An EEG analysis of drug effects after mild head injury in mice

Antal, J.; D’Amore, Antonio; Nerozzi, Dina; Palazzesi, Sergio; Pezzini, G.; Loizzo, Alberto

doi:10.1016/0024-3205(92)90074-y

Cited by 7 publications

(4 citation statements)

References 19 publications

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“…Using this novel approach, we found mTBI resulted in a significant loss in cortical motor map in 2 hours after trauma. This result is consistent with previous behavioral findings in animals showing loss of righting reflex up to at least 2 hours after injury 23 and impaired motor function during rotarod test for up to one day 24 . Our results also support previous findings in concussion patients who was shown to suffer increased cortical silence period, indicative of long term intra-cortical inhibition 25 and in football athletes who sustained concussions performed significantly worse in dexterity, reaction, and movement tests 26 .…”

Section: Discussionsupporting

confidence: 93%

Impaired Glutamate Receptor Function Underlies Early Activity Loss of Ipsilesional Motor Cortex after Closed-Head Mild Traumatic Brain Injury

Nguyen

Al-Juboori

Walerstein

et al. 2021

Journal of Neurotrauma

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Although mild traumatic brain injury (mTBI) accounts for majority of TBI patients, the effects and cellular and molecular mechanisms of mild TBI on cortical neural circuits are still not well understood. Given the transient and non-specific functional deficits following mTBI, it is important to understand whether mTBI causes functional deficits of the brain and the underlying mechanism, particularly during the early stage after injury. Here we used in vivo optogenetic motor mapping to determine longitudinal changes in cortical motor map and in vitro calcium imaging to study how changes in cortical excitability and calcium signals may contribute to the motor deficits in a closed-head mTBI model. In Channelrhodopsin 2 (ChR2)-expressing transgenic mice, we recorded electromyograms (EMG) from biceps muscles induced by scanning blue laser on the motor cortex. There were significant decreases in the size and response amplitude of motor maps of the injured cortex at 2 hours post-mTBI but an increase in motor map size of the contralateral cortex in 12 hours post-mTBI, both of which recovered to baseline level in 24 hours. Calcium imaging of cortical slices prepared from GCaMP6-expressing transgenic mice showed a lower amplitude but longer duration of calcium transients of the injured cortex in 2 hours post-mTBI. Blockade of AMPA or NMDA receptors resulted in smaller amplitude of calcium transients, suggesting impaired function of both receptor types. Imaging of calcium transients evoked by glutamate uncaging revealed reduced response amplitudes and longer duration in 2, 12, and 24 hours after mTBI. Higher percentages of neurons of the injured cortex had longer latency period after uncaging than that of the uninjured neurons. The results suggest that impaired glutamate neurotransmission contributes to functional deficits of the motor cortex in vivo, which supports enhancing glutamate neurotransmission as a potential therapeutic approach for the treatment of mTBI.

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Section: Discussionsupporting

confidence: 93%

Impaired Glutamate Receptor Function Underlies Early Activity Loss of Ipsilesional Motor Cortex after Closed-Head Mild Traumatic Brain Injury

Nguyen

Al-Juboori

Walerstein

et al. 2021

Journal of Neurotrauma

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“…The power and amplitude of total EEG band and of the fast beta band (20 to 40 Hz) decreases immediately after fluid percussion injury in rats and recovers gradually [1,10,17]. Our study confirmed the immediate fall in the power of the beta-2 band following injury.…”

