scholarly journals Neuropeptide VF neurons promote sleep via the serotonergic raphe

2019 ◽  
Author(s):  
Daniel A. Lee ◽  
Grigorios Oikonomou ◽  
Tasha Cammidge ◽  
Young Hong ◽  
David A. Prober
Keyword(s):  
Calcium Imaging ◽  
Neural Circuit ◽  
Raphe Nuclei ◽  
Hypothalamic Neurons ◽  
Optogenetic Stimulation ◽  
Genetic Epistasis ◽  
Normal Sleep ◽  
Genetic Labeling ◽  
Raphé Nuclei ◽  
Stimulation Of

ABSTRACTAlthough several sleep-regulating neurons have been identified, little is known about how they interact with each other for sleep/wake control. We previously identified neuropeptide VF (NPVF) and the hypothalamic neurons that produce it as a sleep-promoting system (Lee et al., 2017). Here we use zebrafish to describe a neural circuit in which neuropeptide VF (npvf)-expressing neurons control sleep via the serotonergic raphe nuclei (RN), a hindbrain structure that promotes sleep in both diurnal zebrafish and nocturnal mice. Using genetic labeling and calcium imaging, we show that npvf-expressing neurons innervate and activate serotonergic RN neurons. We additionally demonstrate that optogenetic stimulation of npvf-expressing neurons induces sleep in a manner that requires NPVF and is abolished when the RN are ablated or lack serotonin. Finally, genetic epistasis demonstrates that NPVF acts upstream of serotonin in the RN to maintain normal sleep levels. These findings reveal a novel hypothalamic-hindbrain circuit for sleep/wake control.

scholarly journals Neuropeptide VF neurons promote sleep via the serotonergic raphe

eLife ◽  
2020 ◽  
Vol 9 ◽  
Author(s):  
Daniel A Lee ◽  
Grigorios Oikonomou ◽  
Tasha Cammidge ◽  
Andrey Andreev ◽  
Young Hong ◽  
...  
Keyword(s):  
Calcium Imaging ◽  
Genetic Evidence ◽  
Neuronal Circuit ◽  
Hypothalamic Neurons ◽  
Neuronal Populations ◽  
Optogenetic Stimulation ◽  
Normal Sleep ◽  
Genetic Labeling ◽  
Raphé Nuclei ◽  
Stimulation Of

Although several sleep-regulating neuronal populations have been identified, little is known about how they interact with each other to control sleep/wake states. We previously identified neuropeptide VF (NPVF) and the hypothalamic neurons that produce it as a sleep-promoting system (Lee et al., 2017). Here we show using zebrafish that npvf-expressing neurons control sleep via the serotonergic raphe nuclei (RN), a hindbrain structure that is critical for sleep in both diurnal zebrafish and nocturnal mice. Using genetic labeling and calcium imaging, we show that npvf-expressing neurons innervate and can activate serotonergic RN neurons. We also demonstrate that chemogenetic or optogenetic stimulation of npvf-expressing neurons induces sleep in a manner that requires NPVF and serotonin in the RN. Finally, we provide genetic evidence that NPVF acts upstream of serotonin in the RN to maintain normal sleep levels. These findings reveal a novel hypothalamic-hindbrain neuronal circuit for sleep/wake control.

Striatal dopamine mediates hallucination-like perception in mice

Science ◽  
2021 ◽  
Vol 372 (6537) ◽  
pp. eabf4740
Author(s):  
K. Schmack ◽  
M. Bosc ◽  
T. Ott ◽  
J. F. Sturgill ◽  
A. Kepecs
Keyword(s):  
Psychotic Disorders ◽  
Neural Circuit ◽  
Dopamine Neurons ◽  
Striatal Dopamine ◽  
Model Organisms ◽  
High Confidence ◽  
Optogenetic Stimulation ◽  
The Brain ◽  
Central Symptom ◽  
Stimulation Of

Hallucinations, a central symptom of psychotic disorders, are attributed to excessive dopamine in the brain. However, the neural circuit mechanisms by which dopamine produces hallucinations remain elusive, largely because hallucinations have been challenging to study in model organisms. We developed a task to quantify hallucination-like perception in mice. Hallucination-like percepts, defined as high-confidence false detections, increased after hallucination-related manipulations in mice and correlated with self-reported hallucinations in humans. Hallucination-like percepts were preceded by elevated striatal dopamine levels, could be induced by optogenetic stimulation of mesostriatal dopamine neurons, and could be reversed by the antipsychotic drug haloperidol. These findings reveal a causal role for dopamine-dependent striatal circuits in hallucination-like perception and open new avenues to develop circuit-based treatments for psychotic disorders.

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.

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
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