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Parvalbumin fast-spiking interneurons are selectively altered by pediatric traumatic brain injury

Abstract

Pediatric traumatic brain injury (TBI) is a leading cause of death and disability in children. Traditionally, ongoing neurodevelopment and neuroplasticity have thought to confer children with an advantage following TBI. However, recent findings indicate that the pediatric brain may be more sensitive to brain injury. Inhibitory interneurons are essential for proper cortical function and implicated in the pathophysiology of TBI, yet few studies have directly examined for TBI induced changes to interneurons themselves. To address this, we examine how inhibitory neurons are altered following controlled cortical impact (CCI) in juvenile mice with targeted Cre-dependent fluorescent labelling of interneurons (Vgat:Cre/Ai9 and PV:Cre/Ai6). While CCI failed to alter the number of excitatory neurons or somatostatin-expressing interneurons in the peri-injury zone it significantly decreased the density of parvalbumin (PV) immunoreactive cells by 71%. However, PV:Cre/Ai6 mice subjected to CCI showed a lesser extent of fluorescently labelled cell loss. PV interneurons are predominantly of a fast-spiking (FS) phenotype and when recorded electrophysiologically from the peri-injury zone exhibited similar intrinsic properties as control neurons. Synaptically, CCI induced a decrease in inhibitory drive onto FS interneurons combined with an increase in the strength of excitatory events. Our results indicate that CCI induced both a loss of PV interneurons and an even greater loss of PV expression. This suggests caution in interpreting changes in PV immunoreactivity alone as direct evidence of interneuronal loss. Further, in contrast with reports in adults TBI in the pediatric brain selectively alter PV-FS interneurons resulting in primarily a loss of interneuronal inhibition.

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