scholarly journals Satiation State-dependent Dopaminergic Control of Food Seeking in Drosophila

2017 ◽  
Author(s):  
Dan Landayan ◽  
David S. Feldman ◽  
Fred W. Wolf
Keyword(s):  
Neural Activity ◽  
Mushroom Body ◽  
Neural Circuits ◽  
Discrete Source ◽  
D1 Receptor ◽  
Neural Pathways ◽  
State Dependent ◽  
Increase Locomotor Activity ◽  
Seeking Behavior ◽  
Food Seeking

Hunger evokes stereotypic behaviors that favor the discovery of nutrients. The neural pathways that coordinate internal and external cues to motivate food seeking behaviors are only partly known. Drosophila that are food deprived increase locomotor activity, are more efficient in locating a discrete source of nutrition, and are willing to overcome adversity to obtain food. Here we developed a semi-naturalistic assay and show that two distinct dopaminergic neural circuits regulate food-seeking behaviors. One group, the PAM neurons, functions in food deprived flies while the other functions in well fed flies, and both promote food seeking. These satiation state-dependent circuits converge on dopamine D1 receptor-expressing Kenyon cells of the mushroom body, where neural activity promotes food seeking behavior independent of satiation state. These findings provide evidence for active food seeking in well-fed flies that is separable from hunger-driven seeking.

scholarly journals Drosophila mushroom bodies integrate hunger and satiety signals to control innate food-seeking behavior

eLife ◽  
2018 ◽  
Vol 7 ◽  
Author(s):  
Chang-Hui Tsao ◽  
Chien-Chun Chen ◽  
Chen-Han Lin ◽  
Hao-Yu Yang ◽  
Suewei Lin
Keyword(s):  
Dopaminergic Neurons ◽  
Mushroom Body ◽  
Energy State ◽  
Fruit Fly ◽  
Mushroom Bodies ◽  
Kenyon Cells ◽  
Control Food ◽  
Seeking Behavior ◽  
Output Neurons ◽  
Food Seeking

The fruit fly can evaluate its energy state and decide whether to pursue food-related cues. Here, we reveal that the mushroom body (MB) integrates hunger and satiety signals to control food-seeking behavior. We have discovered five pathways in the MB essential for hungry flies to locate and approach food. Blocking the MB-intrinsic Kenyon cells (KCs) and the MB output neurons (MBONs) in these pathways impairs food-seeking behavior. Starvation bi-directionally modulates MBON responses to a food odor, suggesting that hunger and satiety controls occur at the KC-to-MBON synapses. These controls are mediated by six types of dopaminergic neurons (DANs). By manipulating these DANs, we could inhibit food-seeking behavior in hungry flies or promote food seeking in fed flies. Finally, we show that the DANs potentially receive multiple inputs of hunger and satiety signals. This work demonstrates an information-rich central circuit in the fly brain that controls hunger-driven food-seeking behavior.

scholarly journals Dissecting neural pathways for forgetting in Drosophila olfactory aversive memory

2015 ◽  
Vol 112 (48) ◽  
pp. E6663-E6672 ◽  
Author(s):  
Yichun Shuai ◽  
Areekul Hirokawa ◽  
Yulian Ai ◽  
Min Zhang ◽  
Wanhe Li ◽  
...  
Keyword(s):  
Reversal Learning ◽  
Dopaminergic Neurons ◽  
Mushroom Body ◽  
Biologically Active ◽  
Molecular Pathways ◽  
Neural Pathways ◽  
Active Process ◽  
Glutamatergic Neurons ◽  
Memory Decay ◽  
Over Time

