JOURNAL OF ANIMAL ECOLOGY
·
2024
·Vol. 94
·期 1
·112-124
·
IF 3.5
Gaoying Gu,Ziqi Wang,Tao Lin,Sainan Wang,Jianjun Li,Shihao Dong,James C. Nieh,Ken Tan
en This link goes to a English section zh This link goes to a Chinese section Predatory threats, even when they do not involve direct consumption (non-consumptive effects, NCEs), can profoundly influence the physiology and behaviour of prey. For example, honeybees that encounter hornet predators show responses similar to fear. However, the physiological mechanisms that are connected with this fear-like response and their effects on bee cognition and olfaction remain largely unknown. We show that bees decreased time spent near the hornet, demonstrated fearful behaviour and moved with greater velocity to escape. After a prolonged 24-h exposure, bees adopted defensive clustering, displayed greater predator avoidance, and experienced a decline in brain dopamine levels. Prolonged predator exposure also diminished bee olfactory sensitivity to odours and their mechanical sensitivity to air currents, contributing to impaired olfactory learning. However, boosting brain dopamine reversed one fear-like behaviour (average bee velocity in the presence of a hornet) and rescued olfactory sensitivity and learning. We therefore provide evidence linking dopamine to sensory and cognitive declines associated with fear in an insect. 摘要 en This link goes to a English section zh This link goes to a Chinese section 即便对猎物不构成直接捕杀(非消耗性捕食效应)，捕食者也可以对猎物的生理和行为造成严重的影响。例如，遭遇胡蜂捕食者时，蜜蜂会产生类似恐惧的反应。 然而，该类似恐惧反应相关的生理机制还没有详细研究，该类似恐惧反应对蜜蜂的认知嗅觉的影响也没有报道。 我们的实验结果表明，蜜蜂在遭遇胡蜂时表现出惧怕行为，表现为减少了在胡蜂附近的停留时间，并以更快的速度逃离。但在24小时的胡蜂胁迫后，蜜蜂表现出防御性集群行为，大脑多巴胺水平下降。长时间的捕食者暴露还降低了蜜蜂对气味的嗅觉敏感度以及气流的机械敏感性，导致嗅觉联想学习能力受损。 然而，人为提高蜜蜂大脑多巴胺水平缓解了它们对胡蜂的恐惧，并在一定程度上恢复了蜜蜂的嗅觉敏感度和学习能力。 因此，我们的研究表明多巴胺参与昆虫恐惧行为的调控，与嗅觉和认知下降密切相关。
研究领域:
昆虫学
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神经生物学
·
行为生态学
✓ 已验证
DOI
高影响因子
Frontiers in Psychiatry
·
2024
·
IF 3.2
Gu Tengyu,Dong Jing,Ge Jing,Feng Jialu,Liu Xiaoliu,Chen Yun,Liu Jianfeng
The claustrum (CLA), a subcortical area between the insular cortex and striatum, innervates almost all cortical regions of the mammalian brain. There is growing evidence that CLA participates in many brain functions, including memory, cognition, and stress response. It is proposed that dysfunction or malfunction of the CLA might be the pathology of some brain diseases, including stress-induced depression and anxiety. However, the role of the CLA in fear memory and anxiety disorders remains largely understudied. Here, we evaluated the influences of neurotoxic lesions of the CLA on auditory-cued fear memory and anxiety-like behaviors in rats.We found that lesions of anterior CLA (aCLA) but not posterior CLA (pCLA) before fear conditioning attenuated fear retrieval, facilitated extinction, and reduced freezing levels during the extinction retention test. Post-learning lesions of aCLA but not pCLA facilitated fear extinction and attenuated freezing behavior during the extinction retention test. Lesions of aCLA or pCLA did not affect anxiety-like behaviors evaluated by the open field test and elevated plus-maze test.These data suggested that aCLA but not pCLA was involved in fear memory and extinction.Future studies are needed to further investigate the anatomical and functional connections of aCLA subareas that are involved in fear conditioning, which will deepen our understanding of CLA functions.
