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Start Over Author "Wickersham, Ian R." Publisher springer science and business media llc
26 results on '"Wickersham, Ian R."'

1. Publisher Correction: Long-term labeling and imaging of synaptically connected neuronal networks in vivo using double-deletion-mutant rabies viruses

Author

Jin, Lei, primary, Sullivan, Heather A., additional, Zhu, Mulangma, additional, Lavin, Thomas K., additional, Matsuyama, Makoto, additional, Fu, Xin, additional, Lea, Nicholas E., additional, Xu, Ran, additional, Hou, YuanYuan, additional, Rutigliani, Luca, additional, Pruner, Maxwell, additional, Babcock, Kelsey R., additional, Ip, Jacque Pak Kan, additional, Hu, Ming, additional, Daigle, Tanya L., additional, Zeng, Hongkui, additional, Sur, Mriganka, additional, Feng, Guoping, additional, and Wickersham, Ian R., additional

Published
2024
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2. Targeting thalamic circuits rescues motor and mood deficits in PD mice

Author

Massachusetts Institute of Technology. Department of Brain and Cognitive Sciences, Zhang, Ying, Roy, Dheeraj S, Zhu, Yi, Chen, Yefei, Aida, Tomomi, Hou, Yuanyuan, Shen, Chenjie, Lea, Nicholas E, Schroeder, Margaret E, Skaggs, Keith M, Sullivan, Heather A, Fischer, Kyle B, Callaway, Edward M, Wickersham, Ian R, Dai, Ji, Li, Xiao-Ming, Lu, Zhonghua, Feng, Guoping, Massachusetts Institute of Technology. Department of Brain and Cognitive Sciences, Zhang, Ying, Roy, Dheeraj S, Zhu, Yi, Chen, Yefei, Aida, Tomomi, Hou, Yuanyuan, Shen, Chenjie, Lea, Nicholas E, Schroeder, Margaret E, Skaggs, Keith M, Sullivan, Heather A, Fischer, Kyle B, Callaway, Edward M, Wickersham, Ian R, Dai, Ji, Li, Xiao-Ming, Lu, Zhonghua, and Feng, Guoping

Abstract

Although bradykinesia, tremor and rigidity are the hallmark motor defects in patients with Parkinson's disease (PD), patients also experience motor learning impairments and non-motor symptoms such as depression1. The neural circuit basis for these different symptoms of PD are not well understood. Although current treatments are effective for locomotion deficits in PD2,3, therapeutic strategies targeting motor learning deficits and non-motor symptoms are lacking4-6. Here we found that distinct parafascicular (PF) thalamic subpopulations project to caudate putamen (CPu), subthalamic nucleus (STN) and nucleus accumbens (NAc). Whereas PF→CPu and PF→STN circuits are critical for locomotion and motor learning, respectively, inhibition of the PF→NAc circuit induced a depression-like state. Whereas chemogenetically manipulating CPu-projecting PF neurons led to a long-term restoration of locomotion, optogenetic long-term potentiation (LTP) at PF→STN synapses restored motor learning behaviour in an acute mouse model of PD. Furthermore, activation of NAc-projecting PF neurons rescued depression-like phenotypes. Further, we identified nicotinic acetylcholine receptors capable of modulating PF circuits to rescue different PD phenotypes. Thus, targeting PF thalamic circuits may be an effective strategy for treating motor and non-motor deficits in PD.

