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Is dopamine transporter-mediated dopaminergic signaling in the retina a noninvasive biomarker for attention-deficit/ hyperactivity disorder? A study in a novel dopamine transporter variant Val559 transgenic mouse model
Title
Is dopamine transporter-mediated dopaminergic signaling in the retina a noninvasive biomarker for attention-deficit/ hyperactivity disorder? A study in a novel dopamine transporter variant Val559 transgenic mouse model.
Creator
Dai, Heng, Jackson, Chad R., Davis, Gwynne L., Blakely, Randy D., McMahon, Douglas G.
Date Issued
2017-12-28
PURL
http://purl.flvc.org/fau/flvc_fau_islandoraimporter_10.1186_s11689-017-9215-8_1634318373
Format
Citation
Analysis of neuroanatomical differences in mice with genetically modified serotonin transporters assessed by structural magnetic resonance imaging
Title
Analysis of neuroanatomical differences in mice with genetically modified serotonin transporters assessed by structural magnetic resonance imaging.
Creator
Ellegood, Jacob, Yee, Yohan, Kerr, Travis M., Muller, Christopher L., Blakely, Randy D., Henkelman, R. Mark, Veenstra-VanderWeele, Jeremy, Lerch, Jason P.
Date Issued
2018-12-10
PURL
http://purl.flvc.org/fau/flvc_fau_islandoraimporter_10.1186_s13229-018-0210-z_1634563542
Format
Citation
Glial loss of the metallo β-lactamase domain containing protein, SWIP-10, induces age- and glutamate-signaling dependent, dopamine neuron degeneration
Title
Glial loss of the metallo β-lactamase domain containing protein, SWIP-10, induces age- and glutamate-signaling dependent, dopamine neuron degeneration.
Creator
Gibson, Chelsea L., Balbona, Joseph T., Niedzwiecki, Ashlin, Rodriguez, Peter, Nguyen, Ken C. Q., Hall, David H., Blakely, Randy D., Bianchi, Laura
Date Issued
2018-03-28
PURL
http://purl.flvc.org/fau/flvc_fau_islandoraimporter_10.1371_journal.pgen.1007269_1634570797
Format
Citation
CELLULAR REQUIREMENTS FOR MBLAC1 EXPRESSION AS ASSESSED IN MBLAC1-/- MOUSE EMBRYONIC FIBROBLASTS
Title
CELLULAR REQUIREMENTS FOR MBLAC1 EXPRESSION AS ASSESSED IN MBLAC1-/- MOUSE EMBRYONIC FIBROBLASTS.
Creator
McGovern, Samantha, Blakely, Randy, Florida Atlantic University, Department of Biomedical Science, Charles E. Schmidt College of Science
Abstract/Description
The majority of research on drug addiction centers on dopamine (DA)- driven synaptic plasticities and how these changes ultimately lead to compulsive drug seeking. However, growing evidence supports a role of glial factors in various steps that lead to drug abuse and addiction. In this regard, significant evidence implicates glial glutamate (Glu) transporters (GLT-1) and cystine/Glu exchangers (xCT) in determining synaptic and extrasynaptic levels of Glu that support the acute and chronic...
Show moreThe majority of research on drug addiction centers on dopamine (DA)- driven synaptic plasticities and how these changes ultimately lead to compulsive drug seeking. However, growing evidence supports a role of glial factors in various steps that lead to drug abuse and addiction. In this regard, significant evidence implicates glial glutamate (Glu) transporters (GLT-1) and cystine/Glu exchangers (xCT) in determining synaptic and extrasynaptic levels of Glu that support the acute and chronic actions of drugs of abuse. -lactam antibiotics have been found in rodent models to upregulate CNS GLT-1 and xCT and thereby contribute to reinstatement after chronic drug exposure and withdrawal. Previously, the Blakely lab identified a glial expressing gene, swip-10, in Caenorhabditis elegans, whose deletion results in the hyperdominergic phenotype Swimming-Induced Paralysis (Swip), supported by Glu signalingdependent DA neuron hyperexcitability that ultimately drives oxidative stress and DA neuron degeneration. Both SWIP-10 and its putative mammalian ortholog MBLAC1 possess a highly conserved metallo -lactamase domain, and MBLAC1 has been found to bind the Glu modulating, b-lactam antibiotic ceftriaxone (Cef). Indeed, immunodepletion studies indicate that MBLAC1 may be the major highaffinity Cef-binding protein in the brain, leading to the hypothesis that MBLAC1 has a Glu modulatory role(s). Recently a functional role of MBLAC1 been proposed, involving activity as a 3’ exonuclease that processes polyA- mRNAs, including RNAs encoding cell replication-dependent histones. How this role, or others, may support the actions of MBLAC1 in the brain and the non-microbial actions of Cef to extracellular Glu homeostasis, is unclear. Recently, the Blakely lab generated Mblac1-/- mice as a tool to investigate these issues. The following work investigated the requirements of MBLAC1 in growth and the actions of Cef in mouse embryonic fibroblasts (MEFs) cultured from either Mblac1+/+ and Mblac1-/- mice. The presented data suggested that Mblac1-/- MEFs display attenuated growth and cell proliferation relative to Mblac1+/+ MEFs. For the first time, the in vitro protective actions of Cef against oxidative stress is shown to be dependent on MBLAC1. The following studies presented contribute to a definition of the role of MBLAC1 and as a Cef binding protein in native preparations, with findings that can drive models for the role of MBLAC1 in the CNS.
