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1,147 results on '"Neve, Rachael L."'

107. Epigenetic regulation of RAC1 induces synaptic remodeling in stress disorders and depression

Author

Golden, Sam A., Christoffel, Daniel J., Heshmati, Mitra, Hodes, Georgia E., Magida, Jane, Davis, Keithara, Cahill, Michael E., Dias, Caroline, Ribeiro, Efrain, Ables, Jessica L., Kennedy, Pamela J., Robison, Alfred J., Gonzalez-Maeso, Javier, Neve, Rachael L., Turecki, Gustavo, Ghose, Subroto, Tamminga, Carol A., and Russo, Scott J.

Subjects
Diagnosis, Care and treatment, Research, Health aspects, Epigenetic inheritance -- Research, Gene therapy -- Health aspects, Major depressive disorder -- Diagnosis -- Care and treatment -- Research, Promoters (Genetics) -- Research
Abstract

The treatment of major depressive disorder (MDD) is confounded by high rates of treatment resistance coupled with low probabilities of achieving lasting remission (1). Such clinical realities, paired with an [...], Depression induces structural and functional synaptic plasticity in brain reward circuits, although the mechanisms promoting these changes and their relevance to behavioral outcomes are unknown. Transcriptional profiling of the nucleus accumbens (NAc) for Rho GTPase-related genes, which are known regulators of synaptic structure, revealed a sustained reduction in RAS-related C3 botulinum toxin substrate 1 (Rac1) expression after chronic social defeat stress. This was associated with a repressive chromatin state surrounding the proximal promoter of Rac1. Inhibition of class 1 histone deacetylases (HDACs) with MS-275 rescued both the decrease in Rac1 transcription after social defeat stress and depression-related behavior, such as social avoidance. We found a similar repressive chromatin state surrounding the RAC1 promoter in the NAc of subjects with depression, which corresponded with reduced RAC1 transcription. Viral-mediated reduction of Rac1 expression or inhibition of Rac1 activity in the NAc increases social defeat-induced social avoidance and anhedonia in mice. Chronic social defeat stress induces the formation of stubby excitatory spines through a Rac1-dependent mechanism involving the redistribution of synaptic cofilin, an actin-severing protein downstream of Rac1. Overexpression of constitutively active Rac1 in the NAc of mice after chronic social defeat stress reverses depression-related behaviors and prunes stubby spines. Taken together, our data identify epigenetic regulation of RAC1 in the NAc as a disease mechanism in depression and reveal a functional role for Rac1 in rodents in regulating stress-related behaviors.

Published
2013
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108. Rapid regulation of depression-related behaviours by control of midbrain dopamine neurons

Author

Chaudhury, Dipesh, Walsh, Jessica J., Friedman, Allyson K., Juarez, Barbara, Ku, Stacy M., Koo, Ja Wook, Ferguson, Deveroux, Tsai, Hsing-Chen, Pomeranz, Lisa, Christoffel, Daniel J., Nectow, Alexander R., Ekstrand, Mats, Domingos, Ana, Mazei-Robison, Michelle S., Mouzon, Ezekiell, Lobo, Mary Kay, Neve, Rachael L., Friedman, Jeffrey M., Russo, Scott J., Deisseroth, Karl, Nestler, Eric J., and Han, Ming-Hu

Subjects
Physiological aspects, Research, Health aspects, Depression (Mood disorder) -- Physiological aspects -- Research, Neuropsychology -- Research -- Physiological aspects -- Health aspects, Mesencephalon -- Research -- Health aspects -- Physiological aspects, Dopaminergic mechanisms -- Research -- Health aspects -- Physiological aspects, Depression, Mental -- Physiological aspects -- Research
Abstract

Ventral tegmental area (VTA) dopamine neurons in the brain's reward circuit have a crucial role in mediating stress responses (1-4), including determining susceptibility versus resilience to social-stress-induced behavioural abnormalities (5). [...]

