory Effect ◽  
Reflex Response ◽  
Ventrolateral Medulla ◽  
Gastrointestinal Hormone ◽  
Sprague Dawley ◽  
Neuronal Inhibition ◽  
Before And After ◽  
Nerve Discharge

The gastrointestinal hormone CCK inhibits a subset of presympathetic neurons in the rostroventrolateral medulla (RVLM) that may be responsible for driving the sympathetic vasomotor outflow to the gastrointestinal circulation. We tested the hypothesis that the central neurocircuitry of this novel sympathoinhibitory reflex involves a relay in the caudal ventrolateral medullary (CVLM) depressor area. Blood pressure and greater splanchnic sympathetic nerve discharge (SSND) or lumbar sympathetic nerve discharge (LSND) were monitored in anesthetised, paralyzed male Sprague-Dawley rats. The effects of phenylephrine (PE, 10 μg/kg iv; baroreflex activation), phenylbiguanide (PBG, 10 μg/kg iv; von Bezold-Jarisch reflex) and CCK (4 or 8 μg/kg iv) on SSND or LSND, were tested before and after bilateral injection of 50–100 nl of the GABAA agonist muscimol (1.75 mM; n = 6, SSND; n = 7, LSND) or the excitatory amino acid antagonist kynurenate (55 mM; n = 7, SSND) into the CVLM. PE and PBG elicited splanchnic and lumbar sympathoinhibitory responses that were abolished by bilateral muscimol or kynurenate injection into the CVLM. Similarly, the inhibitory effect of CCK on SSND was abolished after neuronal inhibition within the CVLM. In contrast, CCK-evoked lumbar sympathoexcitation was accentuated following bilateral CVLM inhibition. In control experiments ( n = 7), these agents were injected outside the CVLM and had no effect on splanchnic sympathoinhibitory responses to PE, PBG, and CCK. In conclusion, neurons in the CVLM are necessary for the splanchnic but not lumbar sympathetic vasomotor reflex response to CCK. This strengthens the view that subpopulations of RVLM neurons supply sympathetic vasomotor outflow to specific vascular territories.

scholarly journals Electroacupuncture Ameliorates the Coronary Occlusion Related Tachycardia and Hypotension in Acute Rat Myocardial Ischemia Model: Potential Role of Hippocampus

2015 ◽  
Vol 2015 ◽  
pp. 1-8 ◽  
Author(s):  
Shengbing Wu ◽  
Jian Cao ◽  
Tianning Zhang ◽  
Yiping Zhou ◽  
Keming Wang ◽  
...  
Keyword(s):  
Myocardial Ischemia ◽  
Neuronal Activity ◽  
Coronary Occlusion ◽  
Heart Function ◽  
Rate Pressure Product ◽  
Ca1 Region ◽  
Cell Counts ◽  
Heart Meridian ◽  
Fos Expression ◽  
Ca1 Area

Mechanisms for electroacupuncture (EA) in disease treatments are still enigmatic. Here, we studied whether hippocampus was involved in the protection of EA stimulation on myocardial ischemia injury. Acute myocardial ischemia (AMI) model was produced. EA stimulation at heart meridian from Shenmen (HT7) to Tongli (HT5) was applied to rats 3 times a day for continuous three days. Coronary occlusion related tachycardia and hypotension, indicated by heart rate, mean arterial pressure, and rate pressure product, were apparently impaired after AMI injury. By contrast, EA stimulating could ameliorate the impairments of heart function (P<0.05). Interestingly, lesion of CA1 region of hippocampus abolished the protection of EA. Neuronal activity in CA1 area was affected by AMI. As evidenced, cell counts, cell types, and frequency of the discharged neurons were facilitated after AMI, while EA stimulation attenuated the abnormalities. Furthermore, c-Fos expression was significantly facilitated in CA1 area after AMI, which was reduced by EA stimulation. Correlations were established between c-Fos expression and cell counts of discharged neurons, as well as between heart function and cell counts of discharged neurons. Taken together, EA stimulation at heart meridian protects against heart dysfunction induced by AMI possibly through suppressing the neuronal activity in CA1 region.

scholarly journals Cardiac spinal deafferentation reduces the susceptibility to sustained ventricular tachycardia in conscious rats