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Date Issued
2019
PURL
http://purl.flvc.org/fau/fd/FA00013395
Subject Headings
Drug addiction--Research, Amino Acid Transport System X-AG, Mice, Fibroblasts
Format
Document (PDF)
Elucidation of a Glial Copper Homeostasis Pathway Regulated by the Caenorhabditis elegans Gene swip-10 with Implications for Systemic Metabolism and Neurodegenerative Disease
Title
Elucidation of a Glial Copper Homeostasis Pathway Regulated by the Caenorhabditis elegans Gene swip-10 with Implications for Systemic Metabolism and Neurodegenerative Disease.
Creator
Rodriguez, Peter Jr., Blakely, Randy D., Florida Atlantic University, Department of Biomedical Science, Charles E. Schmidt College of Medicine
Abstract/Description
Using the Caenorhabditis elegans as a model we have employed forward genetic screens to uncover several novel genetic contributors to dopamine (DA) signaling(1). Follow-up characterization of some of these novel contributors have been detailed in published work from our lab(2), while follow-up studies on other pathways are still underway. Moreover, using the powerful Million Mutation Project library, we have uncovered an important link between primary cilium formation and the regulation of...
Show moreUsing the Caenorhabditis elegans as a model we have employed forward genetic screens to uncover several novel genetic contributors to dopamine (DA) signaling(1). Follow-up characterization of some of these novel contributors have been detailed in published work from our lab(2), while follow-up studies on other pathways are still underway. Moreover, using the powerful Million Mutation Project library, we have uncovered an important link between primary cilium formation and the regulation of the DA transporter dat-1(3). The focus of the body of work detailed in this manuscript is on a glial expressed gene, swip-10, uncovered from our original genetic screen(1, 4, 5). Unlike the other pathways uncovered from our genetic screening, swip-10 does not affect DA signaling via DAT-1 regulation, instead, loss of swip-10 produces excess DA signaling in a glutamate-signaling-dependent manner to cause swimming-induced paralysis (Swip)(4) as well as premature DA neuron degeneration(5). Specifically, the primary aim here was to uncover the molecular pathway by which swip-10 supports these phenotypes.
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Date Issued
2024
PURL
http://purl.flvc.org/fau/fd/FA00014511
Subject Headings
Neurodegenerative Diseases, Glial cells, Caenorhabditis elegans, Copper, Homeostasis
Format
Document (PDF)
Unresponsive Choline Transporter as a Trait Neuromarker and a Causal Mediator of Bottom-Up Attentional Biases
Title
Unresponsive Choline Transporter as a Trait Neuromarker and a Causal Mediator of Bottom-Up Attentional Biases.
Creator
Koshy Cherian, Ajeesh, Kucinski, Aaron, Pitchers, Kyle, Yegla, Brittney, Parikh, Vinay, Kim, Youngsoo, Valuskova, Paulina, Gurnani, Sarika, Lindsley, Craig W., Blakely, Randy D., Sarter, Martin
Date Issued
2017-02-13
PURL
http://purl.flvc.org/fau/flvc_fau_islandoraimporter_10.1523_JNEUROSCI.3499-16.2017_1634323040
Format
Citation
Interrogating the Spatiotemporal Landscape of Neuromodulatory GPCR Signaling by Real-Time Imaging of cAMP in Intact Neurons and Circuits
Title
Interrogating the Spatiotemporal Landscape of Neuromodulatory GPCR Signaling by Real-Time Imaging of cAMP in Intact Neurons and Circuits.
