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Article ; Online: Stress-Induced Neuronal Colony Stimulating Factor 1 Provokes Microglia-Mediated Neuronal Remodeling and Depressive-like Behavior.

Wohleb, Eric S / Terwilliger, Rosemarie / Duman, Catharine H / Duman, Ronald S

2017 Volume 83, Issue 1, Page(s) 38–49

Abstract: Background: Chronic stress exposure causes neuronal atrophy and synaptic deficits in the medial prefrontal cortex (PFC), contributing to development of anxiety- and depressive-like behaviors. Concomitantly, microglia in the PFC undergo morphological and ...

Abstract	Background: Chronic stress exposure causes neuronal atrophy and synaptic deficits in the medial prefrontal cortex (PFC), contributing to development of anxiety- and depressive-like behaviors. Concomitantly, microglia in the PFC undergo morphological and functional changes following stress exposure, suggesting that microglia contribute to synaptic deficits underlying behavioral consequences. Methods: Male and female mice were exposed to chronic unpredictable stress (CUS) to examine the role of neuron-microglia interactions in the medial PFC during development of anxiety- and depressive-like behaviors. Thy1-GFP-M mice were used to assess microglia-mediated neuronal remodeling and dendritic spine density in the medial PFC. Viral-mediated knockdown of neuronal colony stimulating factor 1 (CSF1) was used to modulate microglia function and behavioral consequences after CUS. Results: CUS promoted anxiety- and depressive-like behaviors that were associated with increased messenger RNA levels of CSF1 in the PFC. Increased CSF1 messenger RNA levels were also detected in the postmortem dorsolateral PFC of individuals with depression. Moreover, microglia isolated from the frontal cortex of mice exposed to CUS show elevated CSF1 receptor expression and increased phagocytosis of neuronal elements. Notably, functional alterations in microglia were more pronounced in male mice compared with female mice. These functional changes in microglia corresponded with reduced dendritic spine density on pyramidal neurons in layer 1 of the medial PFC. Viral-mediated knockdown of neuronal CSF1 in the medial PFC attenuated microglia-mediated neuronal remodeling and prevented behavioral deficits caused by CUS. Conclusions: These findings revealed that stress-induced elevations in neuronal CSF1 provokes microglia-mediated neuronal remodeling in the medial PFC, contributing to synaptic deficits and development of anxiety- and depressive-like behavior.
MeSH term(s)	Animals ; Anxiety/metabolism ; Anxiety/pathology ; Chronic Disease ; Depressive Disorder/metabolism ; Depressive Disorder/pathology ; Disease Models, Animal ; Female ; Macrophage Colony-Stimulating Factor/genetics ; Macrophage Colony-Stimulating Factor/metabolism ; Male ; Mice, Inbred C57BL ; Mice, Transgenic ; Microglia/metabolism ; Microglia/pathology ; Neuronal Plasticity/physiology ; Neurons/metabolism ; Neurons/pathology ; Phagocytosis/physiology ; Prefrontal Cortex/metabolism ; Prefrontal Cortex/pathology ; RNA, Messenger/metabolism ; Receptor, Macrophage Colony-Stimulating Factor/metabolism ; Sex Characteristics ; Stress, Psychological/metabolism ; Stress, Psychological/pathology ; Uncertainty
Chemical Substances	RNA, Messenger ; Macrophage Colony-Stimulating Factor (81627-83-0) ; Receptor, Macrophage Colony-Stimulating Factor (EC 2.7.10.1)
Language	English
Publishing date	2017-06-12
Publishing country	United States
Document type	Journal Article
ZDB-ID	209434-4
ISSN	1873-2402 ; 0006-3223
ISSN (online)	1873-2402
ISSN	0006-3223
DOI	10.1016/j.biopsych.2017.05.026
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Article ; Online: Sestrin modulator NV-5138 produces rapid antidepressant effects via direct mTORC1 activation.

Kato, Taro / Pothula, Santosh / Liu, Rong-Jian / Duman, Catharine H / Terwilliger, Rosemarie / Vlasuk, George P / Saiah, Eddine / Hahm, Seung / Duman, Ronald S

The Journal of clinical investigation

2019 Volume 129, Issue 6, Page(s) 2542–2554

Abstract: Preclinical studies demonstrate that rapid acting antidepressants, including ketamine require stimulation of mTORC1 signaling. This pathway is regulated by neuronal activity, endocrine and metabolic signals, notably the amino acid leucine, which ... ...

