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.

Elevated Tau in Military Personnel Relates to Chronic Symptoms Following Traumatic Brain Injury

“…39,[42][43][44] Animal studies have shown that TBI induces long-term neuronal hyperexcitability in the sensory cortex. 39,45 PTSD is commonly associated with alterations in areas of the frontal cortex, hippocampus, amygdala, and overall reductions in neuronal volume. [46][47][48] In addition, the amygdala, which is dysfunctional in PTSD, influences sensory processing through projections to neuromodulatory centers from the forebrain and brainstem, which guide attention, mood and adjust sensory responses to the demands of the environment and internal state of the individual.…”

Inhibitory neuronal changes following a mixed diffuse‐focal model of traumatic brain injury

“…As in our previous TBI studies (Alwis et al, , ; Carron et al, ; Johnstone et al, , , ), a standard rotarod test was used to assess sensorimotor function following injury. Grip strength and sensorimotor function are assessed by recording the maximum rotational speed at which the rats can maintain their position on the rotarod, a rotating cylinder comprising of 18 stainless steel rods (1 mm diameter).…”

Environmental Enrichment Protects Against Sepsis-Associated Encephalopathy-Induced Learning and Memory Deficits by Enhancing the Synthesis and Release of Vasopressin in the Supraoptic Nucleus

“…In fact, previous research showed that there were no differences in the outcomes of MWM or elevated plus maze (EPM) between the sham-EE group and sham group. 13 , 69 , 70 Moreover, studies also revealed no differences in the level of BDNF and inflammatory factors between the sham-EE group and sham group. 69 , 70 , 90 Therefore, we speculated that a sham-EE group might show the same results as the Sham group when compared with the other experimental groups.…”

“…11,12 For example, sensory and memory impairment after traumatic brain injury (TBI) can be relieved by EE, possibly via cortical excitability and reorganization. [13][14][15][16][17] EE was also shown to prevent stroke-induced learning and memory disorder. [18][19][20] Moreover, in models of ethanol binge-drinking or perinatal asphyxia, accumulating evidence points to the positive effects of EE on learning and memory deficits.…”