Published
2013
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112. Deregulation of HDAC1 by p25/Cdk5 in Neurotoxicity

Author

Kim, Dohoon, Frank, Christopher L., Dobbin, Matthew M., Tsunemoto, Rachel K., Tu, Weihong, Peng, Peter L., Guan, Ji-Song, Lee, Byung-Hoon, Moy, Lily Y., Giusti, Paola, Broodie, Nisha, Mazitschek, Ralph, Delalle, Ivanna, Haggarty, Stephen J., Neve, Rachael L., Lu, YouMing, and Tsai, Li-Huei

Published
2008
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116. Regulation of impulsive and aggressive behaviours by a novel lncRNA

Author

Canadian Institutes of Health Research, Fonds de la Recherche en Sante du Québec, Natural Sciences and Engineering Research Council of Canada, Labonté, Benoit, Abdallah, Khaled, Maussion, Gilles, Yerko, Volodymyr, Yang, Jennie, Bittar, Thibault, Quessy, Francis, Golden, Sam A., Navarro, Luis, Checknita, Dave, Gigek, Carolina, Lopez, Juan Pablo, Neve, Rachael L., Russo, Scott J., Tremblay, Richard E., Côté, Gilles, Meaney, Michael J., Mechawar, Naguib, Nestler, Eric J., Turecki, Gustavo, Canadian Institutes of Health Research, Fonds de la Recherche en Sante du Québec, Natural Sciences and Engineering Research Council of Canada, Labonté, Benoit, Abdallah, Khaled, Maussion, Gilles, Yerko, Volodymyr, Yang, Jennie, Bittar, Thibault, Quessy, Francis, Golden, Sam A., Navarro, Luis, Checknita, Dave, Gigek, Carolina, Lopez, Juan Pablo, Neve, Rachael L., Russo, Scott J., Tremblay, Richard E., Côté, Gilles, Meaney, Michael J., Mechawar, Naguib, Nestler, Eric J., and Turecki, Gustavo

Abstract

High impulsive and aggressive traits associate with poor behavioural self-control. Despite their importance in predicting behavioural negative outcomes including suicide, the molecular mechanisms underlying the expression of impulsive and aggressive traits remain poorly understood. Here, we identified and characterized a novel long noncoding RNA (lncRNA), acting as a regulator of the monoamine oxidase A (MAOA) gene in the brain, and named it MAOA-associated lncRNA (MAALIN). Our results show that in the brain of suicide completers, MAALIN is regulated by a combination of epigenetic mechanisms including DNA methylation and chromatin modifications. Elevated MAALIN in the dentate gyrus of impulsive-aggressive suicides was associated with lower MAOA expression. Viral overexpression of MAALIN in neuroprogenitor cells decreased MAOA expression while CRISPR-mediated knock out resulted in elevated MAOA expression. Using viral-mediated gene transfer, we confirmed that MAALIN in the hippocampus significantly decreases MAOA expression and exacerbates the expression of impulsive-aggressive behavioural traits in CD1 aggressive mice. Overall, our findings suggest that variations in DNA methylation mediate the differential expression of a novel lncRNA that acts on MAOA expression to regulate impulsive-aggressive behaviours.

Published
2021

117. A highly homogeneous polymer composed of tetrahedron-like monomers for high-isotropy expansion microscopy

Author

McGovern Institute for Brain Research at MIT, Program in Media Arts and Sciences (Massachusetts Institute of Technology), Massachusetts Institute of Technology. Department of Biological Engineering, Massachusetts Institute of Technology. Center for Neurobiological Engineering, Massachusetts Institute of Technology. Department of Brain and Cognitive Sciences, Koch Institute for Integrative Cancer Research at MIT, Howard Hughes Medical Institute, Gao, Ruixuan, Yu, Chih-Chieh, Gao, Linyi, Piatkevich, Kiryl D, Neve, Rachael L, Munro, James B, Upadhyayula, Srigokul, Boyden, Edward S, McGovern Institute for Brain Research at MIT, Program in Media Arts and Sciences (Massachusetts Institute of Technology), Massachusetts Institute of Technology. Department of Biological Engineering, Massachusetts Institute of Technology. Center for Neurobiological Engineering, Massachusetts Institute of Technology. Department of Brain and Cognitive Sciences, Koch Institute for Integrative Cancer Research at MIT, Howard Hughes Medical Institute, Gao, Ruixuan, Yu, Chih-Chieh, Gao, Linyi, Piatkevich, Kiryl D, Neve, Rachael L, Munro, James B, Upadhyayula, Srigokul, and Boyden, Edward S

