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

摘要

Key points class="unordered" style="list-style-type:disc" id="tjp12810-list-0001">Traumatic brain injury (TBI) in children remains a leading cause of death and disability and it remains poorly understood why children have worse outcomes and longer recover times.TBI has shown to alter cortical excitability and inhibitory drive onto excitatory neurons, yet few studies have directly examined changes to cortical interneurons.This is addressed in the present study using a clinically relevant model of severe TBI (controlled cortical impact) in interneuron cell type specific Cre‐dependent mice.Mice subjected to controlled cortical impact exhibit specific loss of parvalbumin (PV) but not somatostatin immunoreactivity and cell density in the peri‐injury zone.PV interneurons are primarily of a fast‐spiking (FS) phenotype that persisted in the peri‐injury zone but received less frequent inhibitory and stronger excitatory post‐synaptic currents.The targeted loss of PV‐FS interneurons appears to be distinct from previous reports in adult mice suggesting that TBI‐induced pathophysiology is dependent on the age at time of impact.