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

Authors
  • Nichols, Joshua1, 2
  • Bjorklund, George Reed2
  • Newbern, Jason2
  • Anderson, Trent1
  • 1 University of Arizona, College of Medicine - Phoenix, Phoenix, AZ, USA.
  • 2 School of Life Sciences, Arizona State University, AZ, USA.
Type
Published Article
Journal
The Journal of Physiology
Publisher
Wiley (Blackwell Publishing)
Publication Date
Apr 01, 2018
Volume
596
Issue
7
Pages
1277–1293
Identifiers
DOI: 10.1113/JP275393
PMID: 29333742
Source
Medline
Keywords
License
Unknown

Abstract

Paediatric traumatic brain injury (TBI) is a leading cause of death and disability in children. Traditionally, ongoing neurodevelopment and neuroplasticity have been considered to confer children with an advantage following TBI. However, recent findings indicate that the paediatric brain may be more sensitive to brain injury. Inhibitory interneurons are essential for proper cortical function and are implicated in the pathophysiology of TBI, yet few studies have directly investigated TBI-induced changes to interneurons themselves. Accordingly, in the present study, we examine how inhibitory neurons are altered following controlled cortical impact (CCI) in juvenile mice with targeted Cre-dependent fluorescence labelling of interneurons (Vgat:Cre/Ai9 and PV:Cre/Ai6). Although 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 lower extent of fluorescence labelled cell loss. PV interneurons are predominantly of a fast-spiking (FS) phenotype and, when recorded electrophysiologically from the peri-injury zone, exhibited intrinsic properties similar to those of control neurons. Synaptically, CCI induced a decrease in inhibitory drive onto FS interneurons combined with an increase in the strength of excitatory events. The results of the present study indicate that CCI induced both a loss of PV interneurons and an even greater loss of PV expression. This suggests caution is required when interpreting changes in PV immunoreactivity alone as direct evidence of interneuronal loss. Furthermore, in contrast to reports in adults, TBI in the paediatric brain selectively alters PV-FS interneurons, primarily resulting in a loss of interneuronal inhibition.

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