Abstract

Expansion microscopy (ExM) physically magnifies biological specimens to enable nanoscale-resolution imaging using conventional microscopes. Current ExM methods permeate specimens with free-radical-chain-growth-polymerized polyacrylate hydrogels, whose network structure limits the local isotropy of expansion as well as the preservation of morphology and shape at the nanoscale. Here we report that ExM is possible using hydrogels that have a more homogeneous network structure, assembled via non-radical terminal linking of tetrahedral monomers. As with earlier forms of ExM, such 'tetra-gel'-embedded specimens can be iteratively expanded for greater physical magnification. Iterative tetra-gel expansion of herpes simplex virus type 1 (HSV-1) virions by ~10× in linear dimension results in a median spatial error of 9.2 nm for localizing the viral envelope layer, rather than 14.3 nm from earlier versions of ExM. Moreover, tetra-gel-based expansion better preserves the virion spherical shape. Thus, tetra-gels may support ExM with reduced spatial errors and improved local isotropy, pointing the way towards single-biomolecule accuracy ExM.

Published
2021

122. Molecular Adaptations Underlying Susceptibility and Resistance to Social Defeat in Brain Reward Regions

Author

Krishnan, Vaishnav, Han, Ming-Hu, Graham, Danielle L., Berton, Olivier, Renthal, William, Russo, Scott J., LaPlant, Quincey, Graham, Ami, Lutter, Michael, Lagace, Diane C., Ghose, Subroto, Reister, Robin, Tannous, Paul, Green, Thomas A., Neve, Rachael L., Chakravarty, Sumana, Kumar, Arvind, Eisch, Amelia J., Self, David W., Lee, Francis S., Tamminga, Carol A., Cooper, Donald C., Gershenfeld, Howard K., and Nestler, Eric J.

Published
2007
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125. Extinction-induced upregulation in AMPA receptors reduces cocaine-seeking behaviour

Author

Sutton, Michael A., Schmidt, Eric F., Choi, Kwang-Ho, Schad, Christina A., Whisler, Kim, Simmons, Diana, Karanian, David A., Monteggia, Lisa M., Neve, Rachael L., and Self, David W.

Abstract

Author(s): Michael A. Sutton [1, 2]; Eric F. Schmidt [1, 2]; Kwang-Ho Choi [3]; Christina A. Schad [1]; Kim Whisler [3]; Diana Simmons [3]; David A. Karanian [1]; Lisa M. [...]

Published
2003
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127. A viral toolbox for conditional and transneuronal gene expression in zebrafish.

Author

Chie Satou, Neve, Rachael L., Oyibo, Hassana K., Zmarz, Pawel, Kuo-Hua Huang, Bouldoires, Estelle Arn, Takuma Mori, Shin-ichi Higashijima, Keller, Georg B., and Friedrich, Rainer W.

Subjects
*BRACHYDANIO, *GENE expression, *RABIES, *NEURAL circuitry, *FLUORESCENT proteins, *RABIES virus
Abstract

The zebrafish is an important model in systems neuroscience but viral tools to dissect the structure and function of neuronal circuitry are not established. We developed methods for efficient gene transfer and retrograde tracing in adult and larval zebrafish by herpes simplex viruses (HSV1). HSV1 was combined with the Gal4/UAS system to target cell types with high spatial, temporal, and molecular specificity. We also established methods for efficient transneuronal tracing by modified rabies viruses in zebrafish. We demonstrate that HSV1 and rabies viruses can be used to visualize and manipulate genetically or anatomically identified neurons within and across different brain areas of adult and larval zebrafish. An expandable library of viruses is provided to express fluorescent proteins, calcium indicators, optogenetic probes, toxins and other molecular tools. This toolbox creates new opportunities to interrogate neuronal circuits in zebrafish through combinations of genetic and viral approaches. [ABSTRACT FROM AUTHOR]

