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 control (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.
authors.affiliation: 1 Department of Physiology, Monash University , Clayton, VIC, Australia .|2 National Trauma Research Institute, Alfred Hospital , Prahran, VIC, Australia .
authors.forename: Dasuni Sathsara
authors.initials: DS
authors.lastname: Alwis
authors.affiliation: 2 National Trauma Research Institute, Alfred Hospital , Prahran, VIC, Australia .
authors.forename: Edwin Bingbing
authors.initials: EB
authors.lastname: Yan
authors.affiliation: 1 Department of Physiology, Monash University , Clayton, VIC, Australia .
authors.forename: Victoria
authors.initials: V
authors.lastname: Johnstone
authors.affiliation: 1 Department of Physiology, Monash University , Clayton, VIC, Australia .
authors.forename: Simone
authors.initials: S
authors.lastname: Carron
authors.affiliation: 2 National Trauma Research Institute, Alfred Hospital , Prahran, VIC, Australia .
authors.forename: Sarah
authors.initials: S
authors.lastname: Hellewell
authors.affiliation: 2 National Trauma Research Institute, Alfred Hospital , Prahran, VIC, Australia .
authors.forename: Maria Cristina
authors.initials: MC
authors.lastname: Morganti-Kossmann
authors.affiliation: 1 Department of Physiology, Monash University , Clayton, VIC, Australia .
authors.forename: Ramesh
authors.initials: R
authors.lastname: Rajan
mesh_terms: D000818:Animals; D001522:Behavior, Animal / Q000502:physiology; D000070642:Brain Injuries, Traumatic / Q000503:physiopathology*; D000071080:Cortical Excitability / Q000502:physiology*; D004195:Disease Models, Animal; D004777:Environment; D008297:Male; D009473:Neuronal Plasticity / Q000502:physiology*; D009474:Neurons / Q000502:physiology*; D011897:Random Allocation; D051381:Rats; D017207:Rats, Sprague-Dawley; D013003:Somatosensory Cortex / Q000503:physiopathology*; D014738:Vibrissae / Q000502:physiology
keywords: EE; TBI; barrel cortex; electrophysiology