Creator
Muntean, Brian S., Zucca, Stefano, MacMullen, Courtney M., Dao, Maria T., Johnston, Caitlin, Iwamoto, Hideki, Blakely, Randy D., Davis, Ronald L., Martemyanov, Kirill A.
Date Issued
2018-01
PURL
http://purl.flvc.org/fau/flvc_fau_islandoraimporter_10.1016_j.celrep.2017.12.022_1634578549
Format
Citation
Pancreatic deletion of the interleukin-1 receptor disrupts whole body glucose homeostasis and promotes islet β-cell de-differentiation
Title
Pancreatic deletion of the interleukin-1 receptor disrupts whole body glucose homeostasis and promotes islet β-cell de-differentiation.
Creator
Burke, Susan J., Batdorf, Heidi M., Burk, David H., Martin, Thomas M., Mendoza, Tamra, Stadler, Krisztian, Alami, Wateen, Karlstad, Michael D., Robson, Matthew J., Blakely, Randy D., Mynatt, Randall L., Collier, J. Jason
Date Issued
2018-08
PURL
http://purl.flvc.org/fau/flvc_fau_islandoraimporter_10.1016_j.molmet.2018.06.003_1634579597
Format
Citation
p38α MAPK signaling drives pharmacologically reversible brain and gastrointestinal phenotypes in the SERT Ala56 mouse
Title
p38α MAPK signaling drives pharmacologically reversible brain and gastrointestinal phenotypes in the SERT Ala56 mouse.
Creator
Robson, Matthew J., Quinlan, Meagan A., Margolis, Kara Gross, Gajewski-Kurdziel, Paula A., Veenstra-VanderWeele, Jeremy, Gershon, Michael D., Watterson, D. Martin, Blakely, Randy D.
Date Issued
2018-10-08
PURL
http://purl.flvc.org/fau/flvc_fau_islandoraimporter_10.1073_pnas.1809137115_1634648319
Format
Citation
UNAUTHORIZED ACCESS: A visual narrative on the scientific evolution, and artistic exploration of the blood brain barrier disruption protocol.
Title
UNAUTHORIZED ACCESS: A visual narrative on the scientific evolution, and artistic exploration of the blood brain barrier disruption protocol.
Creator
Odibi, Johnson O., McAfee, Francis X., Blakely, Randy, Florida Atlantic University, School of Communication & Multimedia Studies, Dorothy F. Schmidt College of Arts and Letters
Abstract/Description
The blood brain barrier (BBB) is the brain’s defense mechanism in its maintenance of homeostasis. This network comprises an intricate, functional shield for the human brain, equipped with highly specialized cells like pericytes, astrocytic end-feet, endothelial and neuronal cells. This highly organized barrier maintains the brain’s structural integrity by revealing a discriminatory absorbency of molecules based on their molecular weight and ample fat solubility. In view of this impediment to...
Show moreThe blood brain barrier (BBB) is the brain’s defense mechanism in its maintenance of homeostasis. This network comprises an intricate, functional shield for the human brain, equipped with highly specialized cells like pericytes, astrocytic end-feet, endothelial and neuronal cells. This highly organized barrier maintains the brain’s structural integrity by revealing a discriminatory absorbency of molecules based on their molecular weight and ample fat solubility. In view of this impediment to the delivery of many prospective therapeutic agents from crossing the inviolate BBB, a myriad of innovative surgical and pharmacological interventions have been developed to bypass it, one of which is the BBBD protocol.
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Date Issued
2019
PURL
http://purl.flvc.org/fau/fd/FA00013401
Subject Headings
Blood-Brain Barrier, Visualization, Scientific illustration
Format
Document (PDF)
Interrogating the Spatiotemporal Landscape of Neuromodulatory GPCR Signaling by Real-Time Imaging of cAMP in Intact Neurons and Circuits
Title
Interrogating the Spatiotemporal Landscape of Neuromodulatory GPCR Signaling by Real-Time Imaging of cAMP in Intact Neurons and Circuits.