Published
2023

3. Cingulate-motor circuits update rule representations for sequential choice decisions

Author

Massachusetts Institute of Technology. Department of Biology, Takeuchi, Daigo, Roy, Dheeraj, Muralidhar, Shruti, Kawai, Takashi, Bari, Andrea, Lovett, Chanel, Sullivan, Heather A, Wickersham, Ian R, Tonegawa, Susumu, Massachusetts Institute of Technology. Department of Biology, Takeuchi, Daigo, Roy, Dheeraj, Muralidhar, Shruti, Kawai, Takashi, Bari, Andrea, Lovett, Chanel, Sullivan, Heather A, Wickersham, Ian R, and Tonegawa, Susumu

Abstract

AbstractAnterior cingulate cortex mediates the flexible updating of an animal’s choice responses upon rule changes in the environment. However, how anterior cingulate cortex entrains motor cortex to reorganize rule representations and generate required motor outputs remains unclear. Here, we demonstrate that chemogenetic silencing of the terminal projections of cingulate cortical neurons in secondary motor cortex in the rat disrupts choice performance in trials immediately following rule switches, suggesting that these inputs are necessary to update rule representations for choice decisions stored in the motor cortex. Indeed, the silencing of cingulate cortex decreases rule selectivity of secondary motor cortical neurons. Furthermore, optogenetic silencing of cingulate cortical neurons that is temporally targeted to error trials immediately after rule switches exacerbates errors in the following trials. These results suggest that cingulate cortex monitors behavioral errors and updates rule representations in motor cortex, revealing a critical role for cingulate-motor circuits in adaptive choice behaviors.

Published
2023

4. Compensatory remodeling of a septo-hippocampal GABAergic network in the triple transgenic Alzheimer’s mouse model

Author

Wander, Connor M, primary, Li, Ya-Dong, additional, Bao, Hechen, additional, Asrican, Brent, additional, Luo, Yan-Jia, additional, Sullivan, Heather A, additional, Chao, Tzu-Hao Harry, additional, Zhang, Wei-Ting, additional, Chéry, Samantha L, additional, Tart, Dalton S, additional, Chen, Ze-Ka, additional, Shih, Yen-Yu Ian, additional, Wickersham, Ian R, additional, Cohen, Todd J, additional, and Song, Juan, additional

Published
2023
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6. Targeting thalamic circuits rescues motor and mood deficits in PD mice

Author

Zhang, Ying, primary, Roy, Dheeraj S., additional, Zhu, Yi, additional, Chen, Yefei, additional, Aida, Tomomi, additional, Hou, Yuanyuan, additional, Shen, Chenjie, additional, Lea, Nicholas E., additional, Schroeder, Margaret E., additional, Skaggs, Keith M., additional, Sullivan, Heather A., additional, Fischer, Kyle B., additional, Callaway, Edward M., additional, Wickersham, Ian R., additional, Dai, Ji, additional, Li, Xiao-Ming, additional, Lu, Zhonghua, additional, and Feng, Guoping, additional

Published
2022
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7. An amygdala circuit that suppresses social engagement

Author

Picower Institute for Learning and Memory, Massachusetts Institute of Technology. Department of Brain and Cognitive Sciences, McGovern Institute for Brain Research at MIT, Kwon, Jeong-Tae, Ryu, Changhyeon, Lee, Hyeseung, Sheffield, Alec, Fan, Jingxuan, Cho, Daniel H, Bigler, Shivani, Sullivan, Heather A, Choe, Han Kyung, Wickersham, Ian R, Heiman, Myriam, Choi, Gloria B, Picower Institute for Learning and Memory, Massachusetts Institute of Technology. Department of Brain and Cognitive Sciences, McGovern Institute for Brain Research at MIT, Kwon, Jeong-Tae, Ryu, Changhyeon, Lee, Hyeseung, Sheffield, Alec, Fan, Jingxuan, Cho, Daniel H, Bigler, Shivani, Sullivan, Heather A, Choe, Han Kyung, Wickersham, Ian R, Heiman, Myriam, and Choi, Gloria B