Recent studies have identified molecular pathways driving forgetting and supported the notion that forgetting is a biologically active process. The circuit mechanisms of forgetting, however, remain largely unknown. Here we report two sets of Drosophila neurons that account for the rapid forgetting of early olfactory aversive memory. We show that inactivating these neurons inhibits memory decay without altering learning, whereas activating them promotes forgetting. These neurons, including a cluster of dopaminergic neurons (PAM-β′1) and a pair of glutamatergic neurons (MBON-γ4>γ1γ2), terminate in distinct subdomains in the mushroom body and represent parallel neural pathways for regulating forgetting. Interestingly, although activity of these neurons is required for memory decay over time, they are not required for acute forgetting during reversal learning. Our results thus not only establish the presence of multiple neural pathways for forgetting in Drosophila but also suggest the existence of diverse circuit mechanisms of forgetting in different contexts.

scholarly journals Recurrent circuitry is required to stabilize piriform cortex odor representations across brain states

eLife ◽  
2020 ◽  
Vol 9 ◽  
Author(s):  
Kevin A Bolding ◽  
Shivathmihai Nagappan ◽  
Bao-Xia Han ◽  
Fan Wang ◽  
Kevin M Franks
Keyword(s):  
Neural Activity ◽  
Neural Circuits ◽  
Activity Patterns ◽  
Piriform Cortex ◽  
Theoretical Studies ◽  
Pattern Completion ◽  
Attractor Networks ◽  
Attractor Dynamics ◽  
Brain States ◽  
Associative Function

Pattern completion, or the ability to retrieve stable neural activity patterns from noisy or partial cues, is a fundamental feature of memory. Theoretical studies indicate that recurrently connected auto-associative or discrete attractor networks can perform this process. Although pattern completion and attractor dynamics have been observed in various recurrent neural circuits, the role recurrent circuitry plays in implementing these processes remains unclear. In recordings from head-fixed mice, we found that odor responses in olfactory bulb degrade under ketamine/xylazine anesthesia while responses immediately downstream, in piriform cortex, remain robust. Recurrent connections are required to stabilize cortical odor representations across states. Moreover, piriform odor representations exhibit attractor dynamics, both within and across trials, and these are also abolished when recurrent circuitry is eliminated. Here, we present converging evidence that recurrently-connected piriform populations stabilize sensory representations in response to degraded inputs, consistent with an auto-associative function for piriform cortex supported by recurrent circuitry.

scholarly journals Enhanced food motivation in obese mice is controlled by D1R expressing spiny projection neurons in the nucleus accumbens.

2022 ◽  
Author(s):  
Bridget A Matikainen-Ankney ◽  
Alex A Legaria ◽  
Yvan M Vachez ◽  
Caitlin A Murphy ◽  
Yiyan A Pan ◽  
...  
Keyword(s):  
Nucleus Accumbens ◽  
Food Reward ◽  
Ex Vivo ◽  
D1 Receptor ◽  
Physical Work ◽  
Projection Neurons ◽  
Food Motivation ◽  
Obese Mice ◽  
Food Seeking

Obesity is a chronic relapsing disorder that is caused by an excess of caloric intake relative to energy expenditure. In addition to homeostatic feeding mechanisms, there is growing recognition of the involvement of food reward and motivation in the development of obesity. However, it remains unclear how brain circuits that control food reward and motivation are altered in obese animals. Here, we tested the hypothesis that signaling through pro-motivational circuits in the core of the nucleus accumbens (NAc) is enhanced in the obese state, leading to invigoration of food seeking. Using a novel behavioral assay that quantifies physical work during food seeking, we confirmed that obese mice work harder than lean mice to obtain food, consistent with an increase in the relative reinforcing value of food in the obese state. To explain this behavioral finding, we recorded neural activity in the NAc core with both in vivo electrophysiology and cell-type specific calcium fiber photometry. Here we observed greater activation of D1-receptor expressing NAc spiny projection neurons (NAc D1SPNs) during food seeking in obese mice relative to lean mice. With ex vivo slice physiology we identified both pre- and post-synaptic mechanisms that contribute to this enhancement in NAc D1SPN activity in obese mice. Finally, blocking synaptic transmission from D1SPNs decreased physical work during food seeking and attenuated high-fat diet-induced weight gain. These experiments demonstrate that obesity is associated with a selective increase in the activity of D1SPNs during food seeking, which enhances the vigor of food seeking. This work also establishes the necessity of D1SPNs in the development of diet-induced obesity, identifying a novel potential therapeutic target.