Abstract	Preclinical studies demonstrate that rapid acting antidepressants, including ketamine require stimulation of mTORC1 signaling. This pathway is regulated by neuronal activity, endocrine and metabolic signals, notably the amino acid leucine, which activates mTORC1 signaling via binding to the upstream regulator sestrin. Here, we examined the antidepressant actions of NV-5138, a novel highly selective small molecule modulator of sestrin that penetrates the blood brain barrier. The results demonstrate that a single dose of NV-5138 produced rapid and long-lasting antidepressant effects, and rapidly reversed anhedonia caused by chronic stress exposure. The antidepressant actions of NV-5138 required BDNF release as the behavioral responses are blocked by infusion of a BDNF neutralizing antibody into the medial prefrontal cortex (mPFC) or in mice with a knock-in of a BDNF polymorphism that blocks activity dependent BDNF release. NV-5138 administration also rapidly increased synapse number and function in the mPFC, and reversed the synaptic deficits caused by chronic stress. Together, the results demonstrate that NV-5138 produced rapid synaptic and antidepressant behavioral responses via activation of the mTORC1 pathway and BDNF signaling, indicating that pharmacological modulation of sestrin is a novel approach for development of rapid acting antidepressants.
MeSH term(s)	Animals ; Antidepressive Agents/chemistry ; Antidepressive Agents/pharmacokinetics ; Antidepressive Agents/pharmacology ; Behavior, Animal/drug effects ; Brain-Derived Neurotrophic Factor/genetics ; Brain-Derived Neurotrophic Factor/metabolism ; Heat-Shock Proteins/genetics ; Heat-Shock Proteins/metabolism ; Male ; Mechanistic Target of Rapamycin Complex 1/genetics ; Mechanistic Target of Rapamycin Complex 1/metabolism ; Mice ; Mice, Knockout ; Rats ; Rats, Sprague-Dawley ; Synaptic Transmission/drug effects ; Synaptic Transmission/genetics
Chemical Substances	Antidepressive Agents ; Bdnf protein, mouse ; Bdnf protein, rat ; Brain-Derived Neurotrophic Factor ; Heat-Shock Proteins ; Mechanistic Target of Rapamycin Complex 1 (EC 2.7.11.1)
Language	English
Publishing date	2019-04-16
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	3067-3
ISSN	1558-8238 ; 0021-9738
ISSN (online)	1558-8238
ISSN	0021-9738
DOI	10.1172/JCI126859
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Article ; Online: Ketamine rapidly reverses stress-induced impairments in GABAergic transmission in the prefrontal cortex in male rodents.

Ghosal, Sriparna / Duman, Catharine H / Liu, Rong-Jian / Wu, Min / Terwilliger, Rosemarie / Girgenti, Matthew J / Wohleb, Eric / Fogaca, Manoela V / Teichman, Emily M / Hare, Brendan / Duman, Ronald S

Neurobiology of disease

2019 Volume 134, Page(s) 104669

Abstract: Dysfunction of medial prefrontal cortex (mPFC) in association with imbalance of inhibitory and excitatory neurotransmission has been implicated in depression. However, the precise cellular mechanisms underlying this imbalance, particularly for GABAergic ... ...

