Medial vestibular nucleus mediates the cardiorespiratory responses to fastigial nuclear activation and hypercapnia

2004 ◽  
Vol 97 (3) ◽  
pp. 835-842 ◽  
Author(s):  
Joseph P. Hernandez ◽  
Fadi Xu ◽  
Donald T. Frazier
Keyword(s):  
Electrical Stimulation ◽  
Vestibular Nucleus ◽  
Ibotenic Acid ◽  
Medial Vestibular Nucleus ◽  
Ventilatory Responses ◽  
Cardiorespiratory Responses ◽  
Before And After ◽  
Bilateral Lesions ◽  
Spontaneously Breathing ◽  
Stimulation Of

Electrical stimulation of the cerebellar fastigial nucleus (FN) evokes hyperventilation and hypertension responses that are similar to those induced by stimulation of the medial region of the vestibular nucleus (VNM). Because there are mutual projections between these two nuclei morphologically, we hypothesized that the FN-mediated cardiorespiratory responses were related to the integrity of the VNM. Experiments were conducted on 21 anesthetized, tracheotomized, and spontaneously breathing rats. Electrical stimulation (∼10 s) of the FN was used to evoke cardiorespiratory responses, and the same stimulus was repeated 30–45 min after bilateral lesions of the VNM by local microinjection of ibotenic acid (100 mM, 100 nl). We found that FN stimulation-induced hyperventilation and hypertension were attenuated significantly by the lesions. The role of the VNM in the ventilatory responses to chemical challenges was subsequently defined. The animals were exposed to hypercapnia (10% CO2) and hypoxia (10% O2) for 1–2 min randomly before and after VNM lesions. The results showed that VNM lesions significantly attenuated the cardiorespiratory responses to hypercapnia but not to hypoxia, with little effect on baseline respiratory variables. These findings suggest that the VNM is required for full expression of the cardiorespiratory responses to electrical stimulation of the FN as well as to hypercapnia. However, neurons within the VNM do not appear to be critical for maintaining eupneic breathing and the cardiorespiratory responses to hypoxia.

Fastigial nucleus-mediated respiratory responses depend on the medullary gigantocellular nucleus

2001 ◽  
Vol 91 (4) ◽  
pp. 1713-1722 ◽  
Author(s):  
Fadi Xu ◽  
Tongrong Zhou ◽  
Tonya Gibson ◽  
Donald T. Frazier
Keyword(s):  
Electrical Stimulation ◽  
Ibotenic Acid ◽  
Major Effect ◽  
Fastigial Nucleus ◽  
Respiratory Response ◽  
The Right ◽  
Spontaneously Breathing ◽  
Respiratory Responses ◽  
Gigantocellular Nucleus ◽  
Stimulation Of

Electrical stimulation of the rostral fastigial nucleus (FNr) alters respiration via activation of local neurons. We hypothesized that this FNr-mediated respiratory response was dependent on the integrity of the nucleus gigantocellularis of the medulla (NGC). Electrical stimulation of the FNr in 15 anesthetized and tracheotomized spontaneously breathing rats significantly altered ventilation by 35.2 ± 11.0% ( P < 0.01) with the major effect being excitatory (78%). This respiratory response did not significantly differ from control after lesions of the NGC via bilateral microinjection of kainic or ibotenic acid (4.5 ± 1.9%; P > 0.05) but persisted in sham controls. Eight other rats, in which horseradish peroxidase (HRP) solution was previously microinjected into the left NGC, served as nonstimulation controls or were exposed to either 15-min repeated electrical stimulation of the right FNr or hypercapnia for 90 min. Histochemical and immunocytochemical data showed that the right FNr contained clustered HRP-labeled neurons, most of which were double labeled with c-Fos immunoreactivity in both electrically and CO2-stimulated rats. We conclude that the NGC receives monosynaptic FNr inputs and is required for fully expressing FNr-mediated respiratory responses.

