scholarly journals An excitatory ventromedial hypothalamus to paraventricular thalamus circuit that suppresses food intake

2020 ◽  
Vol 11 (1) ◽  
Author(s):  
Jia Zhang ◽  
Dan Chen ◽  
Patrick Sweeney ◽  
Yunlei Yang
Keyword(s):  
Food Intake ◽  
Neural Circuit ◽  
Ventromedial Hypothalamus ◽  
Steroidogenic Factor 1 ◽  
Chemical Genetic ◽  
Optogenetic Stimulation ◽  
Neural Inhibition ◽  
Satiety Center ◽  
Paraventricular Thalamus ◽  
Stimulation Of

AbstractIt is well recognized that ventromedial hypothalamus (VMH) serves as a satiety center in the brain. However, the feeding circuit for the VMH regulation of food intake remains to be defined. Here, we combine fiber photometry, chemo/optogenetics, virus-assisted retrograde tracing, ChR2-assisted circuit mapping and behavioral assays to show that selective activation of VMH neurons expressing steroidogenic factor 1 (SF1) rapidly inhibits food intake, VMH SF1 neurons project dense fibers to the paraventricular thalamus (PVT), selective chemo/optogenetic stimulation of the PVT-projecting SF1 neurons or their projections to the PVT inhibits food intake, and chemical genetic inactivation of PVT neurons diminishes SF1 neural inhibition of feeding. We also find that activation of SF1 neurons or their projections to the PVT elicits a flavor aversive effect, and selective optogenetic stimulation of ChR2-expressing SF1 projections to the PVT elicits direct excitatory postsynaptic currents. Together, our data reveal a neural circuit from VMH to PVT that inhibits food intake.

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 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.

Effect of galanin on food intake in rats: involvement of lateral and ventromedial hypothalamic sites

1993 ◽  
Vol 264 (2) ◽  
pp. R355-R361 ◽  
Author(s):  
R. R. Schick ◽  
S. Samsami ◽  
J. P. Zimmermann ◽  
T. Eberl ◽  
C. Endres ◽  
...  
Keyword(s):  
Food Intake ◽  
Food Consumption ◽  
Paraventricular Nucleus ◽  
Lateral Hypothalamus ◽  
Ventromedial Hypothalamus ◽  
Initial Increase ◽  
Intracerebroventricular Injection ◽  
Fasted Rats ◽  
Stimulation Of ◽  
Cumulative Food Intake

Galanin has previously been reported to elicit feeding in satiated animals when injected into the hypothalamic paraventricular nucleus. It is not known, however, 1) whether this action is due to activation of feeding signals or suppression of satiety signals or both or 2) whether other hypothalamic regions such as the lateral hypothalamus (LH) or the ventromedial hypothalamus (VMH) are involved in this action. The effects of galanin on food intake were therefore examined in satiated and in fasted rats both after intracerebroventricular injection (0.1, 1, and 10 micrograms/10 microliters) and after microinjection (1 and 5 micrograms/0.5 microliters) into the LH and VMH. Twenty minutes after intracerebroventricular injection, galanin significantly and dose dependently augmented food intake by up to sevenfold in freely feeding rats and by up to 79% in fasted animals. The galanin-induced augmentation of cumulative food intake up to 2 h after injection was due to the initial increase in food consumption during the 0 to 20-min interval. This suggests that galanin acts by activation of feeding behavior and not by suppression of satiety signals in these fasted animals, in which satiety signals are presumably not initially operative. Twenty minutes after intrahypothalamic injections into both the LH and VMH, galanin (5 micrograms) significantly increased food consumption, fivefold in freely feeding rats and 30-35% in fasted rats. Thus stimulation of feeding by centrally injected galanin also involves loci within the LH and VMH.

scholarly journals Brain-wide neural dynamics of poststroke recovery induced by optogenetic stimulation

2021 ◽  
Vol 7 (33) ◽  
pp. eabd9465
Author(s):  
Shahabeddin Vahdat ◽  
Arjun Vivek Pendharkar ◽  
Terrance Chiang ◽  
Sean Harvey ◽  
Haruto Uchino ◽  
...  
Keyword(s):  
Functional Recovery ◽  
Primary Motor Cortex ◽  
Neural Circuits ◽  
Neural Circuit ◽  
Neural Dynamics ◽  
Functional Magnetic Resonance ◽  
Resonance Imaging ◽  
Optogenetic Stimulation ◽  
Important Mediator ◽  
Stimulation Of

