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Bridgette D. Semple - One of the best experts on this subject based on the ideXlab platform.

  • Mild traumatic brain injury in adolescent mice alters skull bone properties to influence a subsequent brain impact at adulthood: A pilot study
    Frontiers in Neurology, 2018
    Co-Authors: Thomas J Mccoll, Rhys D. Brady, Sandy R. Shultz, Lauren Lovick, Kyria M. Webster, Stuart J. Mcdonald, Terence J. O'brien, Bridgette D. Semple
    Abstract:

    Mild traumatic brain injuries (mTBI) are common during adolescence, and limited clinical evidence suggests that a younger age at first exposure to a mTBI may lead to worse long-term outcomes. In this study, we hypothesized that a mTBI during adolescence would predispose towards poorer neurobehavioral and neuropathological outcomes after a subsequent injury at adulthood. Mice received a mild weight-drop injury (mTBI) at adolescence (postnatal day 35; P35) and/or at adulthood (P70). Mice were randomized to 6 groups: 'sham' (sham-surgery at P35 only); 'P35' (mTBI at P35 only); 'P35+sham' (mTBI at P35 + sham at P70); 'sham+P70' (sham at P35 + mTBI at P70); 'sham+sham' (sham at both P35 and P70); or 'P35+P70' (mTBI at both P35 and P70). Acute apnea and an extended righting Reflex Time confirmed a mTBI injury at P35 and/or P70. Cognitive, psychosocial, and sensorimotor function was assessed over one week post-injury. Injured groups performed similarly to sham controls across all tasks. Immunofluorescence staining at 1 week detected an increase in glial activation markers in Sham+P70 brains only. Strikingly, 63% of Sham+P70 mice exhibited a skull fracture at impact, compared to 13% of P35+P70 mice. Micro computed tomography of parietal skull bones found that a mTBI at P35 resulted in increased bone volume and strength, which may account for the difference in fracture incidence. In summary, a single mTBI to the adolescent mouse brain did not exacerbate the cerebral effects of a subsequent mTBI in adulthood. However, the head impact at P35 induced significant changes in skull bone structure and integrity. These novel findings support future investigation into the consequences of mTBI on skull bone.

  • data_sheet_1_Mild Traumatic Brain Injury in Adolescent Mice Alters Skull Bone Properties to Influence a Subsequent Brain Impact at Adulthood: A Pilot Study.docx
    2018
    Co-Authors: Thomas J Mccoll, Rhys D. Brady, Sandy R. Shultz, Lauren Lovick, Kyria M. Webster, Stuart J. Mcdonald, Mujun Sun, Terence J. O’brien, Bridgette D. Semple
    Abstract:

    Mild traumatic brain injuries (mTBI) are common during adolescence, and limited clinical evidence suggests that a younger age at first exposure to a mTBI may lead to worse long-term outcomes. In this study, we hypothesized that a mTBI during adolescence would predispose toward poorer neurobehavioral and neuropathological outcomes after a subsequent injury at adulthood. Mice received a mild weight drop injury (mTBI) at adolescence (postnatal day 35; P35) and/or at adulthood (P70). Mice were randomized to 6 groups: ‘sham’ (sham-surgery at P35 only); ‘P35’ (mTBI at P35 only); ‘P35 + sham’ (mTBI at P35 + sham at P70); ‘sham + P70’ (sham at P35 + mTBI at P70); ‘sham + sham’ (sham at both P35 and P70); or ‘P35 + P70’ (mTBI at both P35 and P70). Acute apnea and an extended righting Reflex Time confirmed a mTBI injury at P35 and/or P70. Cognitive, psychosocial, and sensorimotor function was assessed over 1-week post-injury. Injured groups performed similarly to sham controls across all tasks. Immunofluorescence staining at 1 week detected an increase in glial activation markers in Sham + P70 brains only. Strikingly, 63% of Sham + P70 mice exhibited a skull fracture at impact, compared to 13% of P35 + P70 mice. Micro computed tomography of parietal skull bones found that a mTBI at P35 resulted in increased bone volume and strength, which may account for the difference in fracture incidence. In summary, a single mTBI to the adolescent mouse brain did not exacerbate the cerebral effects of a subsequent mTBI in adulthood. However, the head impact at P35 induced significant changes in skull bone structure and integrity. These novel findings support future investigation into the consequences of mTBI on skull bone.

