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Contextual fear extinction and Re-extinction in Carioca High-and Low-Conditioned Freezing Rats

World Journal of Neuroscience 2014年第3期4卷 247-252页

作者： Vitor de Castro Gomes Laura Andrea Leon Daniel Mograbi Fernando Cardenas Jesus Landeira-Fernandez Pontificia Universidade Catolica do Rio de Janeiro Rio de JaneiroBrasil Universidade de Sao Paulo Ribeirao PretoBrasil Institute of Psychiatry Kings CollegeLondonUK Universidad de los Andes BogotaColombia

We recently reported two novel breeding lines of rats known as Carioca High- and Low-conditioned Freezing (CHF and CLF), based on defensive freezing responses to contextual cues previously associated with electric footshock. The present study used animals of the 8th generation of our selective breeding program to investigate both contextual fear extinction and re-extinction. The results consistently showed that CHF animals froze more than CLF animals. Long extinction training was able to extinguish phenotypic differences between lines, but the divergence was restored after just one fear reacquisition training session. These differences disappeared again during re-extinction training. The possible neural mechanisms involved in these two types of learning are discussed.

关键词： Genetic Selection Freezing Response fear extinction

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Ameliorating effect of histamine on impairment of cued fear extinction induced by morphine withdrawal in mice with histidine decarboxylase gene knockout

Ameliorating effect of histamine on impairment of cued fear ...

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中国神经科学学会第四次会员代表大会暨第八届全国学术会议

作者： Ying-Xia GONG~(1 2) Wei-Ping ZHANG~1 Hui-Juan WANG~1 Zhong CHEN~(1 *) 1 Department of Pharmacology Yunyang Medical College Shiyan 2 Department of Pharmacology Institute of Neuroscience School of Medicine Zhejiang University Hangzhou

＜正＞Objective Histamine plays an important role in morphine addiction and memory-dependent behavior.However, little is known about the effect of histamine on impairment of memory after morphine withdrawal.In the present study,a fear conditioning and extinction model was used to investigate the effects of histamine on memory impairment induce by morphine withdrawal in histidine decarboxylase knockout（HDCKO） and wild-type（WT） mice.Methods HDCKO and WT mice were given subcutaneous morphine or saline twice daily for 5 consecutive days.The mice received a cued or contextual fear conditioning session 7 days after the last injection.During subsequent days,mice received four cued or contextual extinction sessions（one session per day）.Western blot was used to test extracellular signal-regulated kinase （ERK） phosphorylation in the amygdala and hippocampus.Results Morphine withdrawal did not affect the acquisition of cued or contextual fear responses,but impaired cued,but not contextual fear extinction.The acquisition of cued and contextual fear responses was accelerated,but extinction of the cued fear response was inhibited in HDCKO mice. Histamine deficiency aggravated the impairment of cued fear extinction induced by morphine withdrawal.Consistent with the behavioral results,morphine withdrawal and histamine deficiency decreased ERK phosphorylation in the amygdala after cued fear extinction.Conclusion These results suggest that morphine withdrawal specifically impairs the cued fear extinction,and histamine ameliorates this impairment by modulating ERK phosphorylation in the amygdala.The improvement by histamine may be explored for possible roles in the prevention or treatment of morphine abuse and relapse.

关键词： fear extinction histamine morphine amygdala HDC knockout mice extracellular signal-regulated kinase

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ASIC1a regulates ventral hippocampal-infralimbic prefrontal plasticity and fear extinction via BDNF-NMDA receptor signaling

ASIC1a regulates ventral hippocampal-infralimbic prefrontal ...

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长三角地区神经科学论坛2017

作者： Qin Wang Xing-Lei Song Qin Jiang Qi Wang Yan-Jiao Wu Wei-Guang Li Tian-Le Xu Collaborative Innovation Center for Brain Science Department of Anatomy and Physiology Shanghai Jiao Tong University School of Medicine