Abstract	Dysfunction of medial prefrontal cortex (mPFC) in association with imbalance of inhibitory and excitatory neurotransmission has been implicated in depression. However, the precise cellular mechanisms underlying this imbalance, particularly for GABAergic transmission in the mPFC, and the link with the rapid acting antidepressant ketamine remains poorly understood. Here we determined the influence of chronic unpredictable stress (CUS), an ethologically validated model of depression, on synaptic markers of GABA neurotransmission, and the influence of a single dose of ketamine on CUS-induced synaptic deficits in mPFC of male rodents. The results demonstrate that CUS decreases GABAergic proteins and the frequency of inhibitory post synaptic currents (IPSCs) of layer V mPFC pyramidal neurons, concomitant with depression-like behaviors. In contrast, a single dose of ketamine can reverse CUS-induced deficits of GABA markers, in conjunction with reversal of CUS-induced depressive-like behaviors. These findings provide further evidence of impairments of GABAergic synapses as key determinants of depressive behavior and highlight ketamine-induced synaptic responses that restore GABA inhibitory, as well as glutamate neurotransmission.
MeSH term(s)	Animals ; Antidepressive Agents/administration & dosage ; Depression/physiopathology ; Disease Models, Animal ; Inhibitory Postsynaptic Potentials/drug effects ; Ketamine/administration & dosage ; Male ; Mice, Inbred C57BL ; Neurons/drug effects ; Neurons/physiology ; Prefrontal Cortex/drug effects ; Prefrontal Cortex/physiopathology ; Stress, Psychological/physiopathology ; Synaptic Transmission/drug effects ; gamma-Aminobutyric Acid/physiology
Chemical Substances	Antidepressive Agents ; gamma-Aminobutyric Acid (56-12-2) ; Ketamine (690G0D6V8H)
Language	English
Publishing date	2019-11-07
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	1211786-9
ISSN	1095-953X ; 0969-9961
ISSN (online)	1095-953X
ISSN	0969-9961
DOI	10.1016/j.nbd.2019.104669
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Article ; Online: Antipsychotic-induced gene regulation in multiple brain regions.

Girgenti, Matthew James / Nisenbaum, Laura K / Bymaster, Franklin / Terwilliger, Rosemarie / Duman, Ronald S / Newton, Samuel Sathyanesan

Journal of neurochemistry

2010 Volume 113, Issue 1, Page(s) 175–187

Abstract: The molecular mechanism of action of antipsychotic drugs is not well understood. Their complex receptor affinity profiles indicate that their action could extend beyond dopamine receptor blockade. Single gene expression studies and high-throughput gene ... ...

Abstract	The molecular mechanism of action of antipsychotic drugs is not well understood. Their complex receptor affinity profiles indicate that their action could extend beyond dopamine receptor blockade. Single gene expression studies and high-throughput gene profiling have shown the induction of genes from several molecular classes and functional categories. Using a focused microarray approach, we investigated gene regulation in rat striatum, frontal cortex, and hippocampus after chronic administration of haloperidol or olanzapine. Regulated genes were validated by in situ hybridization, real-time PCR, and immunohistochemistry. Only limited overlap was observed in genes regulated by haloperidol and olanzapine. Both drugs elicited maximal gene regulation in the striatum and least in the hippocampus. Striatal gene induction by haloperidol was predominantly in neurotransmitter signaling, G-protein coupled receptors, and transcription factors. Olanzapine prominently induced retinoic acid and trophic factor signaling genes in the frontal cortex. The data also revealed the induction of several genes that could be targeted in future drug development efforts. The study uncovered the induction of several novel genes, including somatostatin receptors and metabotropic glutamate receptors. The results demonstrating the regulation of multiple receptors and transcription factors suggests that both typical and atypical antipsychotics could possess a complex molecular mechanism of action.
MeSH term(s)	Animals ; Antipsychotic Agents/pharmacology ; Benzodiazepines/pharmacology ; Brain/drug effects ; Brain/metabolism ; Gene Expression Profiling/methods ; Gene Expression Regulation/drug effects ; Haloperidol/analogs & derivatives ; Haloperidol/pharmacology ; Male ; Neurotransmitter Agents/genetics ; Neurotransmitter Agents/metabolism ; Olanzapine ; Oligonucleotide Array Sequence Analysis/methods ; Rats ; Rats, Sprague-Dawley ; Receptors, G-Protein-Coupled/genetics ; Receptors, G-Protein-Coupled/metabolism ; Signal Transduction/drug effects ; Signal Transduction/genetics ; Transcription Factors/genetics ; Transcription Factors/metabolism
Chemical Substances	Antipsychotic Agents ; Neurotransmitter Agents ; Receptors, G-Protein-Coupled ; Transcription Factors ; Benzodiazepines (12794-10-4) ; haloperidol decanoate (AC20PJ4101) ; Haloperidol (J6292F8L3D) ; Olanzapine (N7U69T4SZR)
Language	English
Publishing date	2010-01-13
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	80158-6
ISSN	1471-4159 ; 0022-3042 ; 1474-1644
ISSN (online)	1471-4159
ISSN	0022-3042 ; 1474-1644
DOI	10.1111/j.1471-4159.2010.06585.x
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Article: Antipsychotic-induced gene regulation in multiple brain regions

