scholarly journals Neural circuit mechanisms of sexual receptivity in Drosophila females

Author(s):  
Kaiyu Wang ◽  
Fei Wang ◽  
Nora Forknall ◽  
Tansy Yang ◽  
Christopher Patrick ◽  
...  

Choosing a mate is one of the most consequential decisions a female will make during her lifetime. This is particularly true for species in which females either mate repeatedly with the same partner or mate infrequently but use the sperm from a single copulation to fertilize eggs over an extended period of time. Drosophila melanogaster uses the latter strategy. Here, we characterize the neural circuitry that implements mating decisions in the female brain. A female fly signals her mating choice by opening her vaginal plates to allow a courting male to copulate1,2. Vaginal plate opening (VPO) occurs in response to the male courtship song and is dependent upon the female's mating status. We sought to understand how these exteroceptive (song) and interoceptive (mating status) inputs are integrated to control VPO. We show that VPO is triggered by a pair of female-specific descending neurons, the vpoDNs. The vpoDNs receive excitatory input from vpoEN auditory neurons, which are tuned to specific features of the melanogaster song. The song responses of vpoDNs, but not vpoENs, are attenuated upon mating, accounting for the reduced receptivity of mated females. This modulation is mediated by pC1 neurons, which encode the female’s mating status3,4 and also provide excitatory input to vpoDNs. The vpoDNs thus directly integrate the external and internal signals to control the mating decisions of Drosophila females.

2019 ◽  
Author(s):  
Yang Wu ◽  
Salil S. Bidaye ◽  
David Mahringer

SummaryLatent neural circuitry in the female brain encoding male-like mating behaviors has been revealed in both mice and flies. InDrosophila, a key component of this circuitry consists of thedoublesex-expressing pC1 neurons, which were deemed to exist in both sexes and function based on the amount of cells being activated. Here, we identify pC1-alpha, a female-specific subtype of pC1, as responsible for inducing persistent male-like social behaviors in females. We demonstrate that activation of a single pC1-alpha neuron is sufficient for such induction in a position- and direction-selective manner, and activity of pC1-alpha neurons as a whole is indispensable for maintaining normal sexual receptivity. These dual functions of pC1-alpha may require different neurotransmission, with acetylcholine specifically required for the former but not the latter. Our findings suggest that pC1-alpha may be the female counterpart of male P1 due to their shared similarities in morphology, lineage, and social promoting function.


2021 ◽  
Vol 7 (22) ◽  
pp. eabf8719
Author(s):  
Yong Han ◽  
Guobin Xia ◽  
Yanlin He ◽  
Yang He ◽  
Monica Farias ◽  
...  

The neural circuitry mechanism that underlies dopaminergic (DA) control of innate feeding behavior is largely uncharacterized. Here, we identified a subpopulation of DA neurons situated in the caudal ventral tegmental area (cVTA) directly innervating DRD1-expressing neurons within the lateral parabrachial nucleus (LPBN). This neural circuit potently suppresses food intake via enhanced satiation response. Notably, this cohort of DAcVTA neurons is activated immediately before the cessation of each feeding bout. Acute inhibition of these DA neurons before bout termination substantially suppresses satiety and prolongs the consummatory feeding. Activation of postsynaptic DRD1LPBN neurons inhibits feeding, whereas genetic deletion of Drd1 within the LPBN causes robust increase in food intake and subsequent weight gain. Furthermore, the DRD1LPBN signaling manifests the central mechanism in methylphenidate-induced hypophagia. In conclusion, our study illuminates a hindbrain DAergic circuit that controls feeding through dynamic regulation in satiety response and meal structure.


2008 ◽  
Vol 100 (3) ◽  
pp. 1384-1396 ◽  
Author(s):  
Weiqing Ji ◽  
Nobuo Suga