Poststroke optogenetic stimulations can promote functional recovery. However, the circuit mechanisms underlying recovery remain unclear. Elucidating key neural circuits involved in recovery will be invaluable for translating neuromodulation strategies after stroke. Here, we used optogenetic functional magnetic resonance imaging to map brain-wide neural circuit dynamics after stroke in mice treated with and without optogenetic excitatory neuronal stimulations in the ipsilesional primary motor cortex (iM1). We identified key sensorimotor circuits affected by stroke. iM1 stimulation treatment restored activation of the ipsilesional corticothalamic and corticocortical circuits, and the extent of activation was correlated with functional recovery. Furthermore, stimulated mice exhibited higher expression of axonal growth–associated protein 43 in the ipsilesional thalamus and showed increased Synaptophysin+/channelrhodopsin+ presynaptic axonal terminals in the corticothalamic circuit. Selective stimulation of the corticothalamic circuit was sufficient to improve functional recovery. Together, these findings suggest early involvement of corticothalamic circuit as an important mediator of poststroke recovery.

scholarly journals Chronic Stimulation of Leptin on Food Intake and Body Weight after Microinjection into the Ventromedial Hypothalamus of Conscious Rats

1970 ◽  
Vol 19 (2) ◽  
pp. 70-75
Author(s):  
Md Shahidul Haque ◽  
Takashi Shimazu
Keyword(s):  
Body Weight ◽  
Food Intake ◽  
Low Dose ◽  
Ventromedial Hypothalamus ◽  
Chronic Stimulation ◽  
Dramatic Effect ◽  
Reduced Body ◽  
Medial Hypothalamus ◽  
Control Body ◽  
Stimulation Of

A very low dose of leptin (50 ng) was microinjected into the ventro-medial hypothalamus (VMH) of each rat daily once for three days. Food intake and body weight were measured after leptin injections. Microinjection of leptin into the VMH reduced food intake by 33.3 % significantly (P<0.01) during three days of leptin injection compared to the control. Body weight was measured after 24 h, 48 h and 72 h of leptin injection. After 24 h (P<0.01) and 48 h (P<0.05) of leptin injection, body weight was reduced significantly compared to that of rat before injection. Similarly, after 72 h of leptin injection, a significant reduced body weight was observed (P<0.1). A significant (P<0.001) reduced changes of body weight were found after 24 h, 48 h and 72 h after injection into the VMH when compared to the respective controls injected with saline. The results suggest that leptin has dramatic effect on reducing body weight by inhibition of food intake.   doi: 10.3329/taj.v19i2.3154 TAJ 2006; 19(2): 70-75

scholarly journals The female-specific VC neurons are mechanically activated, feed-forward motor neurons that facilitate serotonin-induced egg laying in C. elegans

2020 ◽  
Author(s):  
Richard J. Kopchock ◽  
Bhavya Ravi ◽  
Addys Bode ◽  
Kevin M. Collins
Keyword(s):  
Muscle Contraction ◽  
Motor Neurons ◽  
Neural Circuit ◽  
Egg Laying ◽  
Muscle Contractility ◽  
C Elegans ◽  
Optogenetic Stimulation ◽  
Vulval Muscle ◽  
Female Specific ◽  
Stimulation Of

AbstractSuccessful execution of behavior requires the coordinated activity and communication between multiple cell types. Studies using the relatively simple neural circuits of invertebrates have helped to uncover how conserved molecular and cellular signaling events shape animal behavior. To understand the mechanisms underlying neural circuit activity and behavior, we have been studying a simple circuit that drives egg-laying behavior in the nematode worm C. elegans. Here we show that the female-specific, Ventral C (VC) motoneurons are required for vulval muscle contractility and egg laying in response to serotonin. Ca2+ imaging experiments show the VCs are active during times of vulval muscle contraction and vulval opening, and optogenetic stimulation of the VCs promotes vulval muscle Ca2+ activity. However, while silencing of the VCs does not grossly affect steady-state egg-laying behavior, VC silencing does block egg laying in response to serotonin and increases the failure rate of egg-laying attempts. Signaling from the VCs facilitates full vulval muscle contraction and opening of the vulva for efficient egg laying. We also find the VCs are mechanically activated in response to vulval opening. Optogenetic stimulation of the vulval muscles is sufficient to drive VC Ca2+ activity and requires muscle contractility, showing the presynaptic VCs and the postsynaptic vulval muscles can mutually excite each other. Together, our results demonstrate that the VC neurons facilitate efficient execution of egg-laying behavior by coordinating postsynaptic muscle contractility in response to serotonin and mechanosensory feedback.

scholarly journals Optogenetic mapping of feeding and self-stimulation within the lateral hypothalamus of the rat

2019 ◽  
Author(s):  
Kevin R. Urstadt ◽  
Kent C. Berridge
Keyword(s):  
Food Intake ◽  
Eating Behavior ◽  
Lateral Hypothalamus ◽  
Preoptic Area ◽  
Laser Intensity ◽  
Optic Fiber ◽  
Optogenetic Stimulation ◽  
Escape Behaviors ◽  
Self Stimulation ◽  
Stimulation Of

