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Article ; Online: Evaluation of Na

Martinowich, Keri / Das, Debamitra / Sripathy, Srinidhi Rao / Mai, Yishan / Kenney, Rakaia F / Maher, Brady J

2022 Volume 28, Issue 1, Page(s) 76–82

Abstract: Pitt Hopkins Syndrome (PTHS) is a rare syndromic form of autism spectrum disorder (ASD) caused by autosomal dominant mutations in the Transcription Factor 4 (TCF4) gene. TCF4 is a basic helix-loop-helix transcription factor that is critical for ... ...

Abstract	Pitt Hopkins Syndrome (PTHS) is a rare syndromic form of autism spectrum disorder (ASD) caused by autosomal dominant mutations in the Transcription Factor 4 (TCF4) gene. TCF4 is a basic helix-loop-helix transcription factor that is critical for neurodevelopment and brain function through its binding to cis-regulatory elements of target genes. One potential therapeutic strategy for PTHS is to identify dysregulated target genes and normalize their dysfunction. Here, we propose that SCN10A is an important target gene of TCF4 that is an applicable therapeutic approach for PTHS. Scn10a encodes the voltage-gated sodium channel Na
MeSH term(s)	Animals ; Mice ; Autism Spectrum Disorder/drug therapy ; Autism Spectrum Disorder/genetics ; Autism Spectrum Disorder/metabolism ; Facies ; Hyperventilation/genetics ; Intellectual Disability/drug therapy ; Intellectual Disability/genetics ; Intellectual Disability/metabolism ; Transcription Factor 4/genetics ; NAV1.8 Voltage-Gated Sodium Channel/chemistry ; NAV1.8 Voltage-Gated Sodium Channel/metabolism
Chemical Substances	Transcription Factor 4 ; Scn10a protein, mouse ; NAV1.8 Voltage-Gated Sodium Channel
Language	English
Publishing date	2022-10-12
Publishing country	England
Document type	Journal Article ; Review ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	1330655-8
ISSN	1476-5578 ; 1359-4184
ISSN (online)	1476-5578
ISSN	1359-4184
DOI	10.1038/s41380-022-01811-4
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Article ; Online: Manipulation of a genetically and spatially defined sub-population of BDNF-expressing neurons potentiates learned fear and decreases hippocampal-prefrontal synchrony in mice.

Hallock, Henry L / Quillian, Henry M / Mai, Yishan / Maynard, Kristen R / Hill, Julia L / Martinowich, Keri

Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology

2019 Volume 44, Issue 13, Page(s) 2239–2246

Abstract: Brain-derived neurotrophic factor (BDNF) signaling regulates synaptic plasticity in the hippocampus (HC) and prefrontal cortex (PFC), and has been extensively linked with fear memory expression in rodents. Notably, disrupting BDNF production from ... ...

Abstract	Brain-derived neurotrophic factor (BDNF) signaling regulates synaptic plasticity in the hippocampus (HC) and prefrontal cortex (PFC), and has been extensively linked with fear memory expression in rodents. Notably, disrupting BDNF production from promoter IV-derived transcripts enhances fear expression in mice, and decreases fear-associated HC-PFC synchrony, suggesting that Bdnf transcription from promoter IV plays a key role in HC-PFC function during fear memory retrieval. To better understand how promoter IV-derived BDNF controls HC-PFC connectivity and fear expression, we generated a viral construct that selectively targets cells expressing promoter IV-derived Bdnf transcripts ("p4-cells") for tamoxifen-inducible Cre-mediated recombination (AAV8-p4Bdnf-ER
MeSH term(s)	Animals ; Brain-Derived Neurotrophic Factor/genetics ; Brain-Derived Neurotrophic Factor/physiology ; Conditioning, Classical ; Cortical Synchronization ; Fear/physiology ; Hippocampus/metabolism ; Hippocampus/physiology ; Male ; Mice, Inbred C57BL ; Neural Pathways/physiology ; Neuronal Plasticity ; Neurons/physiology ; Prefrontal Cortex/metabolism ; Prefrontal Cortex/physiology
Chemical Substances	Bdnf protein, mouse ; Brain-Derived Neurotrophic Factor
Language	English
Publishing date	2019-06-06
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	639471-1
ISSN	1740-634X ; 0893-133X
ISSN (online)	1740-634X
ISSN	0893-133X
DOI	10.1038/s41386-019-0429-1
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Article ; Online: TrkB Signaling Influences Gene Expression in Cortistatin-Expressing Interneurons.