Section: Other Pathophysiological and Histopathological Responses To supporting

confidence: 91%

Changes in ICBF, morphology and related parameters by fluid percussion injury

et al. 1996

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We investigated the pathophysiological and morphological responses of anaesthetized rats to fluid percussion brain injury generated by an original midline fluid percussion injury device. Following different grades of trauma, lCBF was measured continuously in the right parietal cortex through a burr hole using laser Doppler flowmeter, and physiological parameters were monitored. Pathological changes also were evaluated microscopically. During the first 2 hours following trauma, we found four patterns of cerebral circulatory responses. Little measurable pathophysiological response occurred after percussion pulses of less than 1.33 atmospheres (atm). In animals subjected to pulses of greater than 4.30 atm, lCBF increased synchronously with blood pressure, and then both parameters decreased continuously until death. In animals subjected to pulses of 1.53 to 2.33 atm, trauma produced a transient increase in lCBF with no synchronous rise in blood pressure. In animals subjected to pulses of 2.70 to 3.87 atm, lCBF increased synchronously with blood pressure immediately following the injury, but had decreased markedly by 60 seconds and remained below the pre-injury baseline. Blood pressure recovered to baseline within 4 minutes of the injury. The transient increase in lCBF occurred within 5 seconds following percussion pulses of greater than 1.53 atm and appeared to be independent of the rise in systemic blood pressure. Apnoea occurred in animals subjected to pulses of greater than 1.53 atm, and the duration of apnoea and mortality rate correlated with the magnitude of the applied injury. A power decrease in the electroencephalogram post-injury and a delay in its recovery, both depended on the magnitude of the injury with few regional differences in the beta-2 band power. The distribution and extent of blood-brain barrier disruption and small haemorrhages also correlated with the magnitude of the injury. The number of neurons decreased significantly in both hippocampi by 2 weeks following moderate trauma. The four patterns of lCBF changes demonstrated in the present study, as well as the other responses to injury, may be useful for studying graded models of various diffuse brain injuries.

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“…(C) Variation in mortality rate associated with input energy is shown. Data were collected from the following studies (Manaka and Sano, 1978; Takahashi et al, 1981; Hall, 1985a; Hall, 1985b; Antal et al, 1992; Chen et al, 1996; Chen et al, 1997; Tang et al, 1997a; Tang et al, 1997b; DeFord et al, 2002; Tehranian et al, 2002; Beni-Adani et al, 2003; Pan et al, 2003; Zohar et al, 2003; Creeley et al, 2004; Milman et al, 2005; Tsenter et al, 2008; Israelsson et al, 2009; Kane et al, 2012; Zohar et al, 2011; Albert-Weißenberger et al, 2012). …”

Section: Towards Improving the Biomechanical Relevance Of Tbi In Animmentioning

confidence: 99%

Towards clinical management of traumatic brain injury: a review of models and mechanisms from a biomechanical perspective

Namjoshi

Good²,

Cheng

et al. 2013

Disease Models &Amp; Mechanisms

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Traumatic brain injury (TBI) is a major worldwide healthcare problem. Despite promising outcomes from many preclinical studies, the failure of several clinical studies to identify effective therapeutic and pharmacological approaches for TBI suggests that methods to improve the translational potential of preclinical studies are highly desirable. Rodent models of TBI are increasingly in demand for preclinical research, particularly for closed head injury (CHI), which mimics the most common type of TBI observed clinically. Although seemingly simple to establish, CHI models are particularly prone to experimental variability. Promisingly, bioengineering-oriented research has advanced our understanding of the nature of the mechanical forces and resulting head and brain motion during TBI. However, many neuroscience-oriented laboratories lack guidance with respect to fundamental biomechanical principles of TBI. Here, we review key historical and current literature that is relevant to the investigation of TBI from clinical, physiological and biomechanical perspectives, and comment on how the current challenges associated with rodent TBI models, particularly those involving CHI, could be improved.

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An EEG analysis of drug effects after mild head injury in mice

Cited by 7 publications

References 19 publications

Impaired Glutamate Receptor Function Underlies Early Activity Loss of Ipsilesional Motor Cortex after Closed-Head Mild Traumatic Brain Injury

Impaired Glutamate Receptor Function Underlies Early Activity Loss of Ipsilesional Motor Cortex after Closed-Head Mild Traumatic Brain Injury

Changes in ICBF, morphology and related parameters by fluid percussion injury

Towards clinical management of traumatic brain injury: a review of models and mechanisms from a biomechanical perspective

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