Girgenti, Matthew James / Nisenbaum, Laura K / Bymaster, Franklin / Terwilliger, Rosemarie / Duman, Ronald S / Newton, Samuel Sathyanesan

Journal of neurochemistry. 2010 Apr., v. 113, no. 1

2010

Abstract: J. Neurochem. (2010) 10.1111/j.1471-4159.2010.06585.x The molecular mechanism of action of antipsychotic drugs is not well understood. Their complex receptor affinity profiles indicate that their action could extend beyond dopamine receptor blockade. ... ...

Abstract	J. Neurochem. (2010) 10.1111/j.1471-4159.2010.06585.x The molecular mechanism of action of antipsychotic drugs is not well understood. Their complex receptor affinity profiles indicate that their action could extend beyond dopamine receptor blockade. Single gene expression studies and high-throughput gene profiling have shown the induction of genes from several molecular classes and functional categories. Using a focused microarray approach, we investigated gene regulation in rat striatum, frontal cortex, and hippocampus after chronic administration of haloperidol or olanzapine. Regulated genes were validated by in situ hybridization, real-time PCR, and immunohistochemistry. Only limited overlap was observed in genes regulated by haloperidol and olanzapine. Both drugs elicited maximal gene regulation in the striatum and least in the hippocampus. Striatal gene induction by haloperidol was predominantly in neurotransmitter signaling, G-protein coupled receptors, and transcription factors. Olanzapine prominently induced retinoic acid and trophic factor signaling genes in the frontal cortex. The data also revealed the induction of several genes that could be targeted in future drug development efforts. The study uncovered the induction of several novel genes, including somatostatin receptors and metabotropic glutamate receptors. The results demonstrating the regulation of multiple receptors and transcription factors suggests that both typical and atypical antipsychotics could possess a complex molecular mechanism of action.
Keywords	gene expression ; haloperidol
Language	English
Dates of publication	2010-04
Size	p. 175-187.
Publisher	Blackwell Publishing Ltd
Publishing place	Oxford, UK
Document type	Article
ZDB-ID	80158-6
ISSN	1471-4159 ; 0022-3042 ; 1474-1644
ISSN (online)	1471-4159
ISSN	0022-3042 ; 1474-1644
DOI	10.1111/j.1471-4159.2010.06585.x
Database	NAL-Catalogue (AGRICOLA)

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Article: Single-cell genomics and regulatory networks for 388 human brains.

Emani, Prashant S / Liu, Jason J / Clarke, Declan / Jensen, Matthew / Warrell, Jonathan / Gupta, Chirag / Meng, Ran / Lee, Che Yu / Xu, Siwei / Dursun, Cagatay / Lou, Shaoke / Chen, Yuhang / Chu, Zhiyuan / Galeev, Timur / Hwang, Ahyeon / Li, Yunyang / Ni, Pengyu / Zhou, Xiao / Bakken, Trygve E /

Bendl, Jaroslav / Bicks, Lucy / Chatterjee, Tanima / Cheng, Lijun / Cheng, Yuyan / Dai, Yi / Duan, Ziheng / Flaherty, Mary / Fullard, John F / Gancz, Michael / Garrido-Martín, Diego / Gaynor-Gillett, Sophia / Grundman, Jennifer / Hawken, Natalie / Henry, Ella / Hoffman, Gabriel E / Huang, Ao / Jiang, Yunzhe / Jin, Ting / Jorstad, Nikolas L / Kawaguchi, Riki / Khullar, Saniya / Liu, Jianyin / Liu, Junhao / Liu, Shuang / Ma, Shaojie / Margolis, Michael / Mazariegos, Samantha / Moore, Jill / Moran, Jennifer R / Nguyen, Eric / Phalke, Nishigandha / Pjanic, Milos / Pratt, Henry / Quintero, Diana / Rajagopalan, Ananya S / Riesenmy, Tiernon R / Shedd, Nicole / Shi, Manman / Spector, Megan / Terwilliger, Rosemarie / Travaglini, Kyle J / Wamsley, Brie / Wang, Gaoyuan / Xia, Yan / Xiao, Shaohua / Yang, Andrew C / Zheng, Suchen / Gandal, Michael J / Lee, Donghoon / Lein, Ed S / Roussos, Panos / Sestan, Nenad / Weng, Zhiping / White, Kevin P / Won, Hyejung / Girgenti, Matthew J / Zhang, Jing / Wang, Daifeng / Geschwind, Daniel / Gerstein, Mark