fear extinction is associated with dynamic changes in neuronal activity and connectivity within fear circuits,mainly including hippocampus,medial prefrontal cortex（m PFC）,and amygdala.However,it is still unclear how this extinction-related plasticity is implemented at the molecular and circuit level.Acid-sensing ion channel 1a（ASIC1a）,a member of the degenerin/epithelial Na+channel family,has been reported play an important role in synaptic plasticity and learning and memory,such as fear learning.Here,we identify a critical role of ASIC1a in ventral hippocampus（v HPC）-infralimbic（IL）cortex pathway for fear extinction.We found mice with ASIC1a deletion in v HPC by Cre/lox recombination（ASIC1ac KO）,si RNA or ASIC1a inhibition by Pc TX-1 showed impaired fear extinction,while overexpression of ASIC1a in v HPC facilitated fear extinction in wild type mice.To explore the mechanisms,we did whole-transcriptome analysis with RNA sequencing,and showed that bdnf gene is a likely key molecular substrate recruited by ASIC1ato influence fear extinction.Supporting this possibility,extinction learning induced significant BDNF upregulation in v HPC,which is compromised in ASIC1ac KO mice.Moreover,overexpression of BDNF in v HPC restored the deficiency of fear extinction in ASIC1ac KO mice.By combining optogeneticswithacute slice electrophysiology,we showed that fear extinction learning enhanced excitatory synaptic transmission in the v HPC-IL projection,characterized as the enhanced NMDAR/AMPAR ratio,whichwas severely impaired in ASIC1ac KO mice,and then could be rescued by simultaneous addition of BDNF.Thein-site delivery of BDNF protein to IL also could reverse the impairment of fear extinction induced by v HPCASIC1a deletion.In addition,the similar genetic and pharmacological manipulations of ASIC1a in the IL didn’t have any effect on fear extinction.Together,these results collectively establish a novel molecular pathway involving ASIC1a and BDNF-NMDA receptor signaling specifically in the v HPC-IL circuit that is critical for

关键词： fear extinction ASIC1a ventral hippocampus infralimbic prefrontal cortex BDNF NMDA receptor

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Parvalbumin-Expressing Neurons Network Plasticity and fear extinction

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神经药理学报 2019年第Z1期 18-18页

作者：高天明中国神经科学学会南方医科大学南方医科大学广东省重大精神疾病研究重点实验室南方医科大学精神健康研究教育部重点实验室南方医科大学精神健康研究院

Learning to fear threats in the environment is highly adaptive. However,this form of learning can also lead to pathological fear memories that fuel disorders of fear and anxiety,such as panic disorder and post-traumatic stress disorder(PTSD) in humans. Increasing evidence suggests that the ventral medial prefrontal cortex(vmPFC) is involved in fear extinction. However,no studies have as yet addressed the local network plasticity in fear extinction. Here,we studied the role of parvalbumin(PV) neurons network plasticity in the extinction of cued fear memory and the underlying molecular mechanisms. vmPFC is composed of prelimbic cortex(PL) and infrelimbic cortex(IL). We provide evidence that fear extinction induced a low PV-network configuration in IL cortex but not in PL cortex and this kind of configurationis essential for the extinction.Moreover,by screening an amount of molecules that are known to regulate GABAergic neuronal development,we identified that NRG1-ErbB4 signaling in PV neurons was critical to regulating fear extinction via modulation of PV-networks plasticity. Our study suggests that this signaling may be a potential target for the treatment of fear-related diseases.

关键词： prefrontal cortex parvalbumin neuron network plasticity fear extinction

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The role of α CaMKII in extinction of conditioned fear

The role of α CaMKII in extinction of conditioned fear

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中国神经科学学会第十二届全国学术会议

作者： Jia-Yue WANG Xu-Liang ZHANG Shu-Ming AN Yan-Hong DUAN Xiaohua CAO Key Laboratory of Brain Functional Genomics Ministry of EducationShanghai Key Laboratory of Brain Functional GenomicsSchool of Life SciencesEast China Normal University

Objective Since the impaired fear extinction is one of psychophysiological hallmarks of posttraumatic stress disorder（PTSD）, a deeper understanding of the molecular and neuronal substrates underlying fear extinction has important implications for the treatment of PTSD.It has been reported that there is a link between NMDARdependent long-term depression（LTD） at thalamus-lateral amygdala（T-LA） synapses and fear extinction, especially αCa MKII overexpression impairs NMDAR-dependent LTD in medial prefrontal cortex. However, the role ofαCa MKII in NMDAR-dependent LTD at T-LA synapses and fear extinction remains elusive. Methods Using chemicalgenetic approaches to temporally up-regulateαCa MKII activity in forebrain of mice, and combining molecular biological, electrophysiological with behavioral techniques. Results We found that αCa MKII-F89 G transgenic mice exhibited impaired fear extinction. Notably, in vitro electrophysiological analysis showed normal basal synaptic transmission and LTP, but selectively impaired NMDAR-dependent LTD at T-LA synapses inαCa MKII-F89 G transgenic mice. In accordance with the deficit in NMDARdependent LTD, αCa MKII-F89 G transgenic mice displayed impaired Glu A1-Ser845 dephosphorylation and AMPAR internalization during NMDAR-dependent chemical LTD at T-LA synapses. Furthermore, these deficits were due to the decreased PP2 A activity and increased stargazin expression during NMDAR-dependent LTD. Importantly, above deficits in fear extinction, NMDAR-dependent LTD, Glu A1-Ser845 dephosphorylation and AMPAR internalization, as well as the decreased PP2 A activity and increased stargazin expression could all be reversed by 1-Naphthylmethyl（NM）-PP1, a specific inhibitor of exogenous αCa MKII-F89 G activity. Conclusion Taken together,our results suggest, for the first time, thatαCa MKII overexpression impairs NMDARdependent LTD at T-LA synapses and fear extinction, and supports the notion that there is a close relationship between NMDAR-dependent LTD and fear extinction. Our findings provide