Hyperventilation evoked by activation of the vicinity of the caudal inferior olivary nucleus depends on the fastigial nucleus in anesthetized rats

2008 ◽  
Vol 104 (5) ◽  
pp. 1351-1358 ◽  
Author(s):  
Jianguo Zhuang ◽  
Fadi Xu ◽  
Donald T. Frazier
Keyword(s):  
Electrical Stimulation ◽  
Chemical Activation ◽  
Ibotenic Acid ◽  
Fastigial Nucleus ◽  
Inferior Olivary Nucleus ◽  
Ventilatory Responses ◽  
Respiratory Modulation ◽  
Spontaneously Breathing ◽  
Inferior Olivary ◽  
Olivary Nucleus

Several studies have demonstrated that cerebellar deep nuclei, particularly the rostral fastigial nucleus (FNr), are involved in respiratory modulation. These nuclei receive inputs from the contralateral caudal inferior olivary nuclei of the medulla. The objectives of this study were to determine whether electrical and chemical activation of the vicinity of the caudal inferior olivary nuclei (vIOc) affected respiration and, if true, whether the FNr was involved in the vIOc stimulation-evoked ventilatory responses. Experiments were conducted in 30 anesthetized and spontaneously breathing rats. Our results showed that 1) electrical (25 or 100 μA at 10 or 20 Hz for 10 s) and chemical (1 or 100 mM, 25–50 nl N-methyl-d-aspartate) stimulation of the vIOc augmented ventilation predominantly via increasing tidal volume; 2) the responses to the electrical stimulation were almost eliminated by lesion of the contralateral FNr via microinjection of ibotenic acid; and 3) the respiratory responses to electrical stimulation in the vicinity of the rostral IO were 65–70% smaller compared with that evoked by vIOc stimulation. These findings strongly suggest that vIOc neurons play a significant role in modulation of respiratory activity, largely depending on their projections to the FNr.

Cross-talk along gastrointestinal tract during electrical stimulation: effects and mechanisms of gastric/colonic stimulation on rectal tone in dogs

2005 ◽  
Vol 288 (6) ◽  
pp. G1195-G1198 ◽  
Author(s):  
Shi Liu ◽  
Lijie Wang ◽  
J. D. Z. Chen
Keyword(s):  
Electrical Stimulation ◽  
Inhibitory Effect ◽  
Adrenergic Blockade ◽  
Rectal Compliance ◽  
Rectal Tone ◽  
Before And After ◽  
Sensory Functions ◽  
Sympathetic Pathway ◽  
Colonic Electrical Stimulation ◽  
Stimulation Of

Gastric electrical stimulation (GES) has been shown to alter motor and sensory functions of the stomach. However, its effects on other organs of the gut have rarely been investigated. The study was performed in 12 dogs implanted with two pairs of electrodes, one on the serosa of the stomach and the other on the colon. The study was composed of two experiments. Experiment 1 was designed to study the effects of GES on rectal tone and compliance in nine dogs compared with colonic electrical stimulation (CES). Rectal tone and compliance were assessed before and after GES or CES. Experiment 2 was performed to study the involvement of sympathetic pathway in 8 of the 12 dogs. The rectal tone was recorded for 30–40 min at baseline and 20 min after intravenous guanethidine. GES or CES was given for 20 min 20 min after the initiation of the infusion. It was found that both GES and CES reduced rectal tone with comparable potency. Rectal compliance was altered neither with GES, nor with CES. The inhibitory effect of GES but not CES on rectal tone was abolished by an adrenergic blockade, guanethidine. GES inhibited rectal tone with a comparable potency with CES but did not alter rectal compliance. The inhibitory effect of GES on rectal tone is mediated by the sympathetic pathway. It should be noted that electrical stimulation of one organ of the gut may have a beneficial or adverse effect on another organ of the gut.

Hyperglycemia induced by electrical stimulation of lateral part of dorsal parabrachial nucleus

1988 ◽  
Vol 254 (4) ◽  
pp. E468-E475
Author(s):  
T. Fujiwara ◽  
K. Nagai ◽  
S. Takagi ◽  
H. Nakagawa
Keyword(s):  
Electrical Stimulation ◽  
Glucagon Secretion ◽  
Light Period ◽  
Parabrachial Nucleus ◽  
Lateral Part ◽  
Beta Adrenergic ◽  
Adrenergic Mechanism ◽  
Adrenergic Blocker ◽  
Bilateral Lesions ◽  
Stimulation Of

