Acute and Chronic Neural and Glial Response to Mild Traumatic Brain Injury in the Hippocampus.

Autor:	Dougan CE; Department of Chemical Engineering, University of Massachusetts Amherst, Amherst, MA 01003, USA.; Department of Chemistry and Department of Engineering, Smith College, Northampton, MA 01063., Roberts BL; Neuroscience and Behavior Program, and Department of Psychological and Brain Sciences, University of Massachusetts Amherst, Amherst, MA 01003, USA.; Department of Zoology & Physiology, University of Wyoming, Laramie, WY 83072, USA.; Department of Animal Science, University of Wyoming, Laramie, WY 83072, USA., Crosby AJ; Department of Polymer Science and Engineering, University of Massachusetts Amherst, Amherst, MA 01003, USA., Karatsoreos I; Neuroscience and Behavior Program, and Department of Psychological and Brain Sciences, University of Massachusetts Amherst, Amherst, MA 01003, USA., Peyton SR; Department of Chemical Engineering, University of Massachusetts Amherst, Amherst, MA 01003, USA.
Jazyk:	angličtina
Zdroj:	BioRxiv : the preprint server for biology [bioRxiv] 2024 Apr 02. Date of Electronic Publication: 2024 Apr 02.
DOI:	10.1101/2024.04.01.587620
Abstrakt:	Traumatic brain injury (TBI) is an established risk factor for developing neurodegenerative disease. However, how TBI leads from acute injury to chronic neurodegeneration is limited to post-mortem models. There is a lack of connections between in vitro and in vivo TBI models that can relate injury forces to both macroscale tissue damage and brain function at the cellular level. Needle-induced cavitation (NIC) is a technique that can produce small cavitation bubbles in soft tissues, which allows us to relate small strains and strain rates in living tissue to ensuing acute and chronic cell death, tissue damage, and tissue remodeling. Here, we applied NIC to mouse brain slices to create a new model of TBI with high spatial and temporal resolution. We specifically targeted the hippocampus, which is a brain region critical for learning and memory and an area in which injury causes cognitive pathologies in humans and rodent models. By combining NIC with patch-clamp electrophysiology, we demonstrate that NIC in the Cornu Ammonis (CA)3 region of the hippocampus dynamically alters synaptic release onto CA1 pyramidal neurons in a cannabinoid 1 receptor (CB1R)-dependent manner. Further, we show that NIC induces an increase in extracellular matrix proteins associated with neural repair that is mitigated by CB1R antagonism. Together, these data lay the groundwork for advanced approaches in understanding how TBI impacts neural function at the cellular level, and the development of treatments that promote neural repair in response to brain injury. Competing Interests: DECLARATION OF INTERESTS The authors declare no competing interests.
Databáze:	MEDLINE
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