2011 ◽  
Vol 301 (3) ◽  
pp. R775-R782 ◽  
Author(s):  
Heidi L. Lujan ◽  
Sandhya Krishnan ◽  
Stephen E. DiCarlo
Keyword(s):  
Ventricular Tachycardia ◽  
Myocardial Ischemia ◽  
Ventricular Arrhythmias ◽  
Clinical Work ◽  
Sustained Ventricular Tachycardia ◽  
Rate Pressure Product ◽  
Sprague Dawley ◽  
Metabolic Demand ◽  
Conscious Rats ◽  
Spinal Afferents

The response to myocardial ischemia is complex and involves the cardio-cardiac sympathetic reflex. Specifically, cardiac spinal (sympathetic) afferents are excited by ischemic metabolites and elicit an excitatory sympathetic reflex, which plays a major role in the genesis of ventricular arrhythmias. For example, brief myocardial ischemia leads to ATP release, which activates cardiac spinal afferents through stimulation of P2 receptors. Clinical work with patients and preclinical work with animals document that disruption of this reflex protects against ischemia-induced ventricular arrhythmias. However, the role of afferent signals in the initiation of sustained ventricular tachycardia has not been investigated. Therefore, we tested the hypothesis that cardiac spinal deafferentation reduces the susceptibility to sustained ventricular tachycardia in adult (12–15 wk of age), conscious, male Sprague-Dawley rats. To test this hypothesis, the susceptibility to ventricular tachyarrhythmias produced by occlusion of the left main coronary artery was determined in two groups of conscious rats: 1) deafferentation (bilateral excision of the T1-T5 dorsal root ganglia) and 2) control (sham deafferentation). The ventricular arrhythmia threshold (VAT) was defined as the time from coronary occlusion to sustained ventricular tachycardia resulting in a reduction in arterial pressure. Results document a significantly higher VAT in the deafferentation group (7.0 ± 0.7 min) relative to control (4.3 ± 0.3 min) rats. The decreased susceptibility to tachyarrhythmias with deafferentation was associated with a reduced cardiac metabolic demand (lower rate-pressure product and ST segment elevation) during ischemia.

Local Ionotropic Glutamate Receptors are Required to Trigger and Sustain Ramping of Sympathetic Nerve Activity by Hypothalamic Paraventricular Nucleus TNFα

2021 ◽  
Author(s):  
Aline A. Mourao ◽  
Caroline G. Shimoura ◽  
Mary Ann Andrade ◽  
Tamara T. Truong ◽  
Gustavo R. Pedrino ◽  
...  
Keyword(s):  
Nmda Receptors ◽  
Glutamate Receptors ◽  
Paraventricular Nucleus ◽  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Hypothalamic Paraventricular Nucleus ◽  
Ionotropic Glutamate Receptors ◽  
Sprague Dawley ◽  
Nerve Activity ◽  
Necrosis Factor Alpha

Tumor necrosis factor alpha (TNFa) in the hypothalamic paraventricular nucleus (PVN) contributes to increased sympathetic nerve activity (SNA) in cardiovascular disease models, but mechanisms are incompletely understood. As previously reported, bilateral PVN TNFa (0.6 pmol, 50 nL) induced acute ramping of splanchnic SNA (SSNA) that averaged +64 ± 7% after 60 min and +109 ± 17% after 120 min (P<0.0001, n=10). Given that TNFa can rapidly strengthen glutamatergic transmission, we hypothesized that progressive activation of ionotropic glutamate receptors is critically involved. Compared to vehicle (n=5), prior blockade of PVN AMPA or NMDA receptors in anesthetized (urethane/α-chloralose) adult male Sprague-Dawley rats dose-dependently (ED50: NBQX, 2.48 nmol; APV, 12.33 nmol), but incompletely (Emax: NBQX, 64%; APV, 41%) attenuated TNFα-induced SSNA ramping (n=5/dose). By contrast, combined receptor blockade prevented ramping (1.3 ± 2.1%, P<0.0001, n=5). Whereas separate blockade of PVN AMPA or NMDA receptors (n=5/group) had little effect on continued SSNA ramping when performed 60 min after TNFα injection, combined blockade (n=5) or PVN inhibition with the GABA-A receptor agonist muscimol (n=5) effectively stalled, without reversing, the SSNA ramp. Notably, PVN TNFα increased local TNFα immunofluorescence after 120, but not 60 min. Findings indicate that AMPA and NMDA receptors each contribute to SSNA ramping to PVN TNFα, and that their collective availability and ongoing activity are required to initiate and sustain the ramping response. We conclude that acute sympathetic activation by PVN TNFα involves progressive local glutamatergic excitation that recruits downstream neurons capable of maintaining heightened SSNA, but incapable of sustaining SSNA ramping.

