Citation

Yeh CW, Huang A. eNeuro 2023; 10(10): ENEURO.0340-23.2023.

Copyright

(Copyright © 2023, Society for Neuroscience)

DOI

10.1523/ENEURO.0340-23.2023

PMID

37884345

Abstract

Traumatic brain injury (TBI) affects millions of people annually and is a leading cause of long-term disability. Individuals with this condition commonly manifest behavioral, psychiatric, and cognitive dysfunctions, yet there is inadequate understanding of underlying mechanisms, posing challenges for effective treatments. TBI often arises from physical trauma to the head resulting in focal or diffuse injury, long-term cell loss, and tissue damage depending on injury type. Focal injuries can be modeled with the controlled cortical impact (CCI), while fluid percussion injury (FPI) models diffuse concussive injuries. Furthermore, each type of injury can be further classified based on severity (e.g., mild, moderate, and severe), each with their own unique pathophysiology. In mild TBI, diffuse injury leads to cell loss, diffuse axonal injury, and related circuit alterations in both afferent and efferent networks connecting to the injured cortical area (Krishna et al., 2020). It is recognized that dysfunction of distributed networks after brain injury could contribute to behavioral, emotional, and cognitive postconcussive symptoms. Several neuromodulatory systems participating in the cognitive function, such as the cholinergic, noradrenergic, and dopaminergic systems, are known to be affected by TBI (Shin and Dixon, 2015). However, whether specific subcortical networks are altered after injury and the underlying molecular mechanisms is not known. The study by Dasgupta et al. (2023) addresses this important issue by examining the effect of mild to moderate concussive TBI on basal forebrain (BF) cholinergic neurons (CNs) and locus coeruleus (LC) noradrenergic neurons, both of which are key players in cognitive function, including learning, memory, arousal, and attention ...

Language: en