Behavioral, neurochemical and neuroimmune features of RasGEF1b deficient mice

Heliana de Barros Fernandes, Bruna da Silva Oliveira, Caroline Amaral Machado, Brener Cunha Carvalho, Eliana Cristina de Brito Toscano, Maria Carolina M. da Silva, Érica Leandro Marciano Vieira, Antônio Carlos Pinheiro de Oliveira, Antônio Lúcio Teixeira, Aline Silva de Miranda, Aristóbolo Mendes da Silva

Producción científica: Articlerevisión exhaustiva

Resumen

The factor RasGEF1b is a Ras guanine exchange factor involved in immune responses. Studies have also implicated RasGEF1b in the CNS development. It is still limited the understanding of the role of RasGEF1b in CNS functioning. Using RasGEF1b deficient mice (RasGEF1b-cKO), we investigated the impact of this gene deletion in behavior, cognition, brain neurochemistry and microglia morphology. We showed that RasGEF1b-cKO mice display spontaneous hyperlocomotion and anhedonia. RasGEF1b-cKO mice also exhibited compulsive-like behavior that was restored after acute treatment with the selective serotonin reuptake inhibitor (SSRI) fluoxetine (5 mg/kg). A down-regulation of mRNA of dopamine receptor (Drd1, Drd2, Drd4 and Drd5) and serotonin receptor genes (5Htr1a, 5Htr1b and 5Htr1d) was observed in hippocampus of RasGEF1b-cKO mice. These mice also had reduction of Drd1 and Drd2 in prefrontal cortex and 5Htr1d in striatum. In addition, morphological alterations were observed in RasGEF1b deficient microglia along with decreased levels of hippocampal BDNF. We provided original evidence that the deletion of RasGEF1b leads to unique behavioral features, implicating this factor in CNS functioning.

Idioma originalEnglish (US)
Número de artículo110908
PublicaciónProgress in Neuro-Psychopharmacology and Biological Psychiatry
Volumen129
DOI
EstadoPublished - feb 8 2024
Publicado de forma externa

ASJC Scopus subject areas

  • Pharmacology
  • Biological Psychiatry

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