Environmental enrichment attenuates traumatic brain injury

Induced neuronal hyperexcitability in supragranular layers of sensory cortex

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Abstract

We have previously demonstrated that traumatic brain injury (TBI) induces significant long-term neuronal hyperexcitability in supragranular layers of sensory cortex, coupled with persistent sensory deficits. Hence, we aimed to investigate whether brain plasticity induced by environmental enrichment (EE) could attenuate abnormal neuronal and sensory function post-TBI. TBI (n=22) and sham controls (n=21) animals were randomly assigned housing in either single or enriched conditions for 7-9 weeks. Then, in terminal experiments, extracellular recordings were obtained from barrel cortex neurons in response to whisker motion, including those mimicking motion in awake animals undertaking different tasks. Long-term EE exposure (6 weeks) attenuated TBI-induced hyperexcitability in layers 2/3, such that neuronal activity in TBI animals exposed to EE was restored to control levels. Little to no EE-induced changes in population neuronal responses occurred in input Layer 4 and output Layer 5. However, single cell responses demonstrated EE-induced hypoexcitation in L4 post-TBI. EE was also able to fully ameliorate sensory hypersensitivity post-TBI, although it was not found to improve motor function. Long-term enrichment post-TBI induces changes at both the population and single cell level in the sensory cortex, where EE may act to restore the excitation/inhibition balance in supragranular cortical layers.
Original languageEnglish
Pages (from-to)1084-1101
Number of pages18
JournalJournal of Neurotrauma
Volume33
Issue number11
DOIs
Publication statusPublished - 1 Jun 2016

Keywords

  • barrel cortex
  • EE
  • electrophysiology
  • TBI

Cite this

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title = "Environmental enrichment attenuates traumatic brain injury: Induced neuronal hyperexcitability in supragranular layers of sensory cortex",
abstract = "We have previously demonstrated that traumatic brain injury (TBI) induces significant long-term neuronal hyperexcitability in supragranular layers of sensory cortex, coupled with persistent sensory deficits. Hence, we aimed to investigate whether brain plasticity induced by environmental enrichment (EE) could attenuate abnormal neuronal and sensory function post-TBI. TBI (n=22) and sham controls (n=21) animals were randomly assigned housing in either single or enriched conditions for 7-9 weeks. Then, in terminal experiments, extracellular recordings were obtained from barrel cortex neurons in response to whisker motion, including those mimicking motion in awake animals undertaking different tasks. Long-term EE exposure (6 weeks) attenuated TBI-induced hyperexcitability in layers 2/3, such that neuronal activity in TBI animals exposed to EE was restored to control levels. Little to no EE-induced changes in population neuronal responses occurred in input Layer 4 and output Layer 5. However, single cell responses demonstrated EE-induced hypoexcitation in L4 post-TBI. EE was also able to fully ameliorate sensory hypersensitivity post-TBI, although it was not found to improve motor function. Long-term enrichment post-TBI induces changes at both the population and single cell level in the sensory cortex, where EE may act to restore the excitation/inhibition balance in supragranular cortical layers.",
keywords = "barrel cortex, EE, electrophysiology, TBI",
author = "Alwis, {Duwage Sathsara} and Yan, {Edwin Bingbing} and Victoria Johnstone and Simone Carron and Sarah Hellewell and Morganti-Kossmann, {Maria Cristina} and Ramesh Rajan",
year = "2016",
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AU - Alwis, Duwage Sathsara

AU - Yan, Edwin Bingbing

AU - Johnstone, Victoria

AU - Carron, Simone

AU - Hellewell, Sarah

AU - Morganti-Kossmann, Maria Cristina

AU - Rajan, Ramesh

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N2 - We have previously demonstrated that traumatic brain injury (TBI) induces significant long-term neuronal hyperexcitability in supragranular layers of sensory cortex, coupled with persistent sensory deficits. Hence, we aimed to investigate whether brain plasticity induced by environmental enrichment (EE) could attenuate abnormal neuronal and sensory function post-TBI. TBI (n=22) and sham controls (n=21) animals were randomly assigned housing in either single or enriched conditions for 7-9 weeks. Then, in terminal experiments, extracellular recordings were obtained from barrel cortex neurons in response to whisker motion, including those mimicking motion in awake animals undertaking different tasks. Long-term EE exposure (6 weeks) attenuated TBI-induced hyperexcitability in layers 2/3, such that neuronal activity in TBI animals exposed to EE was restored to control levels. Little to no EE-induced changes in population neuronal responses occurred in input Layer 4 and output Layer 5. However, single cell responses demonstrated EE-induced hypoexcitation in L4 post-TBI. EE was also able to fully ameliorate sensory hypersensitivity post-TBI, although it was not found to improve motor function. Long-term enrichment post-TBI induces changes at both the population and single cell level in the sensory cortex, where EE may act to restore the excitation/inhibition balance in supragranular cortical layers.

AB - We have previously demonstrated that traumatic brain injury (TBI) induces significant long-term neuronal hyperexcitability in supragranular layers of sensory cortex, coupled with persistent sensory deficits. Hence, we aimed to investigate whether brain plasticity induced by environmental enrichment (EE) could attenuate abnormal neuronal and sensory function post-TBI. TBI (n=22) and sham controls (n=21) animals were randomly assigned housing in either single or enriched conditions for 7-9 weeks. Then, in terminal experiments, extracellular recordings were obtained from barrel cortex neurons in response to whisker motion, including those mimicking motion in awake animals undertaking different tasks. Long-term EE exposure (6 weeks) attenuated TBI-induced hyperexcitability in layers 2/3, such that neuronal activity in TBI animals exposed to EE was restored to control levels. Little to no EE-induced changes in population neuronal responses occurred in input Layer 4 and output Layer 5. However, single cell responses demonstrated EE-induced hypoexcitation in L4 post-TBI. EE was also able to fully ameliorate sensory hypersensitivity post-TBI, although it was not found to improve motor function. Long-term enrichment post-TBI induces changes at both the population and single cell level in the sensory cortex, where EE may act to restore the excitation/inhibition balance in supragranular cortical layers.

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