研究领域:
神经科学
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精神病学
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行为神经科学
✓ 已验证
DOI
高影响因子
BEHAVIOURAL BRAIN RESEARCH
·
2025
·
IF 2.3
Yue-Heng Yan,Hong-Kun Wang,Zi-Hao Wang,Rui-Ze Wang,Ruo-Xuan Li,Li-Li Huang,Yan-Yan Wang
NMDA receptors (NMDAR) are vital in CNS activities such as anxiety, memory, and cognition, and the neurobiological mechanisms behind anxiety disorders are exceedingly complicated. The "glutamic acid theory" posits that glutamate excitotoxicity is a key pathophysiological mechanism in anxiety disorders. However, the exact mechanism by which conditioned fear contributes to anxiety disorders remains unknown.Based on the conditioned fear-induced anxiety disorder model, this work aims to investigate changes in NMDAR and related proteins throughout the acquisition and expression of fear memory, as well as the impact on synaptic structural and functional plasticity. Injecting the NMDA receptor endogenous agonist D-Serine (50 μg/μL) and the noncompetitive antagonist MK-801 (1 μg/μL) into the lateral ventricle of the conditioned fear model rats, as well as conducting behavioral observations, show that NMDAR are closely involved in the development of conditioned fear-induced anxiety. Model rats showed significant changes in glutamate (Glu) and γ-aminobutyric acid (GABA) levels in the amygdala (BLA), as well as expression of NMDAR and downstream BDNF/TrkB signaling pathway components. At the same time, model rats exhibited synaptic and neuronal injury, aberrant long-term potentiation (LTP), and decreased expression of essential synaptic proteins SYP and PSD-95. In conclusion, our study demonstrates that NMDAR and synaptic plasticity play a critical role in the development of conditioned fear-induced anxiety, serving as an important reference for understanding the neurobiological underpinnings of anxiety disorders and providing insights into their treatment and new possible targets.
研究领域:
神经科学
·
行为学
·
分子生物学
✓ 已验证
产品关联
DOI
PubMed
高影响因子
Journal of Advanced Research
·
2024
·
IF 11.4
Ya-Bo Zhao,Shi-Zhe Wang,Wen-Ting Guo,Le Wang,Xun Tang,Jin-Nan Li,Lin Xu,Qi-Xin Zhou
Introduction Subtypes of the dipeptidyl peptidase (DPP) family, such as DPP4, are reportedly associated with memory impairment. DPP9 is widely distributed in cells throughout the body, including the brain. However, whether DPP9 regulates memory has not yet been elucidated. Objectives This study aimed to elucidate the role of DPP9 in memory, as well as the underlying molecular mechanism. Methods We performed immunofluorescence on mouse brains to explore the distribution of DPP9 in different brain regions and used AAV vectors to construct knockdown and overexpression models. The effects of changing DPP9 expression on memory were demonstrated through behavioral experiments. Finally, we used electrophysiology, proteomics and affinity purification mass spectrometry (AP-MS) to study the molecular mechanism by which DPP9 affects memory. Results Here, we report that DPP9, which is found almost exclusively in neurons, is expressed and has enzyme activity in many brain regions, especially in the hippocampus. Hippocampal DPP9 expression increases after fear memory formation. Fear memory was impaired by DPP9 knockdown and enhanced by DPP9 protein overexpression in the hippocampus. According to subsequent hippocampal proteomics, multiple pathways, including the peptidase pathway, which can be bidirectionally regulated by DPP9. DPP9 directly interacts with its enzymatic substrate neuropeptide Y (NPY) in neurons. Hippocampal long-term potentiation (LTP) is also bidirectionally regulated by DPP9. Moreover, inhibiting DPP enzyme activity impaired both LTP and memory. In addition, AP-MS revealed that DPP9-interacting proteins are involved in the functions of dendritic spines and axons. By combining AP-MS and proteomics, DPP9 was shown to play a role in regulating actin functions. Conclusion Taken together, our findings reveal that DPP9 affects the CNS not only through enzymatic activity but also through protein–protein interactions. This study provides new insights into the molecular mechanisms of memory and DPP family functions.