Experience-dependent plastic changes in the central sensory systems are due to activation of both the sensory and neuromodulatory systems. Nonspecific changes of cortical auditory neurons elicited by pseudoconditioning are quite different from tone-specific changes of the neurons elicited by auditory fear conditioning. Therefore the neural circuit evoking the nonspecific changes must also be different from that evoking the tone-specific changes. We first examined changes in the response properties of cortical auditory neurons of the big brown bat elicited by pseudoconditioning with unpaired tonal (CSu) and electric leg (USu) stimuli and found that it elicited nonspecific changes to CSu (a heart-rate decrease, an auditory response increase, a broadening of frequency tuning, and a decrease in threshold) and, in addition, a small tone-specific change to CSu (a small short-lasting best-frequency shift) only when CSu frequency was 5 kHz lower than the best frequency of a recorded neuron. We then examined the effects of drugs on the cortical changes elicited by the pseudoconditioning. The development of the nonspecific changes was scarcely affected by atropine (a muscarinic cholinergic receptor antagonist) and mecamylamine (a nicotinic cholinergic receptor antagonist) applied to the auditory cortex and by muscimol (a GABAA-receptor agonist) applied to the somatosensory cortex. However, these drugs abolished the small short-lasting tone-specific change as they abolished the large long-lasting tone-specific change elicited by auditory fear conditioning. Our current results indicate that, different from the tone-specific change, the nonspecific changes depend on neither the cholinergic neuromodulator nor the somatosensory cortex.


2006 ◽  
Vol 43 (6) ◽  
pp. 683-690 ◽  
Author(s):  
Grant Goldsberry ◽  
Dan O'Leary ◽  
Rich Hichwa ◽  
Peg Nopoulos

Objective: The current study was designed to evaluate the neurobiology of reading in a group of men with nonsyndromic clefts of the lip or palate (NSCLP) compared with healthy controls by positron emission tomography. Design: Subjects included eight men with NSCLP compared with six healthy control men. By using radioactively labeled water (O15), regional brain blood flow was obtained during the performance of three simple reading tasks: reading unrelated words, reading unrelated sentences, and reading a story. Results: During each of the reading conditions, NSCLP subjects compared with healthy controls showed increased blood flow in areas previously reported to be involved in language processing and reading (inferior frontal lobe, cerebellum, and occipital lobe). The increased blood flow suggests a possible neural inefficiency. In contrast, when analyzing the brain regions involved in more complex language functioning (reading stories compared with reading only words), control subjects showed an increase in blood flow in a distributed neural circuit, whereas the NSCLP subjects showed a decrease in flow in these regions. Additionally, the NSCLP subjects had activation of several regions not activated in the healthy controls, suggesting a compensatory circuit used for this more complex reading task. Conclusions: These results indicate that subjects with NSCLP show abnormalities in the function of the distributed neural circuitry used for oral reading.


2004 ◽  
Vol 91 (2) ◽  
pp. 666-677 ◽  
Author(s):  
Adam S. Bristol ◽  
Michael A. Sutton ◽  
Thomas J. Carew

The tail-elicited siphon withdrawal reflex (TSW) has been a useful preparation in which to study learning and memory in Aplysia. However, comparatively little is known about the neural circuitry that translates tail sensory input (via the P9 nerves to the pleural ganglion) to final reflex output by siphon motor neurons (MNs) in the abdominal ganglion. To address this question, we examined the functional architecture of the TSW circuit by selectively severing nerves of semi-intact preparations and recording either tail-evoked responses in the siphon MNs or measuring siphon withdrawal responses directly. We found that the neural circuit underlying TSW is functionally lateralized. We next tested whether the expression of learning in the TSW reflects the underlying circuit architecture and shows side-specificity. We tested behavioral and physiological correlates of three forms of learning: sensitization, habituation, and dishabituation. Consistent with the circuit architecture, we found that sensitization and habituation of TSW are expressed in a side-specific manner. Unexpectedly, we found that dishabituation was expressed bilaterally, suggesting that a modulatory pathway bridges the two (ipsilateral) input pathways of the circuit, but this path is only revealed for a specific form of learning, dishabituation. These results suggest that the effects of a descending modulatory signal are differentially “gated” during sensitization and dishabituation.


eLife ◽  
2020 ◽  
Vol 9 ◽  
Author(s):  
David Deutsch ◽  
Diego Pacheco ◽  
Lucas Encarnacion-Rivera ◽  
Talmo Pereira ◽  
Ramie Fathy ◽  
...  

Sustained changes in mood or action require persistent changes in neural activity, but it has been difficult to identify the neural circuit mechanisms that underlie persistent activity and contribute to long-lasting changes in behavior. Here, we show that a subset of Doublesex+ pC1 neurons in the Drosophila female brain, called pC1d/e, can drive minutes-long changes in female behavior in the presence of males. Using automated reconstruction of a volume electron microscopic (EM) image of the female brain, we map all inputs and outputs to both pC1d and pC1e. This reveals strong recurrent connectivity between, in particular, pC1d/e neurons and a specific subset of Fruitless+ neurons called aIPg. We additionally find that pC1d/e activation drives long-lasting persistent neural activity in brain areas and cells overlapping with the pC1d/e neural network, including both Doublesex+ and Fruitless+ neurons. Our work thus links minutes-long persistent changes in behavior with persistent neural activity and recurrent circuit architecture in the female brain.


