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Glycine transporter type 1 (GlyT1) inhibition improves conspecific-provoked immobility in BALB/c mice: Analysis of corticosterone response and glucocorticoid gene expression in cortex and hippocampus.
Burket, Jessica A; Pickle, Jerrah C; Rusk, Allison M; Haynes, Bronson A; Sharp, Julia A; Deutsch, Stephen I.
Afiliación
  • Burket JA; Department of Psychiatry and Behavioral Sciences, Eastern Virginia Medical School, Norfolk, VA, United States; Department of Physiological Sciences, Eastern Virginia Medical School, Norfolk, VA, United States.
  • Pickle JC; Department of Psychiatry and Behavioral Sciences, Eastern Virginia Medical School, Norfolk, VA, United States.
  • Rusk AM; Department of Psychiatry and Behavioral Sciences, Eastern Virginia Medical School, Norfolk, VA, United States.
  • Haynes BA; Department of Physiological Sciences, Eastern Virginia Medical School, Norfolk, VA, United States.
  • Sharp JA; Department of Microbiology and Molecular Cell Biology, Eastern Virginia Medical School, Norfolk, VA, United States.
  • Deutsch SI; Department of Psychiatry and Behavioral Sciences, Eastern Virginia Medical School, Norfolk, VA, United States; Anne Armistead Robinson Endowed Chair in Psychiatry, Department of Psychiatry and Behavioral Sciences, 825 Fairfax Avenue, Suite 710, Norfolk, VA 23507, United States. Electronic address: d
Article en En | MEDLINE | ID: mdl-31962186
Stress reactivity and glucocorticoid signaling alterations are reported in mouse models of autism spectrum disorder (ASD). BALB/c mice display decreased locomotor activity in the presence of stimulus mice and spend less time exploring enclosed stimulus mice; this mouse strain has been validated as an ASD model. VU0410120, a glycine type 1 transporter (GlyT1) inhibitor, improved sociability in BALB/c mice, consistent with data that NMDA Receptor (NMDAR) activation regulates sociability, and the endogenous tone of NMDAR-mediated neurotransmission is altered in this strain. Effects of a prosocial dose of VU0410120 on conspecific-provoked immobility, and relationships between conspecific-provoked immobility and corticosterone response were explored. VU0410120-treated BALB/c mice showed reduced immobility in the presence of conspecifics and increased the conspecific-provoked corticosterone response. However, the intensity of conspecific-provoked immobility in VU0410120-treated BALB/c mice did not differ as a function of corticosterone response. Expression profiles of 88 glucocorticoid signaling associated genes within frontal cortex and hippocampus were examined. BALB/c mice resistant to prosocial effects of VU0410120 had increased mRNA expression of Ddit4, a negative regulator of mTOR signaling. Dysregulated mTOR signaling activity is a convergent finding in several monogenic syndromic forms of ASD. Prosocial effects of VU0410120 in the BALB/c strain may be related to regulatory influences of NMDAR-activation on mTOR signaling activity. Because corticosterone response is a marker of social stress, the current data suggest that the stressfulness of a social encounter alone may not be the sole determinant of increased immobility in BALB/c mice; this strain may also display an element of social disinterest.
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Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Corticosterona / Corteza Cerebral / Proteínas de Transporte de Glicina en la Membrana Plasmática / Glucocorticoides / Hipocampo / Inmovilización Tipo de estudio: Prognostic_studies Límite: Animals Idioma: En Revista: Prog Neuropsychopharmacol Biol Psychiatry Año: 2020 Tipo del documento: Article País de afiliación: Estados Unidos Pais de publicación: Reino Unido

Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Corticosterona / Corteza Cerebral / Proteínas de Transporte de Glicina en la Membrana Plasmática / Glucocorticoides / Hipocampo / Inmovilización Tipo de estudio: Prognostic_studies Límite: Animals Idioma: En Revista: Prog Neuropsychopharmacol Biol Psychiatry Año: 2020 Tipo del documento: Article País de afiliación: Estados Unidos Pais de publicación: Reino Unido