Cortical hypoexcitation defines neuronal responses in the immediate aftermath of traumatic brain injury.

Traumatic brain injury (TBI) from a blow to the head is often associated with complex patterns of brain abnormalities that accompany deficits in cognitive and motor function. Previously we reported that a long-term consequence of TBI, induced with a closed-head injury method modelling human car and...

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Autores principales:	Victoria Philippa Anne Johnstone, Edwin Bingbing Yan, Dasuni Sathsara Alwis, Ramesh Rajan
Formato:	article
Lenguaje:	EN
Publicado:	Public Library of Science (PLoS) 2013
Materias:	Medicine R Science Q
Acceso en línea:	https://doaj.org/article/6833b22572e74bfc99a312b2afbe64a2
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spelling	oai:doaj.org-article:6833b22572e74bfc99a312b2afbe64a22021-11-18T07:46:30ZCortical hypoexcitation defines neuronal responses in the immediate aftermath of traumatic brain injury.1932-620310.1371/journal.pone.0063454https://doaj.org/article/6833b22572e74bfc99a312b2afbe64a22013-01-01T00:00:00Zhttps://www.ncbi.nlm.nih.gov/pmc/articles/pmid/23667624/?tool=EBIhttps://doaj.org/toc/1932-6203Traumatic brain injury (TBI) from a blow to the head is often associated with complex patterns of brain abnormalities that accompany deficits in cognitive and motor function. Previously we reported that a long-term consequence of TBI, induced with a closed-head injury method modelling human car and sporting accidents, is neuronal hyper-excitation in the rat sensory barrel cortex that receives tactile input from the face whiskers. Hyper-excitation occurred only in supra-granular layers and was stronger to complex than simple stimuli. We now examine changes in the immediate aftermath of TBI induced with same injury method. At 24 hours post-trauma significant sensorimotor deficits were observed and characterisation of the cortical population neuronal responses at that time revealed a depth-dependent suppression of neuronal responses, with reduced responses from supragranular layers through to input layer IV, but not in infragranular layers. In addition, increased spontaneous firing rate was recorded in cortical layers IV and V. We postulate that this early post-injury suppression of cortical processing of sensory input accounts for immediate post-trauma sensory morbidity and sets into train events that resolve into long-term cortical hyper-excitability in upper sensory cortex layers that may account for long-term sensory hyper-sensitivity in humans with TBI.Victoria Philippa Anne JohnstoneEdwin Bingbing YanDasuni Sathsara AlwisRamesh RajanPublic Library of Science (PLoS)articleMedicineRScienceQENPLoS ONE, Vol 8, Iss 5, p e63454 (2013)
institution	DOAJ
collection	DOAJ
language	EN
topic	Medicine R Science Q
spellingShingle	Medicine R Science Q Victoria Philippa Anne Johnstone Edwin Bingbing Yan Dasuni Sathsara Alwis Ramesh Rajan Cortical hypoexcitation defines neuronal responses in the immediate aftermath of traumatic brain injury.
description	Traumatic brain injury (TBI) from a blow to the head is often associated with complex patterns of brain abnormalities that accompany deficits in cognitive and motor function. Previously we reported that a long-term consequence of TBI, induced with a closed-head injury method modelling human car and sporting accidents, is neuronal hyper-excitation in the rat sensory barrel cortex that receives tactile input from the face whiskers. Hyper-excitation occurred only in supra-granular layers and was stronger to complex than simple stimuli. We now examine changes in the immediate aftermath of TBI induced with same injury method. At 24 hours post-trauma significant sensorimotor deficits were observed and characterisation of the cortical population neuronal responses at that time revealed a depth-dependent suppression of neuronal responses, with reduced responses from supragranular layers through to input layer IV, but not in infragranular layers. In addition, increased spontaneous firing rate was recorded in cortical layers IV and V. We postulate that this early post-injury suppression of cortical processing of sensory input accounts for immediate post-trauma sensory morbidity and sets into train events that resolve into long-term cortical hyper-excitability in upper sensory cortex layers that may account for long-term sensory hyper-sensitivity in humans with TBI.
format	article
author	Victoria Philippa Anne Johnstone Edwin Bingbing Yan Dasuni Sathsara Alwis Ramesh Rajan
author_facet	Victoria Philippa Anne Johnstone Edwin Bingbing Yan Dasuni Sathsara Alwis Ramesh Rajan
author_sort	Victoria Philippa Anne Johnstone
title	Cortical hypoexcitation defines neuronal responses in the immediate aftermath of traumatic brain injury.
title_short	Cortical hypoexcitation defines neuronal responses in the immediate aftermath of traumatic brain injury.
title_full	Cortical hypoexcitation defines neuronal responses in the immediate aftermath of traumatic brain injury.
title_fullStr	Cortical hypoexcitation defines neuronal responses in the immediate aftermath of traumatic brain injury.
title_full_unstemmed	Cortical hypoexcitation defines neuronal responses in the immediate aftermath of traumatic brain injury.
title_sort	cortical hypoexcitation defines neuronal responses in the immediate aftermath of traumatic brain injury.
publisher	Public Library of Science (PLoS)
publishDate	2013
url	https://doaj.org/article/6833b22572e74bfc99a312b2afbe64a2
work_keys_str_mv	AT victoriaphilippaannejohnstone corticalhypoexcitationdefinesneuronalresponsesintheimmediateaftermathoftraumaticbraininjury AT edwinbingbingyan corticalhypoexcitationdefinesneuronalresponsesintheimmediateaftermathoftraumaticbraininjury AT dasunisathsaraalwis corticalhypoexcitationdefinesneuronalresponsesintheimmediateaftermathoftraumaticbraininjury AT rameshrajan corticalhypoexcitationdefinesneuronalresponsesintheimmediateaftermathoftraumaticbraininjury
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Cortical hypoexcitation defines neuronal responses in the immediate aftermath of traumatic brain injury.

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