scholarly journals A pretectal command system controls hunting behaviour

2019 ◽  
Author(s):  
Paride Antinucci ◽  
Mónica Folgueira ◽  
Isaac H. Bianco

AbstractFor many species, hunting is an innate behaviour that is crucial for survival, yet the circuits that control predatory action sequences are poorly understood. We used larval zebrafish to identify a command system that controls hunting. By combining calcium imaging with a virtual hunting assay, we identified a discrete pretectal region that is selectively active when animals initiate hunting. Targeted genetic labelling allowed us to examine the function and morphology of individual cells and identify two classes of pretectal neuron that project to ipsilateral optic tectum or the contralateral tegmentum. Optogenetic stimulation of single neurons of either class was able to induce sustained hunting sequences, in the absence of prey. Furthermore, laser ablation of these neurons impaired prey-catching and prevented induction of hunting by optogenetic stimulation of the anterior-ventral tectum. In sum, we define a specific population of pretectal neurons that functions as a command system to drive predatory behaviour.Key findingsPretectal neurons are recruited during hunting initiationOptogenetic stimulation of single pretectal neurons can induce predatory behaviourAblation of pretectal neurons impairs huntingPretectal cells comprise a command system controlling hunting behaviour

eLife ◽  
2019 ◽  
Vol 8 ◽  
Author(s):  
Paride Antinucci ◽  
Mónica Folgueira ◽  
Isaac H Bianco

For many species, hunting is an innate behaviour that is crucial for survival, yet the circuits that control predatory action sequences are poorly understood. We used larval zebrafish to identify a population of pretectal neurons that control hunting. By combining calcium imaging with a virtual hunting assay, we identified a discrete pretectal region that is selectively active when animals initiate hunting. Targeted genetic labelling allowed us to examine the function and morphology of individual cells and identify two classes of pretectal neuron that project to ipsilateral optic tectum or the contralateral tegmentum. Optogenetic stimulation of single neurons of either class was able to induce sustained hunting sequences, in the absence of prey. Furthermore, laser ablation of these neurons impaired prey-catching and prevented induction of hunting by optogenetic stimulation of the anterior-ventral tectum. We propose that this specific population of pretectal neurons functions as a command system to induce predatory behaviour.


2016 ◽  
Author(s):  
Ruey-Kuang Cheng ◽  
Seetha Krishnan ◽  
Qian Lin ◽  
Caroline Kibat ◽  
Suresh Jesuthasan

AbstractBackgroundNeural activity in the vertebrate habenula is affected by changes in ambient illumination. The nucleus that links photoreceptors with the habenula is not well characterized. Here, we describe the location, inputs and potential function of this nucleus in larval zebrafish.ResultsHigh-speed calcium imaging shows that onset and offset of light evokes a rapid response in the dorsal left neuropil of the habenula, indicating preferential targeting of this neuropil by afferents mediating response to change in irradiance. Injection of a lipophilic dye into this neuropil led to bilateral labeling of a nucleus in the anterior thalamus that responds to onset and offset of light, and that receives innervation from the retina and pineal organ. Lesioning the neuropil of this thalamic nucleus reduced the habenula response to light. Optogenetic stimulation of the thalamus with channelrhodopsin-2 caused depolarization in the habenula, while manipulation with anion channelrhodopsins inhibited habenula response to light and disrupted climbing and diving that is evoked by irradiance change.ConclusionsA nucleus in the anterior thalamus of larval zebrafish innervates the dorsal left habenula. This nucleus receives input from the retina and pineal, responds to increase and decrease in irradiance, enables habenula responses to change in irradiance, and may function in light-evoked vertical migration.


2019 ◽  
Author(s):  
Daniel A. Lee ◽  
Grigorios Oikonomou ◽  
Tasha Cammidge ◽  
Young Hong ◽  
David A. Prober

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.


eLife ◽  
2020 ◽  
Vol 9 ◽  
Author(s):  
Daniel A Lee ◽  
Grigorios Oikonomou ◽  
Tasha Cammidge ◽  
Andrey Andreev ◽  
Young Hong ◽  
...  