bioRxiv : the preprint server for biology

2024

Abstract: Single-cell genomics is a powerful tool for studying heterogeneous tissues such as the brain. Yet, little is understood about how genetic variants influence cell-level gene expression. Addressing this, we uniformly processed single-nuclei, multi-omics ... ...

Abstract	Single-cell genomics is a powerful tool for studying heterogeneous tissues such as the brain. Yet, little is understood about how genetic variants influence cell-level gene expression. Addressing this, we uniformly processed single-nuclei, multi-omics datasets into a resource comprising >2.8M nuclei from the prefrontal cortex across 388 individuals. For 28 cell types, we assessed population-level variation in expression and chromatin across gene families and drug targets. We identified >550K cell-type-specific regulatory elements and >1.4M single-cell expression-quantitative-trait loci, which we used to build cell-type regulatory and cell-to-cell communication networks. These networks manifest cellular changes in aging and neuropsychiatric disorders. We further constructed an integrative model accurately imputing single-cell expression and simulating perturbations; the model prioritized ~250 disease-risk genes and drug targets with associated cell types.
Language	English
Publishing date	2024-03-30
Publishing country	United States
Document type	Preprint
DOI	10.1101/2024.03.18.585576
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Article ; Online: Peripheral insulin-like growth factor-I produces antidepressant-like behavior and contributes to the effect of exercise.

Duman, Catharine H / Schlesinger, Lee / Terwilliger, Rosemarie / Russell, David S / Newton, Samuel S / Duman, Ronald S

Behavioural brain research

2008 Volume 198, Issue 2, Page(s) 366–371

Abstract: Growth factors in the brain are important to depression and it's treatment and we assessed the ability of peripherally administered insulin-like growth factor-I (IGF-I) to influence behavior related to depression. We found that mice that received chronic ...

Abstract	Growth factors in the brain are important to depression and it's treatment and we assessed the ability of peripherally administered insulin-like growth factor-I (IGF-I) to influence behavior related to depression. We found that mice that received chronic IGF-I treatment showed antidepressant-like behavior in forced-swim and novelty-induced hypophagia (NIH) tests and increased sucrose consumption after chronic mild unpredictable stress exposure. Additionally, peripheral anti-IGF-I administration blocked exercise-induced antidepressant effects in the forced-swim test (FST). These results support the functional relevance of neurotrophic mechanisms to depression and extend this idea to include neurotrophic factors in the periphery.
MeSH term(s)	Animals ; Antidepressive Agents/pharmacology ; Behavior, Animal/drug effects ; Brain-Derived Neurotrophic Factor/genetics ; Brain-Derived Neurotrophic Factor/metabolism ; Depression/drug therapy ; Depression/psychology ; Enzyme-Linked Immunosorbent Assay ; Exercise/psychology ; Humans ; Immunoglobulin G/pharmacology ; In Situ Hybridization ; Injections, Subcutaneous ; Insulin-Like Growth Factor I/administration & dosage ; Insulin-Like Growth Factor I/antagonists & inhibitors ; Insulin-Like Growth Factor I/genetics ; Insulin-Like Growth Factor I/metabolism ; Insulin-Like Growth Factor I/pharmacology ; Insulin-Like Growth Factor I/physiology ; Male ; Mice ; Motor Activity/physiology ; Stress, Physiological/drug effects ; Swimming/physiology ; Time Factors
Chemical Substances	Antidepressive Agents ; Brain-Derived Neurotrophic Factor ; Immunoglobulin G ; Insulin-Like Growth Factor I (67763-96-6)
Language	English
Publishing date	2008-11-14
Publishing country	Netherlands
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, Non-P.H.S.
ZDB-ID	449927-x
ISSN	1872-7549 ; 0166-4328
ISSN (online)	1872-7549
ISSN	0166-4328
DOI	10.1016/j.bbr.2008.11.016
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