scholarly journals Fronto-striatal projections regulate approach-avoidance conflict

2020 ◽  
Author(s):  
Adrienne C. Loewke ◽  
Adelaide R. Minerva ◽  
Alexandra B. Nelson ◽  
Anatol C. Kreitzer ◽  
Lisa A. Gunaydin
Keyword(s):  
Anxiety Disorders ◽  
Avoidance Behavior ◽  
D1 Receptor ◽  
Projection Neurons ◽  
Medium Spiny Neurons ◽  
Neural Pathways ◽  
Spiny Neurons ◽  
Striatal Projection Neurons ◽  
Neural Computations ◽  
Approach Avoidance

ABSTRACTThe dorsomedial prefrontal cortex (dmPFC) has been linked to approach-avoidance behavior and decision-making under conflict, key neural computations thought to be altered in anxiety disorders. However, the heterogeneity of efferent prefrontal projections has obscured identification of the specific top-down neural pathways regulating these anxiety-related behaviors. While the dmPFC-amygdala circuit has long been implicated in controlling reflexive fear responses, recent work suggests that this circuit is less important for avoidance behavior. We hypothesized that dmPFC neurons projecting to the dorsomedial striatum (DMS) represent a subset of prefrontal neurons that robustly encode and drive approach-avoidance behavior. Using fiber photometry recording during the elevated zero maze (EZM) task, we show heightened neural activity in prefrontal and fronto-striatal projection neurons, but not fronto-amydalar projection neurons, during exploration of the anxiogenic open arms of the maze. Additionally, through pathway-specific optogenetics we demonstrate that this fronto-striatal projection preferentially excites postsynaptic D1 receptor-expressing medium spiny neurons in the DMS and bidirectionally controls avoidance behavior. We conclude that this striatal-projecting subpopulation of prefrontal neurons regulates approach-avoidance conflict, supporting a model for prefrontal control of defensive behavior in which the dmPFC-amygdala projection controls reflexive fear behavior and the dmPFC-striatum projection controls anxious avoidance behavior. Our findings identify this fronto-striatal circuit as a valuable therapeutic target for developing interventions to alleviate excessive avoidance behavior in anxiety disorders.

scholarly journals The sigma-1 receptor as key common factor in cocaine and food-seeking behaviors

2019 ◽  
Vol 63 (4) ◽  
pp. R81-R92 ◽  
Author(s):  
David Aguinaga ◽  
Mireia Casanovas ◽  
Rafael Rivas-Santisteban ◽  
Irene Reyes-Resina ◽  
Gemma Navarro ◽  
...  
Keyword(s):  
Eating Disorders ◽  
Drugs Of Abuse ◽  
Common Factor ◽  
G Protein Coupled Receptors ◽  
Sigma 1 Receptor ◽  
New Findings ◽  
Sigma 1 ◽  
Seeking Behavior ◽  
Food Seeking ◽  
G Protein Coupled

Addiction and eating disorders involve brain reward circuits. Binge eating predisposes to addictive behavior, while the cessation of exposure to drugs of abuse leads to reward activities, including intake of tasty foods. Cocaine use is associated with a decrease in food intake, with reversal after drug use is discontinued. Exciting new findings show that receptors for the ‘hunger’ hormone, ghrelin, directly interact with the sigma-1 receptor (σ1R), which is a target of cocaine. σ1Rs are key players in regulating dopaminergic neurotransmission and ghrelin-mediated actions. This review focuses on the σ1 receptor as a general neuroendocrine regulator by directly interacting with neuronal G-protein-coupled receptors. This review also covers the early mechanisms by which cocaine binding to σ1 blocks the food-seeking behavior triggered by ghrelin. Those findings appear as fundamental to understand common mechanisms in drug addiction and eating disorders.