研究领域:
神经科学
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分子生物学
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行为科学
·
蛋白质组学
✓ 已验证
DOI
PubMed
高影响因子
Frontiers in Neuroscience
·
2022
·
IF 5.152
Fan Penghui,Song Yilin,Lu Botao,Wang Yiding,Dai Yuchuan,Xie Jingyu,He Enhui,Xu Zhaojie,Yang Gucheng,Mo Fan,Liu Juntao,Wang Mixia,Cai Xinxia
The medial amygdala (MA) plays an important role in the innate fear circuit. However, the electrophysiological mechanism of MA for processing innate fear needs to be further explored. In this study, we fabricated microelectrode arrays (MEAs) with detecting sites arranged to match the location and shape of MA in mice and detected the electrophysiology in freely behaving mice under 2-methyl-2-thiazoline (2MT)-induced fear. The detection performance of MEA is improved by modifying metal nanoparticles and conductive polymers (PtNPs/PEDOT:PSS). After modification, the impedance magnitude and phase of electrodes were decreased to 27.0 ± 2.3 kΩ and −12.30 ± 0.52°, respectively, leading to a signal-to-noise ratio of 10. Its electrochemical stability and mechanical stability were also verified by cyclic voltammetry (CV) sweeping and ultrasonic vibration. MEAs were then implanted into the MA of mice, and the electrophysiology and behavioral characteristics were synchronously recorded and analyzed. The results showed that 2MT induced strong defensive behaviors in mice, accompanied by increases in the average spike firing rate and local field potential (LFP) power of MA neurons. According to principles commonly applied to cortical extracellular recordings, the recorded neurons are divided into two classes based on waveforms. Statistics showed that about 37% of type 1 neurons (putative GABAergic neurons) and 87% of type 2 neurons (putative glutamatergic neurons) were significantly activated under innate fear. At the same time, the firing rate of some activated neurons had a good linear correlation with the freezing rate.
研究领域:
神经科学
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电生理学
·
行为科学
✓ 已验证
产品关联
DOI
PubMed
高影响因子
BIOFACTORS
·
2023
·
IF 6
Zichen Gui,Jiawen Wang,Yue Zhang,Binbin Wan,Zhiqiang Ke,Zhanhong Ren,Xiaosong Yang,Min Lei,Xiying Guo,Xiufen Liu,Changhan Ouyang,Ninghua Wu,Qingjie Chen
Cognitive impairment is increasingly recognized as an important comorbidity of diabetes progression; however, the underlying molecular mechanism is unclear. Dapagliflozin, an inhibitor of sodium-glucose co-transporter 2 (SGLT2), has shown promising effects against diabetes in rodent experiments and human clinical assays. This study aimed to determine the underlying mechanism and examine the effect of dapagliflozin on diabetic cognitive impairment. To create an in vivo model of diabetic cognitive impairment, streptozotocin (STZ)-induced diabetic mice were used. Dapagliflozin was administered to mice for 8 weeks. The context fear condition and Morris water maze test was used to evaluate mice's behavioral change. Western blotting was used to evaluate protein expression. Hematoxylin and eosin (HE) and Nissl staining were applied to monitor morphological and structural changes. Congo red staining was performed to identify the formation of senile plaques. Mitochondria morphology was examined using a transmission electron microscope, and blood flow in the mouse cerebral cortex was measured using a laser Doppler imaging assay. Comparison to the diabetes mellitus (DM) group, the dapagliflozin group had lower glucose levels. Behavioral studies have shown that dapagliflozin can restore memory deficits in diabetic mice. The murky cell membrane edges and Nissl bodies more difficult to identify in the DM group were revealed by HE and Nissl staining, which were both improved by dapagliflozin treatment. Dapagliflozin inhibited the progression of Aβ generation and the reduced cerebral blood flow in the DM group was rescued. After dapagliflozin treatment, damaged mitochondria and lack of SGLT2 in the hippocampus and cortex of diabetic mice were repaired. Diabetes-induced cognitive dysfunction was attenuated by dapagliflozin and the effect was indirect rather than direct.
研究领域:
药理学
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神经科学
·
糖尿病研究
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产品关联
DOI
PubMed
高影响因子
Frontiers in Neuroscience
·
2022
·
IF 5.152
Ting-Ting Pan,Chao Liu,De-Min Li,Tian-Hao Zhang,Wei Zhang,Shi-Lun Zhao,Qi-Xin Zhou,Bin-Bin Nie,Gao-Hong Zhu,Lin Xu,Hua Liu
Animal contextual fear conditioning (CFC) models are the most-studied forms used to explore the neural substances of posttraumatic stress disorder (PTSD). In addition to the well-recognized hippocampal-amygdalar system, the retrosplenial cortex (RSC) is getting more and more attention due to substantial involvement in CFC, but with a poor understanding of the specific roles of its two major constituents-dysgranular (RSCd) and granular (RSCg). The current study sought to identify their roles and underlying brain network mechanisms during the encoding processing of the rat CFC model. Rats with pharmacologically inactivated RSCd, RSCg, and corresponding controls underwent contextual fear conditioning. [ 18 F]-fluorodeoxyglucose positron emission tomography/computed tomography ( 18 F-FDG PET/CT) scanning was performed for each animal. The 5-h and 24-h retrieval were followed to test the formation of contextual memory. Graph theoretic tools were used to identify the brain metabolic network involved in encoding phase, and changes of nodal (brain region) properties linked, respectively, to disturbed RSCd and RSCg were analyzed. Impaired retrieval occurred in disturbed RSCd animals, not in RSCg ones. The RSC, hippocampus (Hip), amygdala (Amy), piriform cortex (Pir), and visual cortex (VC) are hub nodes of the brain-wide network for contextual fear memory encoding in rats. Nodal degree and efficiency of hippocampus and its connectivity with amygdala, Pir, and VC were decreased in rats with disturbed RSCd, while not in those with suppressed RSCg. The RSC plays its role in contextual fear memory encoding mainly relying on its RSCd part, whose condition would influence the activity of the hippocampal-amygdalar system.