Electrical stimulation of the lateral part of the dorsal parabrachial nucleus (PBD) induces hyperglycemia by enhancing glucagon secretion and suppressing insulin secretion in rats. The mechanism of this effect in the light period was examined by use of blockers of the autonomic nervous system. Hexamethonium, a ganglion blocker, and propranolol, a beta-adrenergic blocker, markedly inhibited the hyperglycemic response to stimulation of the lateral part of the PBD (LPBD). In contrast, phenoxybenzamine, an alpha-adrenergic blocker, and atropine methylnitrate, a muscarinic blocker, had no effect. Because previous studies showed that bilateral lesions of the suprachiasmatic nucleus (SCN) eliminated hyperglycemia induced by intracranial injection of 2-deoxy-D-glucose and that blinding largely suppressed the hyperglycemia, the effects of these two treatments on hyperglycemia induced by electrical stimulation of the LPBD were examined. SCN lesions abolished the hyperglycemic response but did not affect the hyperglucagonemic response. Results 4 wk after orbital enucleation were similar to those after SCN lesions. These findings suggest that the SCN and a beta-adrenergic mechanism are involved in the hyperglycemic response to LPBD stimulation.

Electrical Stimulation of the Guinea Pig Cochlea

1987 ◽  
Vol 96 (4) ◽  
pp. 349-361 ◽  
Author(s):  
Mark J. Maslan ◽  
Josef M. Miller
Keyword(s):  
Electrical Stimulation ◽  
Low Frequency ◽  
Damage Threshold ◽  
Auditory Brainstem ◽  
Cochlear Prosthesis ◽  
Before And After ◽  
Auditory Brainstem Evoked Responses ◽  
Straight Lines ◽  
Histopathologic Findings ◽  
Stimulation Of

As a result of practical considerations, histopathologic findings of the temporal bone in humans with cochlear prosthesis implants have been limited. This project attempts to better define safe parameters of electrical stimulation of the inner ear and compare the safe limits of intracochlear vs. extracochlear stimulation sites. Guinea pigs were implanted with single electrodes either on the promontory or in the scala tympani and were stimulated relative to a remote indifferent for 12 hours distributed over a 4-week period. Electrical auditory brainstem evoked responses (EABRs) were tested before and after each of four 3-hour stimulation sessions. Six weeks after implantation, the animals were killed, and their cochleas were examined under the scanning electron microscope. Intracochlear electrodes exhibited thresholds for damage well below one half of that found for most extracochlear stimulation sites. The function-relating damage threshold (in amperes) to frequency of intracochlear stimulation is represented by two straight lines, with an intercept of 1 kHz. The low-frequency limb exhibited a slope of 3 to 4 dB/octave, whereas the high-frequency limb exhibited a slope of 9 to 10 dB/octave. Extracochlear results were too variable to permit speculation. Changes in EABRs were only variably related to histopathologic findings.

Effect of baroreceptor activity on ventilatory response to chemoreceptor stimulation

1975 ◽  
Vol 39 (3) ◽  
pp. 411-416 ◽  
Author(s):  
D. Heistad ◽  
F. M. Abboud ◽  
A. L. Mark ◽  
P. G. Schmid
Keyword(s):  
Arterial Pressure ◽  
Ventilatory Response ◽  
Carotid Bifurcation ◽  
Carotid Chemoreceptors ◽  
Ventilatory Responses ◽  
Before And After ◽  
Cervical Vagotomy ◽  
Anesthetized Dogs ◽  
Baroreceptor Activation ◽  
Stimulation Of

This study tested the hypothesis that ventilatory responses to chemoreceptor stimulation are affected by the level of arterial pressure and degree of baroreceptor activation. Carotid chemoreceptors were stimulated by injection of nicotine into the common carotid artery of anesthetized dogs. Arterial pressure was reduced by bleeding the animals and raised by transient occlusion of the abdominal aorta. The results indicate that ventilatory responses to chemoreceptor stimulation were augmented by hypotension and depressed by hypertension. In additional studies we excluded the possibility that the findings were produced by a direct effect of changes in arterial pressure on chemoreceptors. Both carotid bifurcations were perfused at constant flow. In one carotid bifurcation, perfusion pressure was raised to stimulate carotid sinus baroreceptors. In the other carotid bifurcation, pressure was constant and nicotine was injected to stimulate carotid chemoreceptors. Stimulation of baroreceptors on one side attenuated the ventilatory response to stimulation of contralateral chemoreceptors. This inhibition was observed before and after bilateral cervical vagotomy. We conclude that there is a major central interaction between baroreceptor and chemoreceptor reflexes so that changes in baroreceptor activity modulate ventilatory responses to chemoreceptor stimulation.