Steven R Passmore - One of the best experts on this subject based on the ideXlab platform.

  • anatomically remote muscle contraction facilitates patellar tendon Reflex reinforcement while mental activity does not a within participants experimental trial
    Chiropractic & Manual Therapies, 2012
    Co-Authors: Steven R Passmore, Paul Bruno
    Abstract:

    The Jendrassik maneuver (JM) is a remote facilitation muscular contraction shown to affect amplitude and temporal components of the human stretch Reflex. Conflicting theoretical models exist regarding the neurological mechanism related to its ability to reinforce Reflex parameters. One mechanism involves the gamma motoneurons of the fusimotor system, which are subject to both physical and mental activity. A second mechanism describes reduced alpha motoneuron presynaptic inhibition, which is not subject to mental activity. In the current study, we determined if mental activity could be used to create a Reflex facilitation comparable to a remote muscle contraction. Using a within-participants design, we investigated the relative effect of the JM and a successfully employed mental task (Stroop task) on the amplitude and temporal components of the patellar tendon Reflex. We found that the addition of mental activity had no influence on the patellar tendon Reflex parameters measured, while the JM provided facilitation (increased Reflex amplitude, decreased total Reflex Time). The findings from this study support the view that the mechanism for the JM is a reduction in presynaptic inhibition of alpha motoneurons as it is influenced by physical and not mental activity.

Shannon T. Marko - One of the best experts on this subject based on the ideXlab platform.

  • a fixed moderate dose combination of tiletamine zolazepam outperforms midazolam in induction of short term immobilization of ball pythons python regius
    PLOS ONE, 2018
    Co-Authors: Lynn J. Miller, Sean A Van Tongeren, Ginger Donnelly, David P. Fetterer, Nicole L. Garza, Matthew G. Lackemeyer, Jesse T. Steffens, Jimmy O. Fiallos, Joshua L. Moore, Shannon T. Marko
    Abstract:

    Laboratory animals are commonly anesthetized to prevent pain and distress and to provide safe handling. Anesthesia procedures are well-developed for common laboratory mammals, but not as well established in reptiles. We assessed the performance of intramuscularly injected tiletamine (dissociative anesthetic) and zolazepam (benzodiazepine sedative) in fixed combination (2 mg/kg and 3 mg/kg) in comparison to 2 mg/kg of midazolam (benzodiazepine sedative) in ball pythons (Python regius). We measured heart and respiratory rates and quantified induction parameters (i.e., Time to loss of righting Reflex, Time to loss of withdrawal Reflex) and recovery parameters (i.e., Time to regain righting Reflex, withdrawal Reflex, normal behavior). Mild decreases in heart and respiratory rates (median decrease of <10 beats per minute and <5 breaths per minute) were observed for most Time points among all three anesthetic dose groups. No statistically significant difference between the median Time to loss of righting Reflex was observed among animals of any group (p = 0.783). However, the withdrawal Reflex was lost in all snakes receiving 3mg/kg of tiletamine+zolazepam but not in all animals of the other two groups (p = 0.0004). In addition, the Time for animals to regain the righting Reflex and resume normal behavior was longer in the drug combination dose groups compared to the midazolam group (p = 0.0055). Our results indicate that midazolam is an adequate sedative for ball pythons but does not suffice to achieve reliable immobilization or anesthesia, whereas tiletamine+zolazepam achieves short-term anesthesia in a dose-dependent manner.

Thomas J Mccoll - One of the best experts on this subject based on the ideXlab platform.