Cannabinoid Cb1 Receptor Antagonists/Inverse Agonists and Food-Seeking Behavior

2011 ◽  
pp. 441-456
Author(s):  
John D. Salamone ◽  
Kelly Sink ◽  
Kristen N. Segovia ◽  
Patrick A. Randall ◽  
Peter J. McLaughlin ◽  
...  
Keyword(s):  
Cb1 Receptor ◽  
Cannabinoid Cb1 Receptor ◽  
Receptor Antagonists ◽  
Inverse Agonists ◽  
Seeking Behavior ◽  
Food Seeking ◽  
Cb1 Receptor Antagonists

scholarly journals Two Different Forms of Arousal in Drosophila Are Oppositely Regulated by the Dopamine D1 Receptor Ortholog DopR via Distinct Neural Circuits

Neuron ◽  
2009 ◽  
Vol 64 (4) ◽  
pp. 522-536 ◽  
Author(s):  
Tim Lebestky ◽  
Jung-Sook C. Chang ◽  
Heiko Dankert ◽  
Lihi Zelnik ◽  
Young-Cho Kim ◽  
...  
Keyword(s):  
Neural Circuits ◽  
Dopamine D1 Receptor ◽  
D1 Receptor

scholarly journals Genetic Manipulation of the Odor-Evoked Distributed Neural Activity in the Drosophila Mushroom Body

Neuron ◽  
2001 ◽  
Vol 29 (1) ◽  
pp. 267-276 ◽  
Author(s):  
Yalin Wang ◽  
Nicholas J.D. Wright ◽  
Hui-Fu Guo ◽  
Zuoping Xie ◽  
Karel Svoboda ◽  
...  
Keyword(s):  
Neural Activity ◽  
Mushroom Body ◽  
Genetic Manipulation

scholarly journals A novel device for real-time measurement and manipulation of licking behavior in head-fixed mice

2018 ◽  
Vol 120 (6) ◽  
pp. 2975-2987 ◽  
Author(s):  
Brice Williams ◽  
Anderson Speed ◽  
Bilal Haider
Keyword(s):  
Real Time ◽  
Neural Activity ◽  
Closed Loop ◽  
Neural Circuits ◽  
Neural Circuit ◽  
Visual Behavior ◽  
Sensory Stimuli ◽  
Neural Recordings ◽  
Control Signals ◽  
Sensory Motor

The mouse has become an influential model system for investigating the mammalian nervous system. Technologies in mice enable recording and manipulation of neural circuits during tasks where they respond to sensory stimuli by licking for liquid rewards. Precise monitoring of licking during these tasks provides an accessible metric of sensory-motor processing, particularly when combined with simultaneous neural recordings. There are several challenges in designing and implementing lick detectors during head-fixed neurophysiological experiments in mice. First, mice are small, and licking behaviors are easily perturbed or biased by large sensors. Second, neural recordings during licking are highly sensitive to electrical contact artifacts. Third, submillisecond lick detection latencies are required to generate control signals that manipulate neural activity at appropriate time scales. Here we designed, characterized, and implemented a contactless dual-port device that precisely measures directional licking in head-fixed mice performing visual behavior. We first determined the optimal characteristics of our detector through design iteration and then quantified device performance under ideal conditions. We then tested performance during head-fixed mouse behavior with simultaneous neural recordings in vivo. We finally demonstrate our device’s ability to detect directional licks and generate appropriate control signals in real time to rapidly suppress licking behavior via closed-loop inhibition of neural activity. Our dual-port detector is cost effective and easily replicable, and it should enable a wide variety of applications probing the neural circuit basis of sensory perception, motor action, and learning in normal and transgenic mouse models. NEW & NOTEWORTHY Mice readily learn tasks in which they respond to sensory cues by licking for liquid rewards; tasks that involve multiple licking responses allow study of neural circuits underlying decision making and sensory-motor integration. Here we design, characterize, and implement a novel dual-port lick detector that precisely measures directional licking in head-fixed mice performing visual behavior, enabling simultaneous neural recording and closed-loop manipulation of licking.

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