Maynard, Kristen R / Kardian, Alisha / Hill, Julia L / Mai, Yishan / Barry, Brianna / Hallock, Henry L / Jaffe, Andrew E / Martinowich, Keri

eNeuro

2020 Volume 7, Issue 1

Abstract: Brain-derived neurotrophic factor (BDNF) signals through its cognate receptor tropomyosin receptor kinase B (TrkB) to promote the function of several classes of inhibitory interneurons. We previously reported that loss of BDNF-TrkB signaling in ... ...

Abstract	Brain-derived neurotrophic factor (BDNF) signals through its cognate receptor tropomyosin receptor kinase B (TrkB) to promote the function of several classes of inhibitory interneurons. We previously reported that loss of BDNF-TrkB signaling in cortistatin (Cort)-expressing interneurons leads to behavioral hyperactivity and spontaneous seizures in mice. We performed bulk RNA sequencing (RNA-seq) from the cortex of mice with disruption of BDNF-TrkB signaling in cortistatin interneurons, and identified differential expression of genes important for excitatory neuron function. Using translating ribosome affinity purification and RNA-seq, we define a molecular profile for Cort-expressing inhibitory neurons and subsequently compare the translatome of normal and TrkB-depleted Cort neurons, revealing alterations in calcium signaling and axon development. Several of the genes enriched in Cort neurons and differentially expressed in TrkB-depleted neurons are also implicated in autism and epilepsy. Our findings highlight TrkB-dependent molecular pathways as critical for the maturation of inhibitory interneurons and support the hypothesis that loss of BDNF signaling in Cort interneurons leads to altered excitatory/inhibitory balance.
MeSH term(s)	Animals ; Brain-Derived Neurotrophic Factor/genetics ; Gene Expression ; Interneurons ; Membrane Glycoproteins ; Mice ; Mice, Inbred C57BL ; Neuropeptides ; Protein-Tyrosine Kinases ; Receptor, trkB
Chemical Substances	Bdnf protein, mouse ; Brain-Derived Neurotrophic Factor ; Membrane Glycoproteins ; Neuropeptides ; cortistatin ; Ntrk2 protein, mouse (EC 2.7.10.1) ; Protein-Tyrosine Kinases (EC 2.7.10.1) ; Receptor, trkB (EC 2.7.10.1)
Language	English
Publishing date	2020-02-10
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2800598-3
ISSN	2373-2822 ; 2373-2822
ISSN (online)	2373-2822
ISSN	2373-2822
DOI	10.1523/ENEURO.0310-19.2019
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Article ; Online: Molecularly Defined Hippocampal Inputs Regulate Population Dynamics in the Prelimbic Cortex to Suppress Context Fear Memory Retrieval.

Hallock, Henry L / Quillian, Henry M / Maynard, Kristen R / Mai, Yishan / Chen, Huei-Ying / Hamersky, Gregory R / Shin, Joo Heon / Maher, Brady J / Jaffe, Andrew E / Martinowich, Keri

Biological psychiatry

2020 Volume 88, Issue 7, Page(s) 554–565

Abstract: Background: Context fear memory dysregulation is a hallmark symptom of several neuropsychiatric disorders, including generalized anxiety disorder and posttraumatic stress disorder. The hippocampus (HC) and prelimbic (PrL) subregion of the medial ... ...

