scholarly journals The zebrafish dorsolateral habenula is required for updating learned behaviors

2019 ◽  
Author(s):  
Fabrizio Palumbo ◽  
Bram Serneels ◽  
Robbrecht Pelgrims ◽  
Emre Yaksi
Keyword(s):  
Cognitive Processes ◽  
Learning Rule ◽  
Potential Outcomes ◽  
Rapid Adaptation ◽  
Conditioned Place Avoidance ◽  
Behavioral Adaptations ◽  
Memory Extinction ◽  
Learned Behaviors ◽  
Place Avoidance ◽  
New Evidence

ABSTRACTOperant conditioning requires multiple cognitive processes, such as learning, prediction of potential outcomes and decision making. It is less clear how interactions of these processes lead to the behavioral adaptations that allow animals to cope with a changing environment. We showed that juvenile zebrafish can perform conditioned place avoidance learning, with an improving performance across development. Ablation of the dorsolateral habenula (dlHb), a brain region involved in associative learning and prediction of outcomes, led to an unexpected improvement in performance and delayed memory extinction. Interestingly, while the control animals exhibited rapid adaptation to a changing learning rule, dlHb ablated animals failed to adapt. Altogether, our results show that the dlHb plays a central role in switching animals’ strategies while integrating new evidence with prior experience.

Time stamp in conditioned place avoidance can be set to different circadian phases

2008 ◽  
Vol 89 (4) ◽  
pp. 591-594 ◽  
Author(s):  
Sean W. Cain ◽  
Robert J. McDonald ◽  
Martin R. Ralph
Keyword(s):  
Time Stamp ◽  
Conditioned Place Avoidance ◽  
Place Avoidance

Amygdala priming results in conditioned place avoidance

2002 ◽  
Vol 71 (3) ◽  
pp. 401-406 ◽  
Author(s):  
Shelley K. Thielen ◽  
Anantha Shekhar
Keyword(s):  
Conditioned Place Avoidance ◽  
Place Avoidance

Pronociceptive effects of a TRPA1 channel agonist methylglyoxal in healthy control and diabetic animals

2013 ◽  
Vol 4 (4) ◽  
pp. 260-260
Author(s):  
Hanna Viisanen ◽  
Maria Lasierra ◽  
Hong Wei ◽  
Ari Koivisto ◽  
Karl E. Åkerman ◽  
...  
Keyword(s):  
Diabetes Mellitus ◽  
Pain Behavior ◽  
Drg Neurons ◽  
Mechanical Hypersensitivity ◽  
Conditioned Place Avoidance ◽  
Healthy Control ◽  
Place Avoidance ◽  
Ongoing Pain ◽  
Endogenous Release

Abstract Aims Methylglyoxal (MG), a reactive carbonyl compound generated in diabetes mellitus (DM), activates the TRPA1 ion channel. Here we studied whether MG induces mechanical hypersensitivity or ongoing pain and whether the pronociceptive effect of MG is changed following its sustained endogenous release in DM. Methods DM was induced by streptozotocin (50-60 mg/kg i.p.) in the rat. MG and Chembridge-5861528 (CHEM), a selective TRPA1 channel antagonist, were administered intraplantarly (i.pl.) in control and diabetic animals. Limb withdrawal to monofilaments was used as an index of hypersensitivity, and observation of sustained pain-like behavior and conditioned place-avoidance test were used to assess ongoing pain. In vitro calcium imaging was used to study whether MG induces sustained activation of dorsal root ganglion (DRG) neurons of diabetic as well as control animals. Results MG produced mechanical hypersensitivity and ongoing pain behavior in control animals, which effects were reduced in diabetic animals. CHEM treatment at a dose suppressing the MG-induced mechanical hypersensitivity failed to suppress the MG-induced ongoing pain behavior. MG was able to produce sustained calcium inflow in DRG neurons of DM as well as control animals. Conclusions The results suggest that MG induces hypersensitivity and ongoing pain that are reduced in diabetes mellitus, possibly due to changes caused by the DM-induced sustained endogenous release of MG. Moreover, the MG-induced mechanical hypersensitivity can be more effectively reversed by a TRPA1 antagonist than the MG-induced ongoing pain behavior.

scholarly journals The Role of Central Amygdala Corticotropin-Releasing Factor in Predator Odor Stress-Induced Avoidance Behavior and Escalated Alcohol Drinking in Rats