2018 ◽  
Author(s):  
Paavo Huoviala ◽  
Michael-John Dolan ◽  
Fiona M. Love ◽  
Philip Myers ◽  
Shahar Frechter ◽  
...  

AbstractEvolution has shaped nervous systems to produce stereotyped behavioural responses to ethologically relevant stimuli. For example when laying eggs, female Drosophila avoid geosmin, an odorant produced by toxic moulds. Here we identify second, third, and fourth order neurons required for this innate olfactory aversion. Connectomics data place these neurons in a complete synaptic circuit from sensory input to descending output. We find multiple levels of valence-specific convergence, including a novel form of axo-axonic input onto second order neurons conveying another danger signal, the pheromone of parasitoid wasps. However, we also observe extensive divergence: second order geosmin neurons connect with a diverse array of 80 third order cell types. We find a pattern of convergence of aversive odour channels at this level. Crossing one more synaptic layer, we identified descending neurons critical for egg-laying aversion. Our data suggest a transition from a labelled line organisation in the periphery to a highly distributed central brain representation that is then coupled to distinct descending pathways.


2014 ◽  
Vol 111 (6) ◽  
pp. 1183-1189 ◽  
Author(s):  
Andrei S. Kozlov ◽  
Timothy Q. Gentner

Recognition of natural stimuli requires a combination of selectivity and invariance. Classical neurobiological models achieve selectivity and invariance, respectively, by assigning to each cortical neuron either a computation equivalent to the logical “AND” or a computation equivalent to the logical “OR.” One powerful OR-like operation is the MAX function, which computes the maximum over input activities. The MAX function is frequently employed in computer vision to achieve invariance and considered a key operation in visual cortex. Here we explore the computations for selectivity and invariance in the auditory system of a songbird, using natural stimuli. We ask two related questions: does the MAX operation exist in auditory system? Is it implemented by specialized “MAX” neurons, as assumed in vision? By analyzing responses of individual neurons to combinations of stimuli we systematically sample the space of implemented feature recombination functions. Although we frequently observe the MAX function, we show that the same neurons that implement it also readily implement other operations, including the AND-like response. We then show that sensory adaptation, a ubiquitous property of neural circuits, causes transitions between these operations in individual neurons, violating the fixed neuron-to-computation mapping posited in the state-of-the-art object-recognition models. These transitions, however, accord with predictions of neural-circuit models incorporating divisive normalization and variable polynomial nonlinearities at the spike threshold. Because these biophysical properties are not tied to a particular sensory modality but are generic, the flexible neuron-to-computation mapping demonstrated in this study in the auditory system is likely a general property.


2020 ◽  
Author(s):  
Richard J. Kopchock ◽  
Bhavya Ravi ◽  
Addys Bode ◽  
Kevin M. Collins

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.


2020 ◽  
Author(s):  
Jacqueline Giovanniello ◽  
Sandra Ahrens ◽  
Kai Yu ◽  
Bo Li

AbstractSubstantial evidence indicates that a microdeletion on human chromosome 16p11.2 is linked to neurodevelopmental disorders including autism spectrum disorders (ASD). Carriers of this deletion show divergent symptoms besides the core features of ASD, such as anxiety and emotional symptoms. The neural mechanisms underlying these symptoms are poorly understood. Here we report mice heterozygous for a deletion allele of the genomic region corresponding to the human 16p11.2 microdeletion locus (i.e., the ‘16p11.2 del/+ mice’) have sex-specific anxiety-related behavioral and neural circuit changes. We found that female, but not male 16p11.2 del/+ mice showed enhanced fear generalization – a hallmark of anxiety disorders – after auditory fear conditioning, and displayed increased anxiety-like behaviors after physical restraint stress. Notably, such sex-specific behavioral changes were paralleled by an increase in activity in central amygdala neurons projecting to the globus pallidus in female, but not male 16p11.2 del/+ mice. Together, these results reveal female-specific anxiety phenotypes related to 16p11.2 microdeletion syndrome and a potential underlying neural circuit mechanism. Our study therefore identifies previously underappreciated sex-specific behavioral and neural changes in a genetic model of 16p11.2 microdeletion syndrome, and highlights the importance of investigating female-specific aspects of this syndrome for targeted treatment strategies.


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