Abstract	Background: Context fear memory dysregulation is a hallmark symptom of several neuropsychiatric disorders, including generalized anxiety disorder and posttraumatic stress disorder. The hippocampus (HC) and prelimbic (PrL) subregion of the medial prefrontal cortex have been linked with context fear memory retrieval in rodents, but the mechanisms by which HC-PrL circuitry regulates this process remain poorly understood. Methods: Spatial and genetic targeting of HC-PrL circuitry was used for RNA sequencing (n = 31), chemogenetic stimulation (n = 44), in vivo calcium imaging (n = 20), ex vivo electrophysiology (n = 8), and molecular regulation of plasticity cascades during fear behavior (context fear retrieval) (n = 16). Results: We showed that ventral HC (vHC) neurons with projections to the PrL cortex (vHC-PrL projectors) are a transcriptomically distinct subpopulation compared with adjacent nonprojecting neurons, and we showed complementary enrichment for diverse neuronal processes and central nervous system-related clinical gene sets. We further showed that stimulation of this population of vHC-PrL projectors suppresses context fear memory retrieval and impairs the ability of PrL neurons to dynamically distinguish between distinct phases of fear learning. Using transgenic and circuit-specific molecular targeting approaches, we demonstrated that unique patterns of activity-dependent gene transcription associated with brain-derived neurotrophic factor signaling within vHC-PrL projectors causally regulated activity in excitatory and inhibitory PrL neurons during context fear memory retrieval. Conclusions: Together, our data show that activity-dependent brain-derived neurotrophic factor release from molecularly distinct vHC-PrL projection neurons modulates postsynaptic signaling in both inhibitory and excitatory PrL neurons, modifying activity in discrete populations of PrL neurons to suppress freezing during context fear memory retrieval.
MeSH term(s)	Fear ; Hippocampus ; Memory ; Population Dynamics ; Prefrontal Cortex
Language	English
Publishing date	2020-04-28
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	209434-4
ISSN	1873-2402 ; 0006-3223
ISSN (online)	1873-2402
ISSN	0006-3223
DOI	10.1016/j.biopsych.2020.04.014
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Article ; Online: Cortistatin-expressing interneurons require TrkB signaling to suppress neural hyper-excitability.

Hill, Julia L / Jimenez, Dennisse V / Mai, Yishan / Ren, Ming / Hallock, Henry L / Maynard, Kristen R / Chen, Huei-Ying / Hardy, Nicholas F / Schloesser, Robert J / Maher, Brady J / Yang, Feng / Martinowich, Keri

Brain structure & function

2018 Volume 224, Issue 1, Page(s) 471–483

Abstract: Signaling of brain-derived neurotrophic factor (BDNF) via tropomyosin receptor kinase B (TrkB) plays a critical role in the maturation of cortical inhibition and controls expression of inhibitory interneuron markers, including the neuropeptide ... ...

Abstract	Signaling of brain-derived neurotrophic factor (BDNF) via tropomyosin receptor kinase B (TrkB) plays a critical role in the maturation of cortical inhibition and controls expression of inhibitory interneuron markers, including the neuropeptide cortistatin (CST). CST is expressed exclusively in a subset of cortical and hippocampal GABAergic interneurons, where it has anticonvulsant effects and controls sleep slow-wave activity (SWA). We hypothesized that CST-expressing interneurons play a critical role in regulating excitatory/inhibitory balance, and that BDNF, signaling through TrkB receptors on CST-expressing interneurons, is required for this function. Ablation of CST-expressing cells caused generalized seizures and premature death during early postnatal development, demonstrating a critical role for these cells in providing inhibition. Mice in which TrkB was selectively deleted from CST-expressing interneurons were hyperactive, slept less and developed spontaneous seizures. Frequencies of spontaneous excitatory post-synaptic currents (sEPSCs) on CST-expressing interneurons were attenuated in these mice. These data suggest that BDNF, signaling through TrkB receptors on CST-expressing cells, promotes excitatory drive onto these cells. Loss of excitatory drive onto CST-expressing cells that lack TrkB receptors may contribute to observed hyperexcitability and epileptogenesis.
MeSH term(s)	Animals ; Behavior, Animal ; Brain/metabolism ; Brain/physiopathology ; Brain Waves ; Brain-Derived Neurotrophic Factor/metabolism ; Excitatory Postsynaptic Potentials ; Hyperkinesis/metabolism ; Hyperkinesis/physiopathology ; Hyperkinesis/prevention & control ; Hyperkinesis/psychology ; Interneurons/metabolism ; Locomotion ; Membrane Glycoproteins/deficiency ; Membrane Glycoproteins/genetics ; Membrane Glycoproteins/metabolism ; Mice, Inbred C57BL ; Mice, Knockout ; Neural Inhibition ; Neuropeptides/deficiency ; Neuropeptides/genetics ; Neuropeptides/metabolism ; Protein-Tyrosine Kinases/deficiency ; Protein-Tyrosine Kinases/genetics ; Protein-Tyrosine Kinases/metabolism ; Seizures/metabolism ; Seizures/physiopathology ; Seizures/prevention & control ; Seizures/psychology ; Sleep ; Synaptic Transmission
Chemical Substances	Bdnf protein, rat ; Brain-Derived Neurotrophic Factor ; Membrane Glycoproteins ; Neuropeptides ; cortistatin ; Ntrk2 protein, mouse (EC 2.7.10.1) ; Protein-Tyrosine Kinases (EC 2.7.10.1)
Language	English
Publishing date	2018-10-30
Publishing country	Germany
Document type	Journal Article
ZDB-ID	2273162-3
ISSN	1863-2661 ; 1863-2653
ISSN (online)	1863-2661
ISSN	1863-2653
DOI	10.1007/s00429-018-1783-1
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Article ; Online: A functional genomics screen identifying blood cell development genes in Drosophila by undergraduates participating in a course-based research experience.