2019 ◽  
Author(s):  
Marcus M. Weera ◽  
Allyson L. Schreiber ◽  
Elizabeth M. Avegno ◽  
Nicholas W. Gilpin
Keyword(s):  
Alcohol Drinking ◽  
Avoidance Behavior ◽  
Conditioned Avoidance ◽  
Corticotropin Releasing Factor ◽  
Predator Odor ◽  
Central Amygdala ◽  
Post Traumatic Stress ◽  
Conditioned Place Avoidance ◽  
Place Avoidance ◽  
Post Traumatic

ABSTRACTPost-traumatic stress disorder (PTSD) is characterized by avoidance of trauma-associated stimuli and amygdala hyperreactivity, and is highly co-morbid with alcohol use disorder (AUD). Our lab uses a predator odor (bobcat urine) stress model that produces conditioned avoidance of an odor-paired context in a subset of rats, mirroring avoidance symptoms that manifest in some but not all humans exposed to trauma. We previously showed that after predator odor stress, Avoiders exhibit escalated alcohol drinking, higher aversion-resistant operant alcohol responding, hyperalgesia, and greater anxiety-like behavior compared to unstressed Controls. We also showed that systemic antagonism of corticotropin-releasing factor-1 receptors (CRFR1) reduced escalation of alcohol drinking in rats not indexed for avoidance, that corticotropin-releasing factor (CRF) infusions into the central amygdala (CeA) produced conditioned place avoidance in stress-naïve rats, and that intra-CeA infusion of a CRFR1 antagonist reduced hyperalgesia in Avoiders. Here, we show that avoidance behavior is persistent after repeated predator odor exposure and is resistant to extinction. In addition, Avoiders showed lower weight gain than Controls after predator odor re-exposure. In the brain, higher avoidance was correlated with higher number of c-Fos+ cells and CRF immunoreactivity in the CeA. Finally, we show that intra-CeA CRFR1 antagonism reversed post-stress escalation of alcohol drinking and reduced avoidance behavior in Avoiders. Collectively, these findings suggest that elucidation of the mechanisms by which CRFR1-gated CeA circuits regulate avoidance behavior and alcohol drinking may lead to better understanding of the neural mechanisms underlying co-morbid PTSD and AUD.

scholarly journals Inactivation of the prelimbic rather than infralimbic cortex impairs acquisition and expression of formalin-induced conditioned place avoidance

2014 ◽  
Vol 569 ◽  
pp. 89-93 ◽  
Author(s):  
Zhao-Cai Jiang ◽  
Qi Pan ◽  
Chun Zheng ◽  
Xiao-Fei Deng ◽  
Jin-Yan Wang ◽  
...  
Keyword(s):  
Infralimbic Cortex ◽  
Conditioned Place Avoidance ◽  
Place Avoidance

scholarly journals Habenula kisspeptin retrieves morphine impaired fear memory in zebrafish

2020 ◽  
Vol 10 (1) ◽  
Author(s):  
Mageswary Sivalingam ◽  
Satoshi Ogawa ◽  
Ishwar S. Parhar
Keyword(s):  
Fear Memory ◽  
Treated Group ◽  
Mrna Levels ◽  
Morphine Treatment ◽  
Conditioned Place Avoidance ◽  
Serotonin System ◽  
Total Brain ◽  
Evolutionarily Conserved ◽  
Place Avoidance

Abstract The habenula is an evolutionarily conserved brain structure, which has recently been implicated in fear memory. In the zebrafish, kisspeptin (Kiss1) is predominantly expressed in the habenula, which has been implicated as a modulator of fear response. Hence, in the present study, we questioned whether Kiss1 has a role in fear memory and morphine-induced fear memory impairment using an odorant cue (alarm substances, AS)-induced fear avoidance paradigm in adult zebrafish, whereby the fear-conditioned memory can be assessed by a change of basal place preference (= avoidance) of fish due to AS-induced fear experience. Subsequently, to examine the possible role of Kiss1 neurons-serotonergic pathway, kiss1 mRNA and serotonin levels were measured. AS exposure triggered fear episodes and fear-conditioned place avoidance. Morphine treatment followed by AS exposure, significantly impaired fear memory with increased time-spent in AS-paired compartment. However, fish administered with Kiss1 (10–21 mol/fish) after morphine treatment had significantly lower kiss1 mRNA levels but retained fear memory. In addition, the total brain serotonin levels were significantly increased in AS- and Kiss1-treated groups as compared to control and morphine treated group. These results suggest that habenular Kiss1 might be involved in consolidation or retrieval of fear memory through the serotonin system.

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