Published
2022
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133. Expression of the transcription factor delta-FosB in the brain controls sensitivity to cocaine

Author

Kelz, Max B., Chen, Jingshan, Carlezon, William A., Jr, Whisler, Kim, Gilden, Lauren, Beckmann, Alison M., Steffen, Cathy, Zhang, Ya-Jun, Marotti, Louis, Self, David W., Tkatch, Tatiana, Baranauskas, Gytis, Surmeier, D. James, Neve, Rachael L., Duman, Ronald S., Picciotto, Marina R., and Nestler, Eric J.

Subjects
Cocaine -- Physiological aspects, Drug abuse -- Physiological aspects, Environmental issues, Science and technology, Zoology and wildlife conservation
Abstract

It has been established that selective induction of delta-FosB in dynorphin/substance-P-containing neurons of the NAc and dorsal striatum in the adult is sufficient to boost an animal's responsiveness to the rewarding and locomotor-activating effects of cocaine. It is possible that induction of delta-FosB by chronic cocaine exposure is a mechanism for quite long-lasting rises in sensitivity to the stimulant and rewarding effects of the drug. This research also showed that increased GluR2 expression in the NAc can explain the enhanced sensitivity to cocaine's rewarding effects noted in the delta-FosB-expressing mice.

Published
1999

140. Alzheimer's disease: a re-examination of the amyloid hypothesis

Author

Neve, Rachael L. and Robakis, Nikolaos K.

Subjects
Alzheimer's disease -- Physiological aspects, Nervous system -- Degeneration, Health, Psychology and mental health
Abstract

Alzheimer's disease (AD) is a neurodegenerative disorder of the brain characterized by the presence of neuritic amyloid plaques and neurofibrillary tangles. Although it most frequently occurs in the elderly, this disorder also afflicts younger patients. The majority of AD cases are late in onset, lack an obvious genetic etiology and are characterized as sporadic, whereas a small percentage of cases are early in onset and segregate strongly within families (FAD), suggesting a genetic etiology. During the past decade it has become evident that the clinical and histopathological phenotypes of this disease are caused by heterogeneous genetic, and probably environmental, factors. Indeed, several genes have been identified that together appear to cause most of the familial forms of the disease, whereas the (epsilon)4 allele of the apolipoprotein E (apoE) gene has been shown to be a significant risk factor for the late onset forms of AD. Despite this evidence of heterogeneity, it has been suggested that all of these factors work through a common pathway by triggering the deposition of amyloid in the brain, which is ultimately responsible for the neuronal degeneration of AD. This is a controversial theory, however, primarily because there is a poor correlation between the concentrations and distribution of amyloid depositions in the brain and several parameters of AD pathology, including degree of dementia, loss of synapses, loss of neurons and abnormalities of the cytoskeleton.

Published
1998

141. Decoding Neural Circuits that Control Compulsive Sucrose Seeking

Author

Matthews, Gillian A., Presbrey, Kara N., Wichmann, Romy, Wildes, Craig P., Nieh, Horng-An Edward, Allsop, Stephen Azariah, Leppla, Christopher Albert, Neve, Rachael L., Tye, Kay, Massachusetts Institute of Technology. Department of Brain and Cognitive Sciences, Picower Institute for Learning and Memory, Nieh, Horng-An Edward, Matthews, Gillian A., Allsop, Stephen Azariah, Presbrey, Kara N., Leppla, Christopher Albert, Wichmann, Romy, Neve, Rachael L., Wildes, Craig P., and Tye, Kay

Subjects
Appetitive Behavior, Behavior, Animal, Biochemistry, Genetics and Molecular Biology(all), Ventral Tegmental Area, Hypothalamus, Sugar consumption, Biology, Inhibitory postsynaptic potential, Article, gamma-Aminobutyric acid, General Biochemistry, Genetics and Molecular Biology, Ventral tegmental area, medicine.anatomical_structure, nervous system, Dopamine, Hypothalamic Area, Lateral, medicine, Excitatory postsynaptic potential, Biological neural network, Animals, GABAergic, Consummatory Behavior, Neuroscience, psychological phenomena and processes, medicine.drug
Abstract