Creator
Brian S. Muntean, Stefano Zucca, Courtney M. MacMullen, Maria T. Dao, Caitlin Johnston, Hideki Iwamoto, Randy D. Blakely, Ronald L. Davis, Kirill A. Martemyanov
Abstract/Description
Modulation of neuronal circuits is key to information processing in the brain. The majority of neuromodulators exert their effects by activating G-proteincoupled receptors (GPCRs) that control the production of second messengers directly impacting cellular physiology. How numerous GPCRs integrate neuromodulatory inputs while accommodating diversity of incoming signals is poorly understood. In this study, we develop an in vivo tool and analytical suite for analyzing GPCR responses by...
Show moreModulation of neuronal circuits is key to information processing in the brain. The majority of neuromodulators exert their effects by activating G-proteincoupled receptors (GPCRs) that control the production of second messengers directly impacting cellular physiology. How numerous GPCRs integrate neuromodulatory inputs while accommodating diversity of incoming signals is poorly understood. In this study, we develop an in vivo tool and analytical suite for analyzing GPCR responses by monitoring the dynamics of a key second messenger, cyclic AMP (cAMP), with excellent quantitative and spatiotemporal resolution in various neurons. Using this imaging approach in combination with CRISPR/Cas9 editing and optogenetics, we interrogate neuromodulatory mechanisms of defined populations of neurons in an intact mesolimbic reward circuit and describe how individual inputs generate discrete second-messenger signatures in a cell- and receptor- specific fashion. This offers a resource for studying native neuronal GPCR signaling in real time.
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Date Issued
2018
PURL
http://purl.flvc.org/fau/fd/FAUIR000525
Format
Document (PDF)
Region-Specific Regulation of Presynaptic Dopamine Homeostasis by D 2 Autoreceptors Shapes the In Vivo Impact of the Neuropsychiatric Disease-Associated DAT Variant Val559
Title
Region-Specific Regulation of Presynaptic Dopamine Homeostasis by D 2 Autoreceptors Shapes the In Vivo Impact of the Neuropsychiatric Disease-Associated DAT Variant Val559.
Creator
Gowrishankar, Raajaram, Gresch, Paul J., Davis, Gwynne L., Katamish, Rania M., Riele, Justin R., Stewart, Adele M., Vaughan, Roxanne A., Hahn, Maureen K., Blakely, Randy D.
Date Issued
2018-05-08
PURL
http://purl.flvc.org/fau/flvc_fau_islandoraimporter_10.1523_JNEUROSCI.0055-18.2018_1634583255
Format
Citation
Truncating SLC5A7 mutations underlie a spectrum of dominant hereditary motor neuropathies
Title
Truncating SLC5A7 mutations underlie a spectrum of dominant hereditary motor neuropathies.
Creator
Salter, Claire G., Beijer, Danique, Hardy, Holly, Barwick, Katy E.S., Bower, Matthew, Mademan, Ines, De Jonghe, Peter, Deconinck, Tine, Russell, Mark A., McEntagart, Meriel M., Chioza, Barry A., Blakely, Randy D., Chilton, John K., De Bleecker, Jan, Baets, Jonathan, Baple, Emma L., Walk, David, Crosby, Andrew H.
Date Issued
2018-04-23
PURL
http://purl.flvc.org/fau/flvc_fau_islandoraimporter_10.1212_NXG.0000000000000222_1634649520
Format
Citation
Choline transporter mutations in severe congenital myasthenic syndrome disrupt transporter localization
Title
Choline transporter mutations in severe congenital myasthenic syndrome disrupt transporter localization.
Creator
Wang, Haicui, Salter, Claire G, Refai, Osama, Hardy, Holly, Barwick, Katy E S, Akpulat, Ugur, Kvarnung, Malin, Chioza, Barry A, Harlalka, Gaurav, Taylan, Fulya, Sejersen, Thomas, Wright, Jane, Zimmerman, Holly H, Karakaya, Mert, Stüve, Burkhardt, Weis, Joachim, Schara, Ulrike, Russell, Mark A, Abdul-Rahman, Omar A, Chilton, John, Blakely, Randy D, Baple, Emma L, Cirak, Sebahattin, Crosby, Andrew H
Date Issued
2017-10-27
PURL
http://purl.flvc.org/fau/flvc_fau_islandoraimporter_10.1093_brain_awx249_1635361980
Format
Citation