AbstractThe lateral hypothalamus (LH) regulates eating and motivation, and includes several anatomical subregions. This study explored localization of function across different LH subregions in controlling food intake stimulated by optogenetic channelrhodopsin excitation, and in supporting laser self-stimulation. We particularly compared the tuberal LH, the posterior LH, and the lateral preoptic area. Local diameters of tissue optogenetically stimulated within LH were assessed by measuring laser-induced Fos plumes and Jun plumes via immunofluorescence surrounding optic fiber tips, and were used to map localization of function for effects elicited by LH optogenetic stimulation. Optogenetic stimulation of the tuberal subsection of the LH behaviorally produced the most robust food intake initially, but produced only mild laser self-stimulation in the same rats. However, after repeated exposures to optogenetic stimulation, tuberal LH behavioral profiles shifted toward more self-stimulation and less food intake. By contrast, stimulation of the lateral preoptic area produced relatively little food intake or self-stimulation, either initially or after extended stimulation experience. Stimulation in the posterior LH subregion supported moderate self-stimulation, but not food intake here, and at higher laser intensity shifted valence to evoke escape behaviors. We conclude that the tuberal LH subregion may best mediate increases in food intake stimulated by optogenetic excitation. However, incentive motivational effects of tuberal LH stimulation may shift toward self-stimulation behavior after repeated stimulation. By contrast, the lateral preoptic area and posterior LH do not as readily elicit either eating behavior or laser self-stimulation, and may be more prone to higher-intensity aversive effects.

Changes in food intake with electrical stimulation of the ventromedial hypothalamus in dogs

1984 ◽  
Vol 60 (6) ◽  
pp. 1253-1257 ◽  
Author(s):  
Frederick D. Brown ◽  
Richard G. Fessler ◽  
Jacob R. Rachlin ◽  
Sean Mullan
Keyword(s):  
Electrical Stimulation ◽  
Food Intake ◽  
Water Intake ◽  
Alternative Therapy ◽  
Daily Intake ◽  
Ventromedial Hypothalamus ◽  
Subcortical White Matter ◽  
Hypothalamic Area ◽  
Content Type ◽  
Stimulation Of

✓ Six adult dogs were implanted stereotaxically with chronic indwelling Medtronic platinum-tipped electrodes in the left ventromedial hypothalamic area (VMH); two dogs with electrodes placed in the subcortical white matter served as controls. Following 24 hours of food deprivation, VMH-stimulated dogs delayed their next meal for a period ranging from 1 to 18 hours. When not stimulated, however, each dog ate immediately upon receiving its food and consumed greater than average daily intake (p < 0.005). The two control dogs ate immediately upon receiving food regardless of whether they were stimulated or not. Dogs that received 1 hour of VMH stimulation every 12 hours for 3 consecutive days maintained an average daily food intake of 35% of normal baseline levels (range 13% to 51%), and water consumption averaged 50% of baseline intake (range 29% to 67%). Both of these results were statistically significant (p < 0.01). After cessation of stimulation, food and water intake returned to normal within 6 to 9 days, with no observable “rebound hyperphagia.” The two animals that received subcortical electrodes showed no change in food or water intake with stimulation. Blood pressure, pulse, respiration, temperature, and gross behavior were not altered during or after stimulation. These results suggest that the use of electrical stimulation of the VMH may be a useful modality for regulating food intake, and deserves further examination as a potential alternative therapy for human morbid obesity.

scholarly journals Relaxin/insulin-like family peptide receptor 4 (Rxfp4) expressing hypothalamic neurons modulate food intake and preference in mice

2021 ◽  
Author(s):  
Jo E Lewis ◽  
Orla RM Woodward ◽  
Christopher A Smith ◽  
Alice E Adriaenssens ◽  
Lawrence Billing ◽  
...  
Keyword(s):  
Food Intake ◽  
Ventromedial Hypothalamus ◽  
Designer Drugs ◽  
Central Nucleus ◽  
Whole Body ◽  
Stria Terminalis ◽  
Bed Nucleus ◽  
Peptide Receptor ◽  
The Central Nervous System ◽  
Paraventricular Thalamus

Relaxin/insulin-like-family peptide receptor-4 (RXFP4), the cognate receptor for insulin-like peptide 5 (INSL5), has previously been implicated in feeding behaviour. To explore Rxfp4 expression and physiology, we generated Rxfp4-Cre mice. Whole body chemogenetic activation (Dq) or inhibition (Di) of Rxfp4-expressing cells using designer receptors exclusively activated by designer drugs (DREADDs) altered food intake and preference. Potentially underlying this effect, Rxfp4-expressing neurons were identified in nodose and dorsal root ganglia and the central nervous system, including the ventromedial hypothalamus (VMH). Single-cell RNA-sequencing defined a cluster of VMH Rxfp4-labelled cells expressing Esr1, Tac1 and Oxtr. VMH-restricted activation of Rxfp4-expressing (RXFP4VMH) cells using AAV-Dq recapitulated the whole body Dq feeding phenotype. Viral tracing demonstrated RXFP4VMH neural projections to the bed nucleus of the stria terminalis, paraventricular hypothalamus, paraventricular thalamus, central nucleus of the amygdala and parabrachial nucleus. These findings identify hypothalamic RXFP4 signalling as a key regulator of food intake and preference.

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