Evans, Cory J / Olson, John M / Mondal, Bama Charan / Kandimalla, Pratyush / Abbasi, Ariano / Abdusamad, Mai M / Acosta, Osvaldo / Ainsworth, Julia A / Akram, Haris M / Albert, Ralph B / Alegria-Leal, Elitzander / Alexander, Kai Y / Ayala, Angelica C / Balashova, Nataliya S / Barber, Rebecca M / Bassi, Harmanjit / Bennion, Sean P / Beyder, Miriam / Bhatt, Kush V /

Bhoot, Chinmay / Bradshaw, Aaron W / Brannigan, Tierney G / Cao, Boyu / Cashell, Yancey Y / Chai, Timothy / Chan, Alex W / Chan, Carissa / Chang, Inho / Chang, Jonathan / Chang, Michael T / Chang, Patrick W / Chang, Stephen / Chari, Neel / Chassiakos, Alexander J / Chen, Iris E / Chen, Vivian K / Chen, Zheying / Cheng, Marsha R / Chiang, Mimi / Chiu, Vivian / Choi, Sharon / Chung, Jun Ho / Contreras, Liset / Corona, Edgar / Cruz, Courtney J / Cruz, Renae L / Dang, Jefferson M / Dasari, Suhas P / De La Fuente, Justin R O / Del Rio, Oscar M A / Dennis, Emily R / Dertsakyan, Petros S / Dey, Ipsita / Distler, Rachel S / Dong, Zhiqiao / Dorman, Leah C / Douglass, Mark A / Ehresman, Allysen B / Fu, Ivy H / Fua, Andrea / Full, Sean M / Ghaffari-Rafi, Arash / Ghani, Asmar Abdul / Giap, Bosco / Gill, Sonia / Gill, Zafar S / Gills, Nicholas J / Godavarthi, Sindhuja / Golnazarian, Talin / Goyal, Raghav / Gray, Ricardo / Grunfeld, Alexander M / Gu, Kelly M / Gutierrez, Natalia C / Ha, An N / Hamid, Iman / Hanson, Ashley / Hao, Celesti / He, Chongbin / He, Mengshi / Hedtke, Joshua P / Hernandez, Ysrael K / Hlaing, Hnin / Hobby, Faith A / Hoi, Karen / Hope, Ashley C / Hosseinian, Sahra M / Hsu, Alice / Hsueh, Jennifer / Hu, Eileen / Hu, Spencer S / Huang, Stephanie / Huang, Wilson / Huynh, Melanie / Javier, Carmen / Jeon, Na Eun / Ji, Sunjong / Johal, Jasmin / John, Amala / Johnson, Lauren / Kadakia, Saurin / Kakade, Namrata / Kamel, Sarah / Kaur, Ravinder / Khatra, Jagteshwar S / Kho, Jeffrey A / Kim, Caleb / Kim, Emily Jin-Kyung / Kim, Hee Jong / Kim, Hyun Wook / Kim, Jin Hee / Kim, Seong Ah / Kim, Woo Kyeom / Kit, Brian / La, Cindy / Lai, Jonathan / Lam, Vivian / Le, Nguyen Khoi / Lee, Chi Ju / Lee, Dana / Lee, Dong Yeon / Lee, James / Lee, Jason / Lee, Jessica / Lee, Ju-Yeon / Lee, Sharon / Lee, Terrence C / Lee, Victoria / Li, Amber J / Li, Jialing / Libro, Alexandra M / Lien, Irvin C / Lim, Mia / Lin, Jeffrey M / Liu, Connie Y / Liu, Steven C / Louie, Irene / Lu, Shijia W / Luo, William Y / Luu, Tiffany / Madrigal, Josef T / Mai, Yishan / Miya, Darron I / Mohammadi, Mina / Mohanta, Sayonika / Mokwena, Tebogo / Montoya, Tonatiuh / Mould, Dallas L / Murata, Mark R / Muthaiya, Janani / Naicker, Seethim / Neebe, Mallory R / Ngo, Amy / Ngo, Duy Q / Ngo, Jamie A / Nguyen, Anh T / Nguyen, Huy C X / Nguyen, Rina H / Nguyen, Thao T T / Nguyen, Vincent T / Nishida, Kevin / Oh, Seo-Kyung / Omi, Kristen M / Onglatco, Mary C / Almazan, Guadalupe Ortega / Paguntalan, Jahzeel / Panchal, Maharshi / Pang, Stephanie / Parikh, Harin B / Patel, Purvi D / Patel, Trisha H / Petersen, Julia E / Pham, Steven / Phan-Everson, Tien M / Pokhriyal, Megha / Popovich, Davis W / Quaal, Adam T / Querubin, Karl / Resendiz, Anabel / Riabkova, Nadezhda / Rong, Fred / Salarkia, Sarah / Sama, Nateli / Sang, Elaine / Sanville, David A / Schoen, Emily R / Shen, Zhouyang / Siangchin, Ken / Sibal, Gabrielle / Sin, Garuem / Sjarif, Jasmine / Smith, Christopher J / Soeboer, Annisa N / Sosa, Cristian / Spitters, Derek / Stender, Bryan / Su, Chloe C / Summapund, Jenny / Sun, Beatrice J / Sutanto, Christine / Tan, Jaime S / Tan, Nguon L / Tangmatitam, Parich / Trac, Cindy K / Tran, Conny / Tran, Daniel / Tran, Duy / Tran, Vina / Truong, Patrick A / Tsai, Brandon L / Tsai, Pei-Hua / Tsui, C Kimberly / Uriu, Jackson K / Venkatesh, Sanan / Vo, Maique / Vo, Nhat-Thi / Vo, Phuong / Voros, Timothy C / Wan, Yuan / Wang, Eric / Wang, Jeffrey / Wang, Michael K / Wang, Yuxuan / Wei, Siman / Wilson, Matthew N / Wong, Daniel / Wu, Elliott / Xing, Hanning / Xu, Jason P / Yaftaly, Sahar / Yan, Kimberly / Yang, Evan / Yang, Rebecca / Yao, Tony / Yeo, Patricia / Yip, Vivian / Yogi, Puja / Young, Gloria Chin / Yung, Maggie M / Zai, Alexander / Zhang, Christine / Zhang, Xiao X / Zhao, Zijun / Zhou, Raymond / Zhou, Ziqi / Abutouk, Mona / Aguirre, Brian / Ao, Chon / Baranoff, Alexis / Beniwal, Angad / Cai, Zijie / Chan, Ryan / Chien, Kenneth Chang / Chaudhary, Umar / Chin, Patrick / Chowdhury, Praptee / Dalie, Jamlah / Du, Eric Y / Estrada, Alec / Feng, Erwin / Ghaly, Monica / Graf, Rose / Hernandez, Eduardo / Herrera, Kevin / Ho, Vivien W / Honeychurch, Kaitlyn / Hou, Yurianna / Huang, Jo M / Ishii, Momoko / James, Nicholas / Jang, Gah-Eun / Jin, Daphne / Juarez, Jesse / Kesaf, Ayse Elif / Khalsa, Sat Kartar / Kim, Hannah / Kovsky, Jenna / Kuang, Chak Lon / Kumar, Shraddha / Lam, Gloria / Lee, Ceejay / Lee, Grace / Li, Li / Lin, Joshua / Liu, Josephine / Ly, Janice / Ma, Austin / Markovic, Hannah / Medina, Cristian / Mungcal, Jonelle / Naranbaatar, Bilguudei / Patel, Kayla / Petersen, Lauren / Phan, Amanda / Phung, Malcolm / Priasti, Nadiyah / Ruano, Nancy / Salim, Tanveer / Schnell, Kristen / Shah, Paras / Shen, Jinhua / Stutzman, Nathan / Sukhina, Alisa / Tian, Rayna / Vega-Loza, Andrea / Wang, Joyce / Wang, Jun / Watanabe, Rina / Wei, Brandon / Xie, Lillian / Ye, Jessica / Zhao, Jeffrey / Zimmerman, Jill / Bracken, Colton / Capili, Jason / Char, Andrew / Chen, Michel / Huang, Pingdi / Ji, Sena / Kim, Emily / Kim, Kenneth / Ko, Julie / Laput, Sean Louise G / Law, Sam / Lee, Sang Kuk / Lee, Olivia / Lim, David / Lin, Eric / Marik, Kyle / Mytych, Josh / O'Laughlin, Andie / Pak, Jensen / Park, Claire / Ryu, Ruth / Shinde, Ashwin / Sosa, Manny / Waite, Nick / Williams, Mane / Wong, Richard / Woo, Jocelyn / Woo, Jonathan / Yepuri, Vishaal / Yim, Dorothy / Huynh, Dan / Wijiewarnasurya, Dinali / Shapiro, Casey / Levis-Fitzgerald, Marc / Jaworski, Leslie / Lopatto, David / Clark, Ira E / Johnson, Tracy / Banerjee, Utpal