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.


2019 ◽  
Author(s):  
S Ceto ◽  
KJ Sekiguchi ◽  
Y Takashima ◽  
A Nimmerjahn ◽  
MH Tuszynski

SummaryNeural stem/progenitor cell grafts integrate into sites of spinal cord injury (SCI) and form anatomical and electrophysiological neuronal relays across lesions. To determine how grafts become synaptically organized and connect with host systems, we performed calcium imaging of neural progenitor cell grafts within sites of SCI, using both in vivo imaging and spinal cord slices. Stem cell grafts organize into localized synaptic networks that are spontaneously active. Following optogenetic stimulation of host corticospinal tract axons regenerating into grafts, distinct and segregated neuronal networks respond throughout the graft. Moreover, optogenetic stimulation of graft axons extending out from the lesion into the denervated spinal cord also trigger responses in local host neuronal networks. In vivo imaging reveals that behavioral stimulation of host elicits focal synaptic responses within grafts. Thus, remarkably, neural progenitor cell grafts form functional synaptic subnetworks in patterns paralleling the normal spinal cord.


2020 ◽  
Author(s):  
Q. Montardy ◽  
M. Wei ◽  
T. Yi ◽  
X. Liu ◽  
Z. Zhou ◽  
...  

AbstractGlutamatergic and GABAergic neurons represent the neural components of the medial vestibular nuclei. We assessed the functional role of glutamatergic and GABAergic neuronal pathways arising from the vestibular nuclei (VN) in the maintenance of gait and balance by optogenetically stimulating the VN in VGluT2-cre and GAD2-cre mice. We demonstrate that glutamatergic, but not GABAergic VN neuronal subpopulation is responsible for immediate and strong posturo-locomotor deficits, comparable to unilateral vestibular deafferentation models. During optogenetic stimulation, the support surface dramatically increased in VNVGluT2+ mice, and rapidly fell back to baseline after stimulation, whilst it remained unchanged during similar stimulation of VNGAD2+ mice. This effect persisted when vestibular compensation was removed. Posturo-locomotor alterations evoked in VNVGluT2+ animals were still present immediately after stimulation, while they disappeared 1h later. Overall, these results indicate a fundamental role for VNVGluT2+ neurons in balance and posturo-locomotor functions, but not for VNGAD2+ neurons, in this specific context. This new optogenetic approach will be useful to characterize the role of the different VN neuronal populations involved in vestibular physiology and pathophysiology.HighlightsFor the first time, Vestibular nuclei were optogenetically stimulated in free-moving animals, to asses for glutamatergic and GABAergic neurons functions in posturo-locomotor behaviors.Brief optogenetic activation of VNVGluT2+, but not VNGAD2+, induced immediate and strong postural deficit.Stimulation of VNVGluT2+ neurons provoked an imbalance with continuous effect on locomotion for a short period of time after stimulation.These results are comparable to the classical vestibular deafferentation models during their peak of deficit, and set optogenetic stimulation as a new model to study vestibular deficits.


2019 ◽  
Author(s):  
Kazutaka Maeda ◽  
Ken-ichi Inoue ◽  
Jun Kunimatsu ◽  
Masahiko Takada ◽  
Okihide Hikosaka

AbstractThe amygdala is uniquely sensitive to emotional events. However, it is not understood whether and how the amygdala uses such emotional signals to control behavior, especially eye movements. We therefore injected muscimol (GABAAagonist) into the central nucleus of amygdala (CeA) in monkeys. This unilateral temporary inactivation suppressed saccades to contralateral but not ipsilateral targets, resulting in longer latencies, hypometric amplitudes, and slower velocity. During free viewing of movies, gaze was distributed mostly in the ipsilateral hemifield. Moreover, CeA inactivation disrupted the tendency of gaze toward social interaction images, which were normally focused on continuously. Conversely, optogenetic stimulation of CeA facilitated saccades to the contralateral side. These findings suggest that CeA controls spatially selective gaze and attention in emotional contexts, and provide a new framework for understanding psychiatric disorders related to amygdala dysfunction.HighlightsCentral amygdala facilitates contralateral saccades selectively.Saccade facilitation is related to motivational goals and social interaction.The amygdala thus controls goal-directed behavior based on emotional contexts.