  • Mild traumatic brain injury in adolescent mice alters skull bone properties to influence a subsequent brain impact at adulthood: A pilot study
    Frontiers in Neurology, 2018
    Co-Authors: Thomas J Mccoll, Rhys D. Brady, Sandy R. Shultz, Lauren Lovick, Kyria M. Webster, Stuart J. Mcdonald, Terence J. O'brien, Bridgette D. Semple
    Abstract:

    Mild traumatic brain injuries (mTBI) are common during adolescence, and limited clinical evidence suggests that a younger age at first exposure to a mTBI may lead to worse long-term outcomes. In this study, we hypothesized that a mTBI during adolescence would predispose towards poorer neurobehavioral and neuropathological outcomes after a subsequent injury at adulthood. Mice received a mild weight-drop injury (mTBI) at adolescence (postnatal day 35; P35) and/or at adulthood (P70). Mice were randomized to 6 groups: 'sham' (sham-surgery at P35 only); 'P35' (mTBI at P35 only); 'P35+sham' (mTBI at P35 + sham at P70); 'sham+P70' (sham at P35 + mTBI at P70); 'sham+sham' (sham at both P35 and P70); or 'P35+P70' (mTBI at both P35 and P70). Acute apnea and an extended righting Reflex Time confirmed a mTBI injury at P35 and/or P70. Cognitive, psychosocial, and sensorimotor function was assessed over one week post-injury. Injured groups performed similarly to sham controls across all tasks. Immunofluorescence staining at 1 week detected an increase in glial activation markers in Sham+P70 brains only. Strikingly, 63% of Sham+P70 mice exhibited a skull fracture at impact, compared to 13% of P35+P70 mice. Micro computed tomography of parietal skull bones found that a mTBI at P35 resulted in increased bone volume and strength, which may account for the difference in fracture incidence. In summary, a single mTBI to the adolescent mouse brain did not exacerbate the cerebral effects of a subsequent mTBI in adulthood. However, the head impact at P35 induced significant changes in skull bone structure and integrity. These novel findings support future investigation into the consequences of mTBI on skull bone.

  • data_sheet_1_Mild Traumatic Brain Injury in Adolescent Mice Alters Skull Bone Properties to Influence a Subsequent Brain Impact at Adulthood: A Pilot Study.docx
    2018
    Co-Authors: Thomas J Mccoll, Rhys D. Brady, Sandy R. Shultz, Lauren Lovick, Kyria M. Webster, Stuart J. Mcdonald, Mujun Sun, Terence J. O’brien, Bridgette D. Semple
    Abstract:

    Mild traumatic brain injuries (mTBI) are common during adolescence, and limited clinical evidence suggests that a younger age at first exposure to a mTBI may lead to worse long-term outcomes. In this study, we hypothesized that a mTBI during adolescence would predispose toward poorer neurobehavioral and neuropathological outcomes after a subsequent injury at adulthood. Mice received a mild weight drop injury (mTBI) at adolescence (postnatal day 35; P35) and/or at adulthood (P70). Mice were randomized to 6 groups: ‘sham’ (sham-surgery at P35 only); ‘P35’ (mTBI at P35 only); ‘P35 + sham’ (mTBI at P35 + sham at P70); ‘sham + P70’ (sham at P35 + mTBI at P70); ‘sham + sham’ (sham at both P35 and P70); or ‘P35 + P70’ (mTBI at both P35 and P70). Acute apnea and an extended righting Reflex Time confirmed a mTBI injury at P35 and/or P70. Cognitive, psychosocial, and sensorimotor function was assessed over 1-week post-injury. Injured groups performed similarly to sham controls across all tasks. Immunofluorescence staining at 1 week detected an increase in glial activation markers in Sham + P70 brains only. Strikingly, 63% of Sham + P70 mice exhibited a skull fracture at impact, compared to 13% of P35 + P70 mice. Micro computed tomography of parietal skull bones found that a mTBI at P35 resulted in increased bone volume and strength, which may account for the difference in fracture incidence. In summary, a single mTBI to the adolescent mouse brain did not exacerbate the cerebral effects of a subsequent mTBI in adulthood. However, the head impact at P35 induced significant changes in skull bone structure and integrity. These novel findings support future investigation into the consequences of mTBI on skull bone.

