15 research outputs found
SRF modulates seizure occurrence, activity induced gene transcription and hippocampal circuit reorganization in the mouse pilocarpine epilepsy model
Über Bildung und Reaktionen von 5-Desoxy-4-hexenofuranos-3-ulosen, einer neuen Klasse α.β-ungesättigter Monosaccharid-Ketone
Bei der Reduktion des Enolacetats 2 mit NaBH4 entsteht neben der 1.2;5.6-Di-O-isopropyliden-α-D-gulofuranose (3) das cis-trans-Gemisch der 4-Hexenofuranosen 4. Das als Zwischenprodukt angenommene α.β-ungesättigte Keton 6 bildet sich aus 2 bei der Umsetzung mit schwachem Alkali. Daneben entsteht das Dimerisierungsprodukt 7. Das sich von der 2-Amino-2-desoxy-D-glucose ableitende Enolacetat 13 erleidet mit NaBH4 eine gleichartige Eliminierung zum Olefin 14
2,6-Diamino-2,6-Didesoxy-D-Allose aus Glukosamin unter Verwendung einer Inversion mit Thionylchlorid
Steroid conjugates. VII. Preparation of N-acetylglucosaminides of 17α- and 17β-estradiol
Serum response factor (SRF) ablation interferes with acute stress-associated immediate and long-term coping mechanisms.
Stress experience modulates behavior, metabolism, and energy expenditure of organisms. One molecular hallmark of an acute stress response is a rapid induction of immediate early genes (IEGs) such as c-Fos and Egr family members. IEG transcription in neurons is mediated by the neuronal activity-driven gene regulator serum response factor (SRF). We show a first role of SRF in immediate and long-lasting acute restraint stress (AS) responses. For this, we employed a standardized mouse phenotyping protocol at the German Mouse Clinic (GMC) including behavioral, metabolic, and cardiologic tests as well as gene expression profiling to analyze the consequences of forebrain-specific SRF deletion in mice exposed to AS. Adult mice with an SRF deletion in glutamatergic neurons (Srf;CaMKIIa-CreERT2) showed hyperactivity, decreased anxiety, and impaired working memory. In response to restraint AS, instant stress reactivity including locomotor behavior and corticosterone induction was impaired in Srf mutant mice. Interestingly, even several weeks after previous AS exposure, SRF-deficient mice showed long-lasting AS-associated changes including altered locomotion, metabolism, energy expenditure, and cardiovascular changes. This suggests a requirement of SRF for mediating long-term stress coping mechanisms in wild-type mice. SRF ablation decreased AS-mediated IEG induction and activity of the actin severing protein cofilin. In summary, our data suggest an SRF function in immediate AS reactions and long-term post-stress-associated coping mechanisms