研究领域:
神经科学
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行为神经科学
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精神病学
·
神经成像
✓ 已验证
DOI
PubMed
高影响因子
Cell Death Discovery
·
2021
·Vol. 7
·期 1
·1-13
·
IF 5.241
Yang Xiu,Li Xu,Liu Le,Chen Yuan-Hao,You Yue,Gao Yin,Liu Yue-Ying,Yang Li,Tong Kun,Chen Di-Shi,Hao Jing-Ru,Sun Nan,Zhao Zi-Ming,Gao Can
Alzheimer’s disease (AD) is characterized by aberrant accumulation of extracellular β-amyloid (Aβ) peptides in the brain. Soluble Aβ oligomers are thought to be the most neurotoxic species and are correlated with cognitive dysfunction in early AD. However, there is still no effective treatment so far. We determined that Pep63, a small peptide, had a neuroprotective effect on synaptic plasticity and memory in our previous study. Here, we developed novel and multifunctional liposomes targeting both Aβ oligomers and fibrils based on a liposome delivery system. Transferrin-Pep63-liposomes (Tf-Pep63-Lip), possessing the ability for blood-brain barrier targeting, were also incorporated with phosphatidic acid (PA) and loaded with neuroprotective Pep63. We discovered that administration of Tf-Pep63-Lip could significantly reduce the Aβ burden in the hippocampus, and improve cognitive deficits in 6-month-old APP/PS1 mice in the Morris-Water maze task and fear-conditioning test with the combined effects of PA and Pep63. Tf-Pep63-Lip could capture Aβ oligomers or fibrils and then facilitated microglial chemotaxis nearby for clearance. Simultaneously, Tf-Pep63-Lip hindered Aβ1-42 aggregation and disaggregated Aβ1-42 assembly due to multivalent PA-Aβ. Pep63 effectively inhibited the binding between EphB2 and Aβ oligomers after release from liposomes and rescued NMDA receptors trafficking, the basis of synaptic plasticity. No side effects were observed in either APP/PS1 or wild-type mice, indicating that Tf-Pep63-Lip might be safe under the dosing regimen used in our experiment. Taken together, our results suggested that Tf-Pep63-Lip may serve as a safe and efficient agent for AD combination therapy.
研究领域:
神经科学
·
药理学
·
分子生物学
·
神经退行性疾病
✓ 已验证
产品关联
DOI
PubMed
高影响因子
JOURNAL OF PSYCHIATRIC RESEARCH
·
2022
·
IF 5.25
Xiahong Li,Yu Gu,Miao Qi,Rongxiang Chen,Daimin Xiao,Ping Yuan,Henry Xiang,Xiuquan Shi
Trauma is a leading cause of mortality and morbidity around the world and many trauma patients could suffer from a series of cognitive and mental disorders including acute stress disorder (ASD). Yet, little research has been done to investigate the influencing factors and pathogenesis of post-traumatic ASD. Therefore, this study investigated main influencing factors and neurobiochemical biomarkers of ASD in trauma patients with a purpose of early clinical identification and intervention. The patients were followed up by general questionnaire and Acute Stress Disorder scale (ASDS). Using the diagnostic criteria of ASD, the study participants were divided into ASD group and non-ASD group. The generalized estimating equation (GEE) multivariate analysis suggested that life stress, sleep less than 8 h, trauma from road traffic crash, overall pain intensity, injury severity, overall fear after trauma were risk factors for ASD. Neutrophil to lymphocyte ratio (NLR) showed a downward trend in both groups ( P < 0.05), and the ASD group was higher than the non-ASD group ( P = 0.015). Glu to GABA ratio (GGR) in the ASD group were higher than the non-ASD group ( P < 0.001). Both patient demographics and patient's condition could impact the risk of developing ASD after a major injury.
研究领域:
精神病学
·
神经科学
·
创伤医学
·
生物标志物研究
✓ 已验证
产品关联
DOI
PubMed
高影响因子
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