Metoclopramide blocks the phenyl diguanide and 5-hydroxytryptamine induced cardiorespiratory reflexes in cats and dogs

1988 ◽  
Vol 66 (6) ◽  
pp. 776-782 ◽  
Author(s):  
K. Ravi ◽  
N. B. Dev
Keyword(s):  
Left Atrial ◽  
Right Atrial ◽  
Excitatory Effect ◽  
Reflex Responses ◽  
Cardiorespiratory Responses ◽  
C Fiber ◽  
Spontaneously Breathing ◽  
Cardiac Receptors ◽  
Sensory Endings ◽  
Stimulation Of

The effects of metoclopramide on the reflex cardiorespiratory responses elicited by stimulation of pulmonary J receptors by right atrial injections of phenyl diguanide (PDG), 5-hydroxytryptamine (5-HT), and capsaicin were investigated in anesthetized spontaneously breathing cats. It was observed that while metoclopramide blocked the responses to PDG and 5-HT injections, it spared the responses to capsaicin injections. Similarly, metoclopramide was without effect on the reflex responses following activation of pulmonary C-fiber receptors (J receptors) by capsaicin in dogs. Reflex cardiorespiratory responses elicited by left atrial injections of PDG and 5-HT, owing to stimulation of cardiac receptors in cats, and reflex responses following right or left atrial injections of PDG and 5-HT, owing to stimulation of aortic chemoreceptors in dogs, were also found to be blocked by metoclopramide. Afferent impulse activity recorded from aortic chemoreceptors of dogs showed that while metoclopramide depressed the excitatory effect of PDG and 5-HT on them, it did not produce any effect on their spontaneous activity and their excitation by hypoxia. The results from the reflex studies show that metoclopramide is capable of antagonizing the reflex responses following the activation of the cardiopulmonary afferents by PDG and 5-HT. Based on the effects on aortic chemoreceptor afferents, it is suggested that PDG, 5-HT, and metoclopramide may be acting upon the regenerative region of the sensory endings.

Effects of neck muscle activities during rhythmic jaw movements by stimulation of the medial vestibular nucleus in rats

2011 ◽  
Vol 86 (5-6) ◽  
pp. 447-453 ◽  
Author(s):  
Yoshihide Satoh ◽  
Eriko Yajima ◽  
Yasuhiro Nagamine ◽  
Ken’Ichi Ishizuka ◽  
Toshiki Murakami
Keyword(s):  
Vestibular Nucleus ◽  
Medial Vestibular Nucleus ◽  
Neck Muscle ◽  
Jaw Movements ◽  
Stimulation Of

Central GABAergic mechanisms are involved in apnea induced by SLN stimulation in piglets

2001 ◽  
Vol 90 (4) ◽  
pp. 1570-1576 ◽  
Author(s):  
Jalal M. Abu-Shaweesh ◽  
Ismail A. Dreshaj ◽  
Musa A. Haxhiu ◽  
Richard J. Martin
Keyword(s):  
Electrical Stimulation ◽  
Phrenic Nerve ◽  
Superior Laryngeal Nerve ◽  
Laryngeal Nerve ◽  
Receptor Blocker ◽  
Inspiratory Time ◽  
Before And After ◽  
Four Levels ◽  
Stimulation Of

Stimulation of the superior laryngeal nerve (SLN) results in apnea in animals of different species, the mechanism of which is not known. We studied the effect of the GABAA receptor blocker bicuculline, given intravenously and intracisternally, on apnea induced by SLN stimulation. Eighteen 5- to 10-day-old piglets were studied: bicuculline was administered intravenously to nine animals and intracisternally to nine animals. The animals were anesthetized and then decerebrated, vagotomized, ventilated, and paralyzed. The phrenic nerve responses to four levels of electrical SLN stimulation were measured before and after bicuculline. SLN stimulation caused a significant decrease in phrenic nerve amplitude, phrenic nerve frequency, minute phrenic activity, and inspiratory time ( P < 0.01) that was proportional to the level of electrical stimulation. Increased levels of stimulation were more likely to induce apnea during stimulation that often persisted beyond cessation of the stimulus. Bicuculline, administered intravenously or intracisternally, decreased the SLN stimulation-induced decrease in phrenic nerve amplitude, minute phrenic activity, and phrenic nerve frequency ( P < 0.05). Bicuculline also reduced SLN-induced apnea and duration of poststimulation apnea ( P < 0.05). We conclude that centrally mediated GABAergic pathways are involved in laryngeal stimulation-induced apnea.

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