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Your search keyword '"H De Jesus-Cortes"' showing total 5 results
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5 results on '"H De Jesus-Cortes"'

1. Forebrain elimination of cacna1c mediates anxiety-like behavior in mice

Author

Amy S. Lee, H De Jesus-Cortes, Aditi M Rajadhyaksha, Anjali M. Rajadhyaksha, Franz Hofmann, J K Britt, Anni S. Lee, Andrew A. Pieper, Keith L. Gonzales, Sven Moosmang, and S Ra

Subjects
medicine.medical_specialty, Elevated plus maze, Calcium Channels, L-Type, Prefrontal Cortex, Striatum, Anxiety, Nucleus accumbens, Open field, Mice, 03 medical and health sciences, Cellular and Molecular Neuroscience, Prosencephalon, 0302 clinical medicine, Internal medicine, medicine, Animals, Maze Learning, Prefrontal cortex, Letter to the Editor, Molecular Biology, 030304 developmental biology, Mice, Knockout, 0303 health sciences, Ventral tegmental area, Disease Models, Animal, Psychiatry and Mental health, Endocrinology, medicine.anatomical_structure, Gene Knockdown Techniques, Forebrain, Psychology, Neuroscience, 030217 neurology & neurosurgery, Basolateral amygdala
Abstract

The CACNA1C gene encoding the Cav1.2 subunit of the L-type calcium channel has emerged as a new candidate gene for neuropsychiatric disease, including bipolar disorder, major depression, schizophrenia and autism.1, 2, 3 We report that global haploinsufficiency, forebrain-specific elimination and prefrontal cortex (PFC)-specific knockdown of cacna1c all increase anxiety-related behavior in mice, a prominent component of the forms of neuropsychiatric disease in which aberrations in CACNA1C have been implicated, without affecting compulsive behavior. Constitutive cacna1c heterozygous mice (HET) were evaluated in three behavioral assays related to anxiety: open field test, light–dark conflict test and elevated plus maze (EPM). HETs displayed anxiety-like behavior in the EPM (Figure 1a), spending significantly less time exploring the open arms compared with wild-type littermate controls (WT; F1,19=6.437; P

Published
2012
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2. Dissociation of functional and structural plasticity of dendritic spines during NMDAR and mGluR-dependent long-term synaptic depression in wild-type and fragile X model mice.

Author

Thomazeau A, Bosch M, Essayan-Perez S, Barnes SA, De Jesus-Cortes H, and Bear MF

Subjects
Animals, Dendritic Spines metabolism, Fragile X Mental Retardation Protein genetics, Fragile X Mental Retardation Protein metabolism, Hippocampus metabolism, Mice, Mice, Knockout, Neuronal Plasticity, Long-Term Synaptic Depression, Receptors, N-Methyl-D-Aspartate metabolism
Abstract

Many neurodevelopmental disorders are characterized by impaired functional synaptic plasticity and abnormal dendritic spine morphology, but little is known about how these are related. Previous work in the Fmr1 -/y mouse model of fragile X (FX) suggests that increased constitutive dendritic protein synthesis yields exaggerated mGluR5-dependent long-term synaptic depression (LTD) in area CA1 of the hippocampus, but an effect on spine structural plasticity remains to be determined. In the current study, we used simultaneous electrophysiology and time-lapse two photon imaging to examine how spines change their structure during LTD induced by activation of mGluRs or NMDA receptors (NMDARs), and how this plasticity is altered in Fmr1 -/y mice. We were surprised to find that mGluR activation causes LTD and AMPA receptor internalization, but no spine shrinkage in either wildtype or Fmr1 -/y mice. In contrast, NMDAR activation caused spine shrinkage as well as LTD in both genotypes. Spine shrinkage was initiated by non-ionotropic (metabotropic) signaling through NMDARs, and in wild-type mice this structural plasticity required activation of mTORC1 and new protein synthesis. In striking contrast, NMDA-induced spine plasticity in Fmr1 -/y mice was no longer dependent on acute activation of mTORC1 or de novo protein synthesis. These findings reveal that the structural consequences of mGluR and metabotropic NMDAR activation differ, and that a brake on spine structural plasticity, normally provided by mTORC1 regulation of protein synthesis, is absent in FX. Increased constitutive protein synthesis in FX appears to modify functional and structural plasticity induced through different glutamate receptors., (© 2020. The Author(s).)

Published
2021
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3. Corrigendum: Wild-type microglia do not reverse pathology in mouse models of Rett syndrome.

Author

Wang J, Wegener JE, Huang TW, Sripathy S, De Jesus-Cortes H, Xu P, Tran S, Knobbe W, Leko V, Britt J, Starwalt R, McDaniel L, Ward CS, Parra D, Newcomb B, Lao U, Nourigat C, Flowers DA, Cullen S, Jorstad NL, Yang Y, Glaskova L, Vigneau S, Kozlitina J, Yetman MJ, Jankowsky JL, Reichardt SD, Reichardt HM, Gärtner J, Bartolomei MS, Fang M, Loeb K, Keene CD, Bernstein I, Goodell M, Brat DJ, Huppke P, Neul JL, Bedalov A, and Pieper AA

Published
2015
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4. Wild-type microglia do not reverse pathology in mouse models of Rett syndrome.

Author

Wang J, Wegener JE, Huang TW, Sripathy S, De Jesus-Cortes H, Xu P, Tran S, Knobbe W, Leko V, Britt J, Starwalt R, McDaniel L, Ward CS, Parra D, Newcomb B, Lao U, Nourigat C, Flowers DA, Cullen S, Jorstad NL, Yang Y, Glaskova L, Vingeau S, Kozlitina J, Yetman MJ, Jankowsky JL, Reichardt SD, Reichardt HM, Gärtner J, Bartolomei MS, Fang M, Loeb K, Keene CD, Bernstein I, Goodell M, Brat DJ, Huppke P, Neul JL, Bedalov A, and Pieper AA

Subjects
Animals, Female, Male, Disease Progression, Methyl-CpG-Binding Protein 2 metabolism, Microglia cytology, Microglia physiology, Rett Syndrome pathology
Published
2015
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5. Discovery of a neuroprotective chemical, (S)-N-(3-(3,6-dibromo-9H-carbazol-9-yl)-2-fluoropropyl)-6-methoxypyridin-2-amine [(-)-P7C3-S243], with improved druglike properties.

Author

Naidoo J, De Jesus-Cortes H, Huntington P, Estill S, Morlock LK, Starwalt R, Mangano TJ, Williams NS, Pieper AA, and Ready JM

Subjects
Animals, Area Under Curve, Disease Models, Animal, Drug Discovery, Magnetic Resonance Spectroscopy, Mice, Mice, Inbred C57BL, Neuroprotective Agents pharmacokinetics, Parkinson Disease pathology, Spectrometry, Mass, Electrospray Ionization, Substantia Nigra pathology, Carbazoles pharmacology, Neuroprotective Agents pharmacology
Abstract

(-)-P7C3-S243 is a neuroprotective aminopropyl carbazole with improved druglike properties compared with previously reported compounds in the P7C3 class. It protects developing neurons in a mouse model of hippocampal neurogenesis and protects mature neurons within the substantia nigra in a mouse model of Parkinson's disease. A short, enantioselective synthesis provides the neuroprotective agent in optically pure form. It is nontoxic, orally bioavailable, metabolically stable, and able to cross the blood-brain barrier. As such, it represents a valuable lead compound for the development of drugs to treat neurodegenerative diseases and traumatic brain injury.

Published
2014
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