关键词： αCaMKII fear extinction long-term depression lateral amygdala PTSD

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T-type Ca2+ channels in thalamic control of behavior

T-type Ca2+ channels in thalamic control of behavior

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中国神经科学学会第四次会员代表大会暨第八届全国学术会议

作者： Sukchan Lee Soojung Lee Huisu Kim Guk Bae Kim Ingie Hong Sukwoo Choi Sung-Yon Kim Sang Jeong Kim Hee-Sup Shin Department of Physiology SeoulNational University College of Medicine and Neuroscience Research Institute Medical Research CenterKorea School of Biological Sciences College of Natural SciencesSeoul National UniversityKorea Department of Physiology Seoul National University College of Medicine and Neuroscience Research Institute Medical Research CenterKorea

Objective The Mediodorsal thalamus(MD) is a part of the limbic system and connects reciprocally with the prefrontal cortex,the amygdala and the hippocampus,which comprise a network of structures involved in fear memory. However,the contribution of the MD to fear behavior is poorly understood.Phospholipase C(PLC) b4 is expressed intensely in the MD but very lightly in the prefrontal cortex and the amygdala,the two key regions known to regulate fear extinction.Methods Here,we examined a role of the MD using the PLCb4 knock-out(PLCb4) mice in the formation and extinction of auditory-conditioned fear.Results The PLCb4 mice showed normal acquisition and long-term memory of auditory-conditioned fear.However,the mutant was severely impaired in fear extinction.Patch clamp recording on the mutant MD neurons in thalamic slices showed an increase of low threshold Ca currents mediated via T-type Ca channels compared to the wild type.An infusion in vivo of T-type channel blocker into the MD ameliorated the impaired extinction phenotype in PLCb4 and facilitated the extinction in wild type mice.Conclusion These results suggest that the mediodorsal thalamus is involved in the control of fear extinction and T-type Ca channels play an inhibitory role in this process.

关键词： T-type Ca2+ channels mediodorsal nucleus thalamus fear extinction

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Sleep Disturbances and fear-Associated Behavioral Changes in a Mouse Model of PTSD

Sleep Disturbances and Fear-Associated Behavioral Changes in...

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中国睡眠研究会第十一届全国学术年会

作者： Yu-dong YAN Zhi-li HUANG Su-rong YANG Fudan University

Exposure to life-threatening events or following traumatic events, a subset of individuals may suffer from persistent pathological symptoms such as those seen in post-traumatic stress disorder（PTSD）. PTSD is a growing issue worldwide, strongly impairing patients’ quality of life and social functions. Intrusion symptom, avoidance symptom, negative cognition/mood symptoms and arousal symptoms lasting for 1 month or longer after exposure are characteristics of PTSD. Sleep disturbances, including insomnia, nightmares and hyper-arousal, are the primary presenting concern among individuals and are considered hallmark symptoms, setting as diagnostic criteria of PTSD. Ameliorating sleep disturbances among at-risk individuals would be a viable target for the prevention and treatment of PTSD. FDA-approved selective serotonin reuptake inhibitors drug（SSRIs）, paroxetine and sertraline, are widely used for PTSD treatment. Nevertheless, little evidence showed sleep disturbances could be improved by SSRIs. The underlying neurobiological mechanisms of sleep disturbances following trauma exposure are still poorly understood and appropriate mouse models are in demand.In this study, we measured long-term sleep alterations in response to stress exposure in a mouse model of PTSD induced by single prolonged stress（mSPS）, a modified mouse paradigm based on a most prevalent rat model SPS. Adult male C57 BL/6 J mice, instrumented with electrodes for EEG and EMG recording were exposed to a series of severe and multimodal stressors, including 2 h restraint, 10 min forced swim, exposure to soiled rat bedding scent, and exposure to ether until unconsciousness. The results showed an increase in rapid eye movement（REM） sleep during the light period, with raised number of REM sleep episodes and transitions from non-rapid eye movement（NREM） to REM sleep. The distribution of episode length of REM sleep also altered. Even though no differences were shown in waking amount, medium-length wake episode decreased significantly in both light and dark pe

关键词： post-traumatic stress disorder mouse single prolonged stress sleep disorder fear extinction

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