  • Mild Traumatic Brain Injury in Adolescent Mice Alters Skull Bone Properties to Influence a Subsequent Brain Impact at Adulthood: A Pilot Study
    Frontiers Media S.A., 2018
    Co-Authors: Thomas J Mccoll, Rhys D. Brady, Sandy R. Shultz, Lauren Lovick, Kyria M. Webster, Mujun Sun, Stuart J. Mcdonald
    Abstract:

    Mild traumatic brain injuries (mTBI) are common during adolescence, and limited clinical evidence suggests that a younger age at first exposure to a mTBI may lead to worse long-term outcomes. In this study, we hypothesized that a mTBI during adolescence would predispose toward poorer neurobehavioral and neuropathological outcomes after a subsequent injury at adulthood. Mice received a mild weight drop injury (mTBI) at adolescence (postnatal day 35; P35) and/or at adulthood (P70). Mice were randomized to 6 groups: ‘sham’ (sham-surgery at P35 only); ‘P35’ (mTBI at P35 only); ‘P35 + sham’ (mTBI at P35 + sham at P70); ‘sham + P70’ (sham at P35 + mTBI at P70); ‘sham + sham’ (sham at both P35 and P70); or ‘P35 + P70’ (mTBI at both P35 and P70). Acute apnea and an extended righting Reflex Time confirmed a mTBI injury at P35 and/or P70. Cognitive, psychosocial, and sensorimotor function was assessed over 1-week post-injury. Injured groups performed similarly to sham controls across all tasks. Immunofluorescence staining at 1 week detected an increase in glial activation markers in Sham + P70 brains only. Strikingly, 63% of Sham + P70 mice exhibited a skull fracture at impact, compared to 13% of P35 + P70 mice. Micro computed tomography of parietal skull bones found that a mTBI at P35 resulted in increased bone volume and strength, which may account for the difference in fracture incidence. In summary, a single mTBI to the adolescent mouse brain did not exacerbate the cerebral effects of a subsequent mTBI in adulthood. However, the head impact at P35 induced significant changes in skull bone structure and integrity. These novel findings support future investigation into the consequences of mTBI on skull bone

Bruce F Ohara - One of the best experts on this subject based on the ideXlab platform.

  • resolvins at d1 and e1 differentially impact functional outcome post traumatic sleep and microglial activation following diffuse brain injury in the mouse
    Brain Behavior and Immunity, 2015
    Co-Authors: Rachel K Rowe, Jordan L Harrison, Bruce F Ohara, Timothy W Ellis
    Abstract:

    Abstract Traumatic brain injury (TBI) is induced by mechanical forces which initiate a cascade of secondary injury processes, including inflammation. Therapies which resolve the inflammatory response may promote neural repair without exacerbating the primary injury. Specific derivatives of omega-3 fatty acids loosely grouped as specialized pro-resolving lipid mediators (SPMs) and termed resolvins promote the active resolution of inflammation. In the current study, we investigate the effect of two resolvin molecules, RvE1 and AT-RvD1, on post-traumatic sleep and functional outcome following diffuse TBI through modulation of the inflammatory response. Adult, male C57BL/6 mice were injured using a midline fluid percussion injury (mFPI) model (6–10 min righting Reflex Time for brain-injured mice). Experimental groups included mFPI administered RvE1 (100 ng daily), AT-RvD1 (100 ng daily), or vehicle (sterile saline) and counterbalanced with uninjured sham mice. Resolvins or saline were administered daily for seven consecutive days beginning 3 days prior to TBI to evaluate proof-of-principle to improve outcome. Immediately following diffuse TBI, post-traumatic sleep was recorded for 24 h post-injury. For days 1–7 post-injury, motor outcome was assessed by rotarod. Cognitive function was measured at 6 days post-injury using novel object recognition (NOR). At 7 days post-injury, microglial activation was quantified using immunohistochemistry for Iba-1. In the diffuse brain-injured mouse, AT-RvD1 treatment, but not RvE1, mitigated motor and cognitive deficits. RvE1 treatment significantly increased post-traumatic sleep in brain-injured mice compared to all other groups. RvE1 treated mice displayed a higher proportion of ramified microglia and lower proportion of activated rod microglia in the cortex compared to saline or AT-RvD1 treated brain-injured mice. Thus, RvE1 treatment modulated post-traumatic sleep and the inflammatory response to TBI, albeit independently of improvement in motor and cognitive outcome as seen in AT-RvD1-treated mice. This suggests AT-RvD1 may impart functional benefit through mechanisms other than resolution of inflammation alone.

