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. 2020 Mar;34(3):3855-3873.
doi: 10.1096/fj.201902257RR. Epub 2020 Jan 12.

Interference of neuronal activity-mediated gene expression through serum response factor deletion enhances mortality and hyperactivity after traumatic brain injury

Philip Förstner  1 , Bernd Knöll  1
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Interference of neuronal activity-mediated gene expression through serum response factor deletion enhances mortality and hyperactivity after traumatic brain injury

Philip Förstner et al. FASEB J. 2020 Mar.

Abstract

Traumatic brain injury (TBI) is one of the most frequent causes of brain injury and mortality in young adults with detrimental sequelae such as cognitive impairments, epilepsy, and attention-deficit hyperactivity disorder. TBI modulates the neuronal excitability resulting in propagation of a neuronal activity-driven gene expression program. However, the impact of such neuronal activity mediated gene expression in TBI has been poorly studied. In this study we analyzed mouse mutants of the prototypical neuronal activity-dependent transcription factor SRF (serum response factor) in a weight-drop TBI model. Neuron-restricted SRF deletion elevated TBI inflicted mortality suggesting a neuroprotective SRF function during TBI. Behavioral inspection uncovered elevated locomotor activity in Srf mutant mice after TBI in contrast to hypoactivity observed in wild-type littermates. This indicates an SRF role in modulation of TBI-associated alterations in locomotor activity. Finally, induction of a neuronal activity induced gene expression program composed of immediate early genes (IEGs) such as Egr1, Egr2, Egr3, Npas4, Atf3, Arc, Ptgs2, and neuronal pentraxins (Nptx2) was compromised upon SRF depletion. Overall, our data show a role of neuronal activity-mediated gene transcription during TBI and suggest a molecular link between TBI and such post-TBI neurological comorbidities involving hyperactivity phenotypes.

Keywords: Egr; c-Fos; hematoma; hyperactivity; immediate early gene; transcription.

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REFERENCES

    1. Stocchetti N, Zanier ER. Chronic impact of traumatic brain injury on outcome and quality of life: a narrative review. Crit Care. 2016;20:148.
    1. Bruns J Jr, Hauser WA. The epidemiology of traumatic brain injury: a review. Epilepsia. 2003;44(Suppl 10):2-10.
    1. Vos BC, Nieuwenhuijsen K, Sluiter JK. Consequences of traumatic brain injury in professional American football players. Clinical Journal of Sport Medicine. 2018;28:91-99.
    1. Verellen RM, Cavazos JE. Post-traumatic epilepsy: an overview. Therapy. 2010;7:527-531.
    1. Rogers JM, Read CA. Psychiatric comorbidity following traumatic brain injury. Brain Inj. 2007;21:1321-1333.

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