Medullary lateral tegmental field: control of respiratory rate and vagal lung inflation afferent influences on sympathetic nerve discharge

2005 ◽  
Vol 288 (5) ◽  
pp. R1396-R1410 ◽  
Author(s):  
Shaun W. Phillips ◽  
Gerard L. Gebber ◽  
Susan M. Barman
Keyword(s):  
Respiratory Rate ◽  
Sympathetic Nerve ◽  
Artificial Ventilation ◽  
Critical Role ◽  
Lung Inflation ◽  
Chemical Inactivation ◽  
A Value ◽  
Relationship Of ◽  
The Relationship ◽  
Nerve Discharge

We used spectral analysis and event-triggered averaging to determine the effects of chemical inactivation of the medullary lateral tegmental field (LTF) on 1) the relationship of intratracheal pressure (ITP, an index of vagal lung inflation afferent activity) to sympathetic nerve discharge (SND) and phrenic nerve activity (PNA) and 2) central respiratory rate in paralyzed, artificially ventilated dial-urethane-anesthetized cats. ITP-SND coherence value at the frequency of artificial ventilation was significantly ( P < 0.05; n = 18) reduced from 0.73 ± 0.04 (mean ± SE) to 0.24 ± 0.04 after bilateral microinjection of muscimol into the LTF. Central respiratory rate was unexpectedly increased in 12 of these experiments (0.28 ± 0.03 vs. 0.95 ± 0.25 Hz). The ITP-PNA coherence value was variably affected by chemical inactivation of the LTF. It was unchanged when central respiratory rate was also not altered, decreased when respiratory rate was increased above the rate of artificial ventilation, and increased when respiratory rate was raised from a value below the rate of artificial ventilation to the same frequency as the ventilator. Chemical inactivation of the LTF increased central respiratory rate in four of six vagotomized cats but did not significantly affect the PNA-SND coherence value. These data demonstrate that the LTF 1) plays a critical role in mediating the effects of vagal lung inflation afferents on SND but not PNA, 2) helps maintain central respiratory rate in the physiological range, but 3) is not involved in the coupling of central respiratory and sympathetic circuits.

scholarly journals Differential Effects of Refeeding on Melanocortin-Responsive Neurons in the Hypothalamic Paraventricular Nucleus

Endocrinology ◽  
2008 ◽  
Vol 149 (9) ◽  
pp. 4329-4335 ◽  
Author(s):  
Edith Sánchez ◽  
Praful S. Singru ◽  
Runa Acharya ◽  
Monica Bodria ◽  
Csaba Fekete ◽  
...  
Keyword(s):  
Gene Expression ◽  
Paraventricular Nucleus ◽  
Hypothalamic Paraventricular Nucleus ◽  
Mrna Levels ◽  
Sprague Dawley ◽  
Early Action ◽  
Sprague Dawley Rats ◽  
Melanocortin Signaling ◽  
Agouti Related Protein ◽  
Serum Tsh

To explore the effect of refeeding on recovery of TRH gene expression in the hypothalamic paraventricular nucleus (PVN) and its correlation with the feeding-related neuropeptides in the arcuate nucleus (ARC), c-fos immunoreactivity (IR) in the PVN and ARC 2 h after refeeding and hypothalamic TRH, neuropeptide Y (NPY) and agouti-related protein (AGRP) mRNA levels 4, 12, and 24 h after refeeding were studied in Sprague-Dawley rats subjected to prolonged fasting. Despite rapid reactivation of proopiomelanocortin neurons by refeeding as demonstrated by c-fos IR in ARC α-MSH-IR neurons and ventral parvocellular subdivision PVN neurons, c-fos IR was present in only 9.7 ± 1.1% hypophysiotropic TRH neurons. Serum TSH levels remained suppressed 4 and 12 h after the start of refeeding, returning to fed levels after 24 h. Fasting reduced TRH mRNA compared with fed animals, and similar to TSH, remained suppressed at 4 and 12 h after refeeding, returning toward normal at 24 h. AGRP and NPY gene expression in the ARC were markedly elevated in fasting rats, AGRP mRNA returning to baseline levels 12 h after refeeding and NPY mRNA remaining persistently elevated even at 24 h. These data raise the possibility that refeeding-induced activation of melanocortin signaling exerts differential actions on its target neurons in the PVN, an early action directed at neurons that may be involved in satiety, and a later action on hypophysiotropic TRH neurons involved in energy expenditure, potentially mediated by sustained elevations in AGRP and NPY. This response may be an important homeostatic mechanism to allow replenishment of depleted energy stores associated with fasting.

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