  • diffuse brain injury does not affect chronic sleep patterns in the mouse
    Brain Injury, 2014
    Co-Authors: Rachel K Rowe, Jordan L Harrison, Bruce F Ohara, Jonathan Lifshitz
    Abstract:

    AbstractPrimary objective: To test if the current model of diffuse brain injury produces chronic sleep disturbances similar to those reported by TBI patients.Methods and procedures: Adult male C57BL/6 mice were subjected to moderate midline fluid percussion injury (n = 7; 1.4 atm; 6–10 minutes righting Reflex Time) or sham injury (n = 5). Sleep–wake activity was measured post-injury using a non-invasive, piezoelectric cage system. Chronic sleep patterns were analysed weekly for increases or decreases in percentage sleep (hypersomnia or insomnia) and changes in bout length (fragmentation).Main outcomes and results: During the first week after diffuse TBI, brain-injured mice exhibited increased mean percentage sleep and mean bout length compared to sham-injured mice. Further analysis indicated the increase in mean percentage sleep occurred during the dark cycle. Injury-induced changes in sleep, however, did not extend beyond the first week post-injury and were not present in weeks 2–5 post-injury.Conclusion...

  • recovery of neurological function despite immediate sleep disruption following diffuse brain injury in the mouse clinical relevance to medically untreated concussion
    Sleep, 2014
    Co-Authors: Rachel K Rowe, Jordan L Harrison, Bruce F Ohara, Jonathan Lifshitz
    Abstract:

    STUDY OBJECTIVE: We investigated the relationship between immediate disruption of posttraumatic sleep and functional outcome in the diffuse brain-injured mouse. DESIGN: Adult male C57BL/6 mice were subjected to moderate midline fluid percussion injury (n = 65; 1.4 atm; 6-10 min righting Reflex Time) or sham injury (n = 44). Cohorts received either intentional sleep disruption (minimally stressful gentle handling) or no sleep disruption for 6 h following injury. Following disruption, serum corticosterone levels (enzyme-linked immunosorbent assay) and posttraumatic sleep (noninvasive piezoelectric sleep cages) were measured. For 1-7 days postinjury, sensorimotor outcome was assessed by Rotarod and a modified Neurological Severity Score (NSS). Cognitive function was measured using Novel Object Recognition (NOR) and Morris water maze (MWM) in the first week postinjury. SETTING: Neurotrauma research laboratory. MEASUREMENTS AND RESULTS: Disrupting posttraumatic sleep for 6 h did not affect serum corticosterone levels or functional outcome. In the hour following the first dark onset, sleep-disrupted mice exhibited a significant increase in sleep; however, this increase was not sustained and there was no rebound of lost sleep. Regardless of sleep disruption, mice showed a Time-dependent improvement in Rotarod performance, with brain-injured mice having significantly shorter latencies on day 7 compared to sham. Further, brain-injured mice, regardless of sleep disruption, had significantly higher NSS scores postinjury compared with sham. Cognitive behavioral testing showed no group differences among any treatment group measured by MWM and NOR. CONCLUSION: Short-duration disruption of posttraumatic sleep did not affect functional outcome, measured by motor and cognitive performance. These data raise uncertainty about posttraumatic sleep as a mechanism of recovery from diffuse brain injury.