The lateral hypothalamic (LH) projection to the ventral tegmental area (VTA) has been linked to reward processing, but the computations within the LH-VTA loop that give rise to specific aspects of behavior have been difficult to isolate. We show that LH-VTA neurons encode the learned action of seeking a reward, independent of reward availability. In contrast, LH neurons downstream of VTA encode reward-predictive cues and unexpected reward omission. We show that inhibiting the LH-VTA pathway reduces “compulsive” sucrose seeking but not food consumption in hungry mice. We reveal that the LH sends excitatory and inhibitory input onto VTA dopamine (DA) and GABA neurons, and that the GABAergic projection drives feeding-related behavior. Our study overlays information about the type, function, and connectivity of LH neurons and identifies a neural circuit that selectively controls compulsive sugar consumption, without preventing feeding necessary for survival, providing a potential target for therapeutic interventions for compulsive-overeating disorder., JPB Foundation, Whitehall Foundation, Klingenstein Foundation, Brain & Behavior Research Foundation (Young Investigator Award), Alfred P. Sloan Foundation, National Institute of Mental Health (U.S.) (NIH R01-MH102441-01), National Institutes of Health (U.S.) (Director’s New Investigator Award DP2-DK-102256-01), National Science Foundation (U.S.). Graduate Research Fellowship, Integrative Neuronal Systems Fellowship, Training Program in the Neurobiology of Learning and Memory, Massachusetts Institute of Technology. Simons Center for the Social Brain (Postdoctoral Fellowship), Jeffrey and Nancy Halis Fellowship, Henry E. Singleton Fund, James R. Killian Fellowship, NWO of the Netherlands (Rubicon Award)

Published
2015
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143. Absence of Duplication of Chromosome 21 Genes in Familial and Sporadic Alzheimer's Disease

Author

St George-Hyslop, Peter H., Tanzi, Rudolph E., Polinsky, Ronald J., Neve, Rachael L., Pollen, Daniel, Drachman, David, Growdon, John, Cupples, L. Adrienne, Nee, Linda, Myers, Richard H., O'Sullivan, Dianne, Watkins, Paul C., Amos, Jean A., Deutsch, Curtis K., Bodfish, James W., Kinsbourne, Marcel, Feldman, Robert G., Bruni, Amalia, Amaducci, Luigi, Foncin, Jean-Francois, and Gusella, James F.

Published
1987

147. Beta-amyloid precursor protein binds to a neurite-promoting IKVAV site of laminin

Author

Kibbey, Maura C., Jucker, Mathias, Weeks, Benjamin S., Neve, Rachael L., Van Nostrand, William E., and Kleinman, Hynda K.

Subjects
Laminin -- Analysis, Protein binding -- Analysis, Nerves -- Research, Science and technology
Abstract

A beta-amyloid precursor protein (APP) binds the -Ile-Lys-Val-Ala-Val-site C 1KVAV on the laminin A chain. Studies proved that this chain induces neurite outgrowth and cell attachment. Antisera for various epitopes of APP can identify LBP110, which is part of the APP group. APP, identified in turn by LBP110 antiserum, has a vital role to play in neurite outgrowth.

Published
1993

148. RGS9 Modulates Dopamine Signaling in the Basal Ganglia

Author

Rahman, Zia, Schwarz, Johannes, Gold, Stephen J, Zachariou, Venetia, Wein, Marc N, Choi, Kwang-Ho, Kovoor, Abraham, Chen, Ching-Kang, DiLeone, Ralph J, Schwarz, Sigrid C, Selley, Dana E, Sim-Selley, Laura J, Barrot, Michel, Luedtke, Robert R, Self, David, Neve, Rachael L, Lester, Henry A, Simon, Melvin I, and Nestler, Eric J

Published
2003
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