Abstract

Innate social behaviours, such as mating and fighting, are fundamental to animal reproduction and survival1. However, social engagements can also put an individual at risk2. Little is known about the neural mechanisms that enable appropriate risk assessment and the suppression of hazardous social interactions. Here we identify the posteromedial nucleus of the cortical amygdala (COApm) as a locus required for the suppression of male mating when a female mouse is unhealthy. Using anatomical tracing, functional imaging and circuit-level epistatic analyses, we show that suppression of mating with an unhealthy female is mediated by the COApm projections onto the glutamatergic population of the medial amygdalar nucleus (MEA). We further show that the role of the COApm-to-MEA connection in regulating male mating behaviour relies on the neuromodulator thyrotropin-releasing hormone (TRH). TRH is expressed in the COApm, whereas the TRH receptor (TRHR) is found in the postsynaptic MEA glutamatergic neurons. Manipulating neural activity of TRH-expressing neurons in the COApm modulated male mating behaviour. In the MEA, activation of the TRHR pathway by ligand infusion inhibited mating even towards healthy female mice, whereas genetic ablation of TRHR facilitated mating with unhealthy individuals. In summary, we reveal a neural pathway that relies on the neuromodulator TRH to modulate social interactions according to the health status of the reciprocating individual. Individuals must balance the cost of social interactions relative to the benefit, as deficits in the ability to select healthy mates may lead to the spread of disease.

Published
2022

8. Organization of the inputs and outputs of the mouse superior colliculus

Author

Benavidez, Nora L., primary, Bienkowski, Michael S., additional, Zhu, Muye, additional, Garcia, Luis H., additional, Fayzullina, Marina, additional, Gao, Lei, additional, Bowman, Ian, additional, Gou, Lin, additional, Khanjani, Neda, additional, Cotter, Kaelan R., additional, Korobkova, Laura, additional, Becerra, Marlene, additional, Cao, Chunru, additional, Song, Monica Y., additional, Zhang, Bin, additional, Yamashita, Seita, additional, Tugangui, Amanda J., additional, Zingg, Brian, additional, Rose, Kasey, additional, Lo, Darrick, additional, Foster, Nicholas N., additional, Boesen, Tyler, additional, Mun, Hyun-Seung, additional, Aquino, Sarvia, additional, Wickersham, Ian R., additional, Ascoli, Giorgio A., additional, Hintiryan, Houri, additional, and Dong, Hong-Wei, additional

Published
2021
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9. Connectivity characterization of the mouse basolateral amygdalar complex

Author

Hintiryan, Houri, primary, Bowman, Ian, additional, Johnson, David L., additional, Korobkova, Laura, additional, Zhu, Muye, additional, Khanjani, Neda, additional, Gou, Lin, additional, Gao, Lei, additional, Yamashita, Seita, additional, Bienkowski, Michael S., additional, Garcia, Luis, additional, Foster, Nicholas N., additional, Benavidez, Nora L., additional, Song, Monica Y., additional, Lo, Darrick, additional, Cotter, Kaelan R., additional, Becerra, Marlene, additional, Aquino, Sarvia, additional, Cao, Chunru, additional, Cabeen, Ryan P., additional, Stanis, Jim, additional, Fayzullina, Marina, additional, Ustrell, Sarah A., additional, Boesen, Tyler, additional, Tugangui, Amanda J., additional, Zhang, Zheng-Gang, additional, Peng, Bo, additional, Fanselow, Michael S., additional, Golshani, Peyman, additional, Hahn, Joel D., additional, Wickersham, Ian R., additional, Ascoli, Giorgio A., additional, Zhang, Li I., additional, and Dong, Hong-Wei, additional

Published
2021
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10. Distinct prefrontal top-down circuits differentially modulate sensorimotor behavior

Author

Picower Institute for Learning and Memory, Massachusetts Institute of Technology. Department of Brain and Cognitive Sciences, McGovern Institute for Brain Research at MIT, Huda, Rafiq, Sipe, Grayson O, Breton-Provencher, Vincent, Cruz, K Guadalupe, Pho, Gerald N, Adam, Elie, Gunter, Liadan M, Sullins, Austin, Wickersham, Ian R, Sur, Mriganka, Picower Institute for Learning and Memory, Massachusetts Institute of Technology. Department of Brain and Cognitive Sciences, McGovern Institute for Brain Research at MIT, Huda, Rafiq, Sipe, Grayson O, Breton-Provencher, Vincent, Cruz, K Guadalupe, Pho, Gerald N, Adam, Elie, Gunter, Liadan M, Sullins, Austin, Wickersham, Ian R, and Sur, Mriganka