G3 (Bethesda, Md.)

2021 Volume 11, Issue 1

Abstract: Undergraduate students participating in the UCLA Undergraduate Research Consortium for Functional Genomics (URCFG) have conducted a two-phased screen using RNA interference (RNAi) in combination with fluorescent reporter proteins to identify genes ... ...

Abstract	Undergraduate students participating in the UCLA Undergraduate Research Consortium for Functional Genomics (URCFG) have conducted a two-phased screen using RNA interference (RNAi) in combination with fluorescent reporter proteins to identify genes important for hematopoiesis in Drosophila. This screen disrupted the function of approximately 3500 genes and identified 137 candidate genes for which loss of function leads to observable changes in the hematopoietic development. Targeting RNAi to maturing, progenitor, and regulatory cell types identified key subsets that either limit or promote blood cell maturation. Bioinformatic analysis reveals gene enrichment in several previously uncharacterized areas, including RNA processing and export and vesicular trafficking. Lastly, the participation of students in this course-based undergraduate research experience (CURE) correlated with increased learning gains across several areas, as well as increased STEM retention, indicating that authentic, student-driven research in the form of a CURE represents an impactful and enriching pedagogical approach.
MeSH term(s)	Animals ; Blood Cells ; Drosophila/genetics ; Genomics/education ; Humans ; Students ; Universities
Language	English
Publishing date	2021-02-12
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2629978-1
ISSN	2160-1836 ; 2160-1836
ISSN (online)	2160-1836
ISSN	2160-1836
DOI	10.1093/g3journal/jkaa028
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Article ; Online: Evaluation of Na

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Article ; Online: Manipulation of a genetically and spatially defined sub-population of BDNF-expressing neurons potentiates learned fear and decreases hippocampal-prefrontal synchrony in mice.

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Article ; Online: TrkB Signaling Influences Gene Expression in Cortistatin-Expressing Interneurons.

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Article ; Online: Molecularly Defined Hippocampal Inputs Regulate Population Dynamics in the Prelimbic Cortex to Suppress Context Fear Memory Retrieval.

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Article ; Online: Cortistatin-expressing interneurons require TrkB signaling to suppress neural hyper-excitability.

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Article ; Online: A functional genomics screen identifying blood cell development genes in Drosophila by undergraduates participating in a course-based research experience.

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