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.

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 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)

Firing pattern and location of respiratory neurons in cat medullary raphe nuclei

1993 ◽  
Vol 161 (2) ◽  
pp. 149-152 ◽  
Author(s):  
Masae Hosogai ◽  
Satoshi Matsuo ◽  
Shozo Nakao
Keyword(s):  
Firing Pattern ◽  
Raphe Nuclei ◽  
Respiratory Neurons ◽  
Medullary Raphe ◽  
Raphé Nuclei

The role of the medullary raphe nuclei in regulation of cholinergic outflow to the airways

1998 ◽  
Vol 69 (1) ◽  
pp. 64-71 ◽  
Author(s):  
M.A. Haxhiu ◽  
B. Erokwu ◽  
V. Bhardwaj ◽  
I.A. Dreshaj
Keyword(s):  
Raphe Nuclei ◽  
Medullary Raphe ◽  
Raphé Nuclei

scholarly journals Quipazine Elicits Swallowing in the Arterially Perfused Rat Preparation: A Role for Medullary Raphe Nuclei?

2020 ◽  
Vol 21 (14) ◽  
pp. 5120
Author(s):  
Victor Bergé-Laval ◽  
Christian Gestreau
Keyword(s):  
Therapeutic Option ◽  
Experimental Studies ◽  
Raphe Nuclei ◽  
Excitatory Effect ◽  
Motor Patterns ◽  
Systemic Injection ◽  
Medullary Raphe ◽  
Raphé Nuclei ◽  
Stimulation Of

Pharmacological neuromodulation of swallowing may represent a promising therapeutic option to treat dysphagia. Previous studies suggested a serotonergic control of swallowing, but mechanisms remain poorly understood. Here, we investigated the effects of the serotonergic agonist quipazine on swallowing, using the arterially perfused working heart-brainstem (in situ) preparation in rats. Systemic injection of quipazine produced single swallows with motor patterns and swallow-breathing coordination similar to spontaneous swallows, and increased swallow rate with moderate changes in cardiorespiratory functions. Methysergide, a 5-HT2 receptor antagonist, blocked the excitatory effect of quipazine on swallowing, but had no effect on spontaneous swallow rate. Microinjections of quipazine in the nucleus of the solitary tract were without effect. In contrast, similar injections in caudal medullary raphe nuclei increased swallow rate without changes in cardiorespiratory parameters. Thus, quipazine may exert an excitatory effect on raphe neurons via stimulation of 5-HT2A receptors, leading to increased excitability of the swallowing network. In conclusion, we suggest that pharmacological stimulation of swallowing by quipazine in situ represents a valuable model for experimental studies. This work paves the way for future investigations on brainstem serotonergic modulation, and further identification of neural populations and mechanisms involved in swallowing and/or swallow-breathing interaction.

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