Abstract

© 2020, The Author(s). Sensorimotor behaviors require processing of behaviorally relevant sensory cues and the ability to select appropriate responses from a vast behavioral repertoire. Modulation by the prefrontal cortex (PFC) is thought to be key for both processes, but the precise role of specific circuits remains unclear. We examined the sensorimotor function of anatomically distinct outputs from a subdivision of the mouse PFC, the anterior cingulate cortex (ACC). Using a visually guided two-choice behavioral paradigm with multiple cue-response mappings, we dissociated the sensory and motor response components of sensorimotor control. Projection-specific two-photon calcium imaging and optogenetic manipulations show that ACC outputs to the superior colliculus, a key midbrain structure for response selection, principally coordinate specific motor responses. Importantly, ACC outputs exert control by reducing the innate response bias of the superior colliculus. In contrast, ACC outputs to the visual cortex facilitate sensory processing of visual cues. Our results ascribe motor and sensory roles to ACC projections to the superior colliculus and the visual cortex and demonstrate for the first time a circuit motif for PFC function wherein anatomically non-overlapping output pathways coordinate complementary but distinct aspects of visual sensorimotor behavior.

Published
2021

11. An amygdala circuit that suppresses social engagement

Author

Kwon, Jeong-Tae, primary, Ryu, Changhyeon, additional, Lee, Hyeseung, additional, Sheffield, Alec, additional, Fan, Jingxuan, additional, Cho, Daniel H., additional, Bigler, Shivani, additional, Sullivan, Heather A., additional, Choe, Han Kyung, additional, Wickersham, Ian R., additional, Heiman, Myriam, additional, and Choi, Gloria B., additional

Published
2021
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14. Nontoxic, double-deletion-mutant rabies viral vectors for retrograde targeting of projection neurons

Author

Chatterjee, Soumya, primary, Sullivan, Heather A., additional, MacLennan, Bryan J., additional, Xu, Ran, additional, Hou, YuanYuan, additional, Lavin, Thomas K., additional, Lea, Nicholas E., additional, Michalski, Jacob E., additional, Babcock, Kelsey R., additional, Dietrich, Stephan, additional, Matthews, Gillian A., additional, Beyeler, Anna, additional, Calhoon, Gwendolyn G., additional, Glober, Gordon, additional, Whitesell, Jennifer D., additional, Yao, Shenqin, additional, Cetin, Ali, additional, Harris, Julie A., additional, Zeng, Hongkui, additional, Tye, Kay M., additional, Reid, R. Clay, additional, and Wickersham, Ian R., additional

Published
2018
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15. Erratum: Corrigendum: Lhx6-positive GABA-releasing neurons of the zona incerta promote sleep

Author

Liu, Kai, primary, Kim, Juhyun, additional, Kim, Dong Won, additional, Stephanie Zhang, Yi, additional, Bao, Hechen, additional, Denaxa, Myrto, additional, Lim, Szu-Aun, additional, Kim, Eileen, additional, Liu, Chang, additional, Wickersham, Ian R., additional, Pachnis, Vassilis, additional, Hattar, Samer, additional, Song, Juan, additional, Brown, Solange P., additional, and Blackshaw, Seth, additional

Published
2017
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16. Reversing behavioural abnormalities in mice exposed to maternal inflammation

Author

Shin Yim, Yeong, primary, Park, Ashley, additional, Berrios, Janet, additional, Lafourcade, Mathieu, additional, Pascual, Leila M., additional, Soares, Natalie, additional, Yeon Kim, Joo, additional, Kim, Sangdoo, additional, Kim, Hyunju, additional, Waisman, Ari, additional, Littman, Dan R., additional, Wickersham, Ian R., additional, Harnett, Mark T., additional, Huh, Jun R., additional, and Choi, Gloria B., additional