2020 ◽  
Author(s):  
Cornelis Immanuel van der Zouwen ◽  
Joël Boutin ◽  
Maxime Fougère ◽  
Aurélie Flaive ◽  
Mélanie Vivancos ◽  
...  

AbstractBackgroundStimulation of the Mesencephalic Locomotor Region (MLR) is increasingly considered as a target to improve locomotor function in Parkinson’s disease, spinal cord injury and stroke. A key function of the MLR is to control the speed of forward symmetrical locomotor movements. However, the ability of freely moving mammals to integrate environmental cues to brake and turn during MLR stimulation is poorly documented.Objective/hypothesisWe investigated whether freely behaving mice could brake or turn based on environmental cues during MLR stimulation.MethodsWe stimulated the cuneiform nucleus in mice expressing channelrhodopsin in Vglut2-positive neurons in a Cre-dependent manner (Vglut2-ChR2-EYFP) using optogenetics. We detected locomotor movements using deep learning. We used patch-clamp recordings to validate the functional expression of channelrhodopsin and neuroanatomy to visualize the stimulation sites.ResultsOptogenetic stimulation of the MLR evoked locomotion and increasing laser power increased locomotor speed. Gait diagram and limb kinematics were similar during spontaneous and optogenetic-evoked locomotion. Mice could brake and make sharp turns (∼90⁰) when approaching a corner during MLR stimulation in an open-field arena. The speed during the turn was scaled with the speed before the turn, and with the turn angle. In a reporter mouse, many Vglut2-ZsGreen neurons were immunopositive for glutamate in the MLR. Patch-clamp recordings in Vglut2-ChR2-EYFP mice show that blue light evoked short latency spiking in MLR neurons.ConclusionMLR glutamatergic neurons are a relevant target to improve locomotor activity without impeding the ability to brake and turn when approaching an obstacle, thus ensuring smooth and adaptable navigation.Highlights-Mice brake and turn when approaching the arena’s corner during MLR-evoked locomotion-Speed decrease is scaled to speed before the turn during MLR-evoked locomotion-Turn angle is scaled to turn speed during MLR-evoked locomotion-Gait and limb kinematics are similar during spontaneous and MLR-evoked locomotion


1962 ◽  
Vol 39 (3) ◽  
pp. 423-430
Author(s):  
H. L. Krüskemper ◽  
F. J. Kessler ◽  
E. Steinkrüger

ABSTRACT 1. Reserpine does not inhibit the tissue respiration of liver in normal male rats (in vitro). 2. The decrease of tissue respiration of the liver with simultaneous morphological stimulation of the thyroid gland after long administration of reserpine is due to a minute inhibition of the hormone synthesis in the thyroid gland. 3. The morphological alterations of the thyroid in experimental hypothyroidism due to perchlorate can not be prevented with reserpine.


1960 ◽  
Vol XXXIII (II) ◽  
pp. 230-250 ◽  
Author(s):  
Eileen E. Hill

ABSTRACT A method for the fractionation of the urinary 17-ketogenic steroids with no oxygen grouping at C11 and those oxygenated at C11, is applied to the clinical problems of congenital adrenal hyperplasia. In normal children the mean ratio of the non-oxygenated to oxygenated steroids is 0.24. In childrern with congenital adrenal hyperplasia the ratio is 2.3. The reason for this difference in ratio is discussed. The changes in ratio found under stimulation of the adrenal gland with exogenous or endogenous corticotrophin and the suppression with cortisone therapy are studied. This test can be applied to isolated samples of urine, a major advantage in paediatric practice, and can be carried out in routine laboratories. It is found to be reliable in the diagnosis and sensitive in the control of congenital adrenal hyperplasia.


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