scholarly journals Effects of electrical stimulation of the medullary raphe nuclei on respiratory movement in rats

2006 ◽  
Vol 192 (5) ◽  
pp. 507-507
Author(s):  
Ying Cao ◽  
Yutaka Fujito ◽  
Kiyoji Matsuyama ◽  
Mamoru Aoki
Keyword(s):  
Electrical Stimulation ◽  
Respiratory Movement ◽  
Raphe Nuclei ◽  
Medullary Raphe ◽  
Raphé Nuclei ◽  
Stimulation Of

scholarly journals Medullary raphe nuclei activate the lumbosacral defecation center through the descending serotonergic pathway to regulate colorectal motility in rats

2018 ◽  
Vol 314 (3) ◽  
pp. G341-G348 ◽  
Author(s):  
Hiroyuki Nakamori ◽  
Kiyotada Naitou ◽  
Yuuki Horii ◽  
Hiroki Shimaoka ◽  
Kazuhiro Horii ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Electrical Stimulation ◽  
Raphe Nuclei ◽  
Lumbosacral Spinal Cord ◽  
Pelvic Nerves ◽  
Medullary Raphe ◽  
Raphé Nuclei ◽  
Type 3 ◽  
Stimulation Of

Colorectal motility is regulated by two defecation centers located in the brain and spinal cord. In previous studies, we have shown that administration of serotonin (5-HT) in the lumbosacral spinal cord causes enhancement of colorectal motility. Because spinal 5-HT is derived from neurons of the medullary raphe nuclei, including the raphe magnus, raphe obscurus, and raphe pallidus, we examined whether stimulation of the medullary raphe nuclei enhances colorectal motility via the lumbosacral defecation center. Colorectal pressure was recorded with a balloon in vivo in anesthetized rats. Electrical stimulation of the medullary raphe nuclei failed to enhance colorectal motility. Because GABAergic neurons can be simultaneously activated by the raphe stimulation and released GABA masks accelerating actions of the raphe nuclei on the lumbosacral defecation center, a GABAA receptor antagonist was preinjected intrathecally to manifest excitatory responses. When spinal GABAA receptors were blocked by the antagonist, electrical stimulation of the medullary raphe nuclei increased colorectal contractions. This effect of the raphe nuclei was inhibited by intrathecal injection of 5-hydroxytryptamine type 2 (5-HT2) and type 3 (5-HT3) receptor antagonists. In addition, injection of a selective 5-HT reuptake inhibitor in the lumbosacral spinal cord augmented the raphe stimulation-induced enhancement of colorectal motility. Transection of the pelvic nerves, but not transection of the colonic nerves, prevented the effect of the raphe nuclei on colorectal motility. These results demonstrate that activation of the medullary raphe nuclei causes augmented contractions of the colorectum via 5-HT2 and 5-HT3 receptors in the lumbosacral defecation center. NEW & NOTEWORTHY We have shown that electrical stimulation of the medullary raphe nuclei causes augmented contractions of the colorectum via pelvic nerves in rats. The effect of the medullary raphe nuclei on colorectal motility is exerted through activation of 5-hydroxytryptamine type 2 and type 3 receptors in the lumbosacral defecation center. The descending serotoninergic raphespinal tract represents new potential therapeutic targets against colorectal dysmotility such as irritable bowel syndrome.

In vivo release of serotonin in cat dorsal vagal complex and cervical ventral horn induced by electrical stimulation of the medullary raphe nuclei

1990 ◽  
Vol 535 (2) ◽  
pp. 227-236 ◽  
Author(s):  
Ernst Brodin ◽  
Bengt Linderoth ◽  
Michel Goiny ◽  
Yuji Yamamoto ◽  
Bertil Gazelius ◽  
...  
Keyword(s):  
Electrical Stimulation ◽  
Ventral Horn ◽  
Raphe Nuclei ◽  
Dorsal Vagal Complex ◽  
In Vivo Release ◽  
Medullary Raphe ◽  
Raphé Nuclei ◽  
Stimulation Of

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.

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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