Published
2017
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17. Lhx6-positive GABA-releasing neurons of the zona incerta promote sleep

Author

Liu, Kai, primary, Kim, Juhyun, additional, Kim, Dong Won, additional, Zhang, Yi Stephanie, additional, Bao, Hechen, additional, Denaxa, Myrto, additional, Lim, Szu-Aun, additional, Kim, Eileen, additional, Liu, Chang, additional, Wickersham, Ian R., additional, Pachnis, Vassilis, additional, Hattar, Samer, additional, Song, Juan, additional, Brown, Solange P., additional, and Blackshaw, Seth, additional

Published
2017
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19. A circuit mechanism for differentiating positive and negative associations

Author

Namburi, Praneeth, primary, Beyeler, Anna, additional, Yorozu, Suzuko, additional, Calhoon, Gwendolyn G., additional, Halbert, Sarah A., additional, Wichmann, Romy, additional, Holden, Stephanie S., additional, Mertens, Kim L., additional, Anahtar, Melodi, additional, Felix-Ortiz, Ada C., additional, Wickersham, Ian R., additional, Gray, Jesse M., additional, and Tye, Kay M., additional

Published
2015
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26. Assembly and operation of the autopatcher for automated intracellular neural recording in vivo

Author

Annabelle C. Singer, Ian R. Wickersham, Craig R. Forest, Suhasa B. Kodandaramaiah, Gregory L. Holst, Edward S. Boyden, Michael L. McKinnon, Giovanni Talei Franzesi, Massachusetts Institute of Technology. Department of Biological Engineering, Massachusetts Institute of Technology. Department of Brain and Cognitive Sciences, Massachusetts Institute of Technology. Media Laboratory, McGovern Institute for Brain Research at MIT, Wickersham, Ian R., and Boyden, Edward

Subjects
Automation, Laboratory, 0301 basic medicine, Laboratory methods, Patch-Clamp Techniques, Time Factors, Computer science, Extramural, Training time, Article, General Biochemistry, Genetics and Molecular Biology, Mice, 03 medical and health sciences, 030104 developmental biology, 0302 clinical medicine, Automated patch clamp, In vivo, Cellular neuroscience, Animals, Patch clamp, Surgical preparation, Neuroscience, 030217 neurology & neurosurgery
Abstract

Whole-cell patch clamping in vivo is an important neuroscience technique that uniquely provides access to both suprathreshold spiking and subthreshold synaptic events of single neurons in the brain. This article describes how to set up and use the autopatcher, which is a robot for automatically obtaining high-yield and high-quality whole-cell patch clamp recordings in vivo. By following this protocol, a functional experimental rig for automated whole-cell patch clamping can be set up in 1 week. High-quality surgical preparation of mice takes ~1 h, and each autopatching experiment can be carried out over periods lasting several hours. Autopatching should enable in vivo intracellular investigations to be accessible by a substantial number of neuroscience laboratories, and it enables labs that are already doing in vivo patch clamping to scale up their efforts by reducing training time for new lab members and increasing experimental durations by handling mentally intensive tasks automatically., National Eye Institute, National Institute of Mental Health (U.S.) (1-U01-MH106027-01), United States. National Institutes of Health (EY023173), National Science Foundation (U.S.) (HER 0965945), National Science Foundation (U.S.) (CISE 1110947), National Science Foundation (U.S.) (5T90DA032466), Georgia Institute of Technology, United States. National Institutes of Health (1R01EY023173), New York Stem Cell Foundation (Robertson Neuroscience Investigator Award), United States. National Institutes of Health (1DP1NS087724), United States. National Institutes of Health (1R24MH106075), United States. National Institutes of Health (1R01MH103910)

Published
2016
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