Effect of acute stretch injury on action potential and network activity of rat neocortical neurons in culture

Magou, George C.; Pfister, Bryan J.; Berlin, Joshua R.

doi:10.1016/j.brainres.2015.07.056

Cited by 26 publications

(11 citation statements)

References 46 publications

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“…Additionally, this GABA-mediated inhibition, particularly in the deeper layers, may be partially explained by the neuronal response to mechanical perturbation. Literature investigating the cortical mechanotransduction involved in traumatic brain injury has shown that a mechanical or stretch injury substantially increased GABA concentrations in vitro, thereby reducing spontaneous single unit activity [41][42][43]. While intracortical MEA implantation may be better modeled as a stab injury, micromotion-induced tissue strain may produce similar mechanical responses.…”

Section: Discussionmentioning

confidence: 99%

Influence of Implantation Depth on the Performance of Intracortical Probe Recording Sites

et al. 2021

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Microelectrode arrays (MEAs) enable the recording of electrical activity from cortical neurons which has implications for basic neuroscience and neuroprosthetic applications. The design space for MEA technology is extremely wide where devices may vary with respect to the number of monolithic shanks as well as placement of microelectrode sites. In the present study, we examine the differences in recording ability between two different MEA configurations: single shank (SS) and multi-shank (MS), both of which consist of 16 recording sites implanted in the rat motor cortex. We observed a significant difference in the proportion of active microelectrode sites over the 8-week indwelling period, in which SS devices exhibited a consistent ability to record activity, in contrast to the MS arrays which showed a marked decrease in activity within 2 weeks post-implantation. Furthermore, this difference was revealed to be dependent on the depth at which the microelectrode sites were located and may be mediated by anatomical heterogeneity, as well as the distribution of inhibitory neurons within the cortical layers. Our results indicate that the implantation depth of microelectrodes within the cortex needs to be considered relative to the chronic performance characterization.

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Section: Discussionmentioning

confidence: 99%

Influence of Implantation Depth on the Performance of Intracortical Probe Recording Sites

et al. 2021

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“…Although both cortical neurons and primary sensory neurons have been reported to sustain similar morphological impairments and altered electrophysiological manifestations in response to stretch injury [7,10,38,[90][91][92], they are functionally different and have different extracellular environments in vivo. Those local environments can alter their postinjury cellular cascades, which can induce distinct inflammatory responses and regenerative capacity after mechanical stimulation [93,94].…”

Section: Discussionmentioning

confidence: 99%

Tissue Strain Reorganizes Collagen With a Switchlike Response That Regulates Neuronal Extracellular Signal-Regulated Kinase Phosphorylation In Vitro: Implications for Ligamentous Injury and Mechanotransduction

Zhang

Stablow

Shenoy

et al. 2016

Journal of Biomechanical Engineering

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Excessive loading of ligaments can activate the neural afferents that innervate the collagenous tissue, leading to a host of pathologies including pain. An integrated experimental and modeling approach was used to define the responses of neurons and the surrounding collagen fibers to the ligamentous matrix loading and to begin to understand how macroscopic deformation is translated to neuronal loading and signaling. A neuron-collagen construct (NCC) developed to mimic innervation of collagenous tissue underwent tension to strains simulating nonpainful (8%) or painful ligament loading (16%). Both neuronal phosphorylation of extracellular signal-regulated kinase (ERK), which is related to neuroplasticity (R 2 ! 0.041; p 0.0171) and neuronal aspect ratio (AR) (R 2 ! 0.250; p < 0.0001), were significantly correlated with tissue-level strains. As NCC strains increased during a slowly applied loading (1%/s), a "switchlike" fiber realignment response was detected with collagen reorganization occurring only above a transition point of 11.3% strain. A finite-element based discrete fiber network (DFN) model predicted that at bulk strains above the transition point, heterogeneous fiber strains were both tensile and compressive and increased, with strains in some fibers along the loading direction exceeding the applied bulk strain. The transition point identified for changes in collagen fiber realignment was consistent with the measured strain threshold (11.7% with a 95% confidence interval of 10.2-13.4%) for elevating ERK phosphorylation after loading. As with collagen fiber realignment, the greatest degree of neuronal reorientation toward the loading direction was observed at the NCC distraction corresponding to painful loading. Because activation of neuronal ERK occurred only at strains that produced evident collagen fiber realignment, findings suggest that tissue strain-induced changes in the micromechanical environment, especially altered local collagen fiber kinematics, may be associated with mechanotransduction signaling in neurons.

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“…In experimental models, the typical definition for mTBI is one in which there is no significant cell death, but detrimental gene expression or functional responses 6 7 . Previous work had indicated that the threshold for in vitro mTBI was a uniaxial or multiaxial ~10% strain with pulse durations ranging from 25 to 50 ms 5 44 45 46 47 . The strain and strain rate parameters utilized in our current study fall within the bounds of these published values.…”

Section: Discussionmentioning

confidence: 99%

Acetazolamide Mitigates Astrocyte Cellular Edema Following Mild Traumatic Brain Injury

Sturdivant

Smith

Ali

et al. 2016

Sci Rep

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Non-penetrating or mild traumatic brain injury (mTBI) is commonly experienced in accidents, the battlefield and in full-contact sports. Astrocyte cellular edema is one of the major factors that leads to high morbidity post-mTBI. Various studies have reported an upregulation of aquaporin-4 (AQP4), a water channel protein, following brain injury. AZA is an antiepileptic drug that has been shown to inhibit AQP4 expression and in this study we investigate the drug as a therapeutic to mitigate the extent of mTBI induced cellular edema. We hypothesized that mTBI-mediated astrocyte dysfunction, initiated by increased intracellular volume, could be reduced when treated with AZA. We tested our hypothesis in a three-dimensional in vitro astrocyte model of mTBI. Samples were subject to no stretch (control) or one high-speed stretch (mTBI) injury. AQP4 expression was significantly increased 24 hours after mTBI. mTBI resulted in a significant increase in the cell swelling within 30 min of mTBI, which was significantly reduced in the presence of AZA. Cell death and expression of S100B was significantly reduced when AZA was added shortly before mTBI stretch. Overall, our data point to occurrence of astrocyte swelling immediately following mTBI, and AZA as a promising treatment to mitigate downstream cellular mortality.

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Effect of acute stretch injury on action potential and network activity of rat neocortical neurons in culture

Cited by 26 publications

References 46 publications

Influence of Implantation Depth on the Performance of Intracortical Probe Recording Sites

Influence of Implantation Depth on the Performance of Intracortical Probe Recording Sites

Tissue Strain Reorganizes Collagen With a Switchlike Response That Regulates Neuronal Extracellular Signal-Regulated Kinase Phosphorylation In Vitro: Implications for Ligamentous Injury and Mechanotransduction

Acetazolamide Mitigates Astrocyte Cellular Edema Following Mild Traumatic Brain Injury

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