Sacral Spinal Cord

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David J. Bennett - One of the best experts on this subject based on the ideXlab platform.

  • Tail muscle parvalbumin content is decreased in chronic Sacral Spinal Cord injured rats with spasticity
    Experimental physiology, 2011
    Co-Authors: R. Luke Harris, David J. Bennett, Max A. Levine, Charles T. Putman
    Abstract:

    In rats, chronic Sacral Spinal isolation eliminates both descending and afferent inputs to motoneurons supplying the segmental tail muscles, eliminating daily tail muscle EMG activity. In contrast, chronic Sacral Spinal Cord transection preserves afferent inputs, causing tail muscle spasticity that generates quantitatively normal daily EMG. Compared with normal rats, rats with Spinal isolation and transection/spasticity provide a chronic model of progressive neuromuscular injury. Using normal, Spinal isolated and spastic rats, we characterized the activity dependence of calcium-handling protein expression for parvalbumin, fast sarco(endo)plasmic reticulum Ca2+-ATPase (SERCA1) and slow SERCA2. As these proteins may influence fatigue resistance, we also assayed the activities of oxidative (citrate synthase; CS) and glycolytic enzymes (glyceraldehyde phosphate dehydrogenase; GAPDH). We hypothesized that, compared with normal rats, chronic isolation would cause decreased parvalbumin, SERCA1 and SERCA2 expression and CS and GAPDH activities. We further hypothesized that chronic spasticity would promote recovery of parvalbumin, SERCA1 and SERCA2 expression and of CS and GAPDH activities. Parvalbumin, SERCA1 and SERCA2 were quantified with Western blotting. Citrate synthase and GAPDH activities were quantified photometrically. Compared with normal rats, Spinal isolation caused large decreases in parvalbumin (95%), SERCA1 (70%) and SERCA2 (68%). Compared with Spinal isolation, spasticity promoted parvalbumin recovery (ninefold increase) and a SERCA2-to-SERCA1 transformation (84% increase in the ratio of SERCA1 to SERCA2). Compared with normal values, CS and GAPDH activities decreased in isolated and spastic muscles. In conclusion, with complete paralysis due to Spinal isolation, parvalbumin expression is nearly eliminated, but with muscle spasticity after Spinal Cord transection, parvalbumin expression partly recovers. Additionally, spasticity after transection causes a slow-to-fast SERCA isoform transformation that may be compensatory for decreased parvalbumin content.

  • Animal Models of Movement Disorders - CHAPTER L3 – The Spastic Rat with Sacral Spinal Cord Injury
    Animal Models of Movement Disorders, 2005
    Co-Authors: P. J. Harvey, Monica A. Gorassini, David J. Bennett
    Abstract:

    Although the spasticity that follows Spinal Cord injury in humans is common, it has been difficult to study experimentally because Spinal Cord injury in animals produces only comparatively mild spasticity. Spasticity occurs in humans without complete Spinal Cord transections, whereas in animals such as rats and cats, incomplete Spinal Cord injury only leads to mild hyperreflexia. However, these cats have inconvenient and traumatic functional impairments, requiring twice-daily bladder and bowel expression. Bladder infection, pressure sores, and impaired locomotion can lead to significant morbidity and mortality. Thus, the complete Spinal cat is an impractical model, and many groups have used hemisections, partial transections, and contusions to study Spinal Cord injury, even though spasticity is not always prominent. By using Sacral Spinal Cord lesions in rats, a model of spasticity that is convenient to study in the awake state and requires minimal care is developed. Furthermore, the small diameter of the Spinal Cord at this level allows for electrophysiological study of adult spastic motoneurons and reflexes in vitro. This preparation has been central to the understanding of how plateau potentials lead to the intense muscle spasms characteristic of Spinal spasticity. Ongoing experiments are elucidating the underlying currents associated with plateaus and the neuromodulators that are involved in the development of these plateaus in the months following the injury.

  • spastic long lasting reflexes in the awake rat after Sacral Spinal Cord injury
    Journal of Neurophysiology, 2004
    Co-Authors: David J. Bennett, P. J. Harvey, Leo Sanelli, C L Cooke, Monica A. Gorassini
    Abstract:

    Following chronic Sacral Spinal Cord transection in rats the affected tail muscles exhibit marked spasticity, with characteristic long-lasting tail spasms evoked by mild stimulation. The purpose of...

  • spastic long lasting reflexes of the chronic Spinal rat studied in vitro
    Journal of Neurophysiology, 2004
    Co-Authors: P. J. Harvey, David J. Bennett
    Abstract:

    Over the months following Sacral Spinal Cord transection in adult rats, a pronounced spasticity syndrome emerges in the affected tail musculature, where long-lasting muscle spasms can be evoked by ...

  • Spastic long-lasting reflexes in the awake rat after Sacral Spinal Cord injury
    Journal of neurophysiology, 2004
    Co-Authors: David J. Bennett, P. J. Harvey, Leo Sanelli, C L Cooke, Monica A. Gorassini
    Abstract:

    Following chronic Sacral Spinal Cord transection in rats the affected tail muscles exhibit marked spasticity, with characteristic long-lasting tail spasms evoked by mild stimulation. The purpose of the present paper was to characterize the long-lasting reflex seen in tail muscles in response to electrical stimulation of the tail nerves in the awake spastic rat, including its development with time and relation to spasticity. Before and after Sacral Spinal transection, surface electrodes were placed on the tail for electrical stimulation of the caudal nerve trunk (mixed nerve) and for reCording EMG from segmental tail muscles. In normal and acute Spinal rats caudal nerve trunk stimulation evoked little or no EMG reflex. By 2 wk after injury, the same stimulation evoked long-lasting reflexes that were 1) very low threshold, 2) evoked from rest without prior EMG activity, 3) of polysynaptic latency with >6 ms central delay, 4) about 2 s long, and 5) enhanced by repeated stimulation (windup). These reflexes produced powerful whole tail contractions (spasms) and developed gradually over the weeks after the injury (< or =52 wk tested), in close parallel to the development of spasticity. Pure low-threshold cutaneous stimulation, from electrical stimulation of the tip of the tail, also evoked long-lasting spastic reflexes, not seen in acute Spinal or normal rats. In acute Spinal rats a strong C-fiber stimulation of the tip of the tail (20 x T) could evoke a weak EMG response lasting about 1 s. Interestingly, when this C-fiber stimulation was used as a conditioning stimulation to depolarize the motoneuron pool in acute Spinal rats, a subsequent low-threshold stimulation of the caudal nerve trunk evoked a 300-500 ms long reflex, similar to the onset of the long-lasting reflex in chronic Spinal rats. A similar conditioned reflex was not seen in normal rats. Thus there is an unusually long low-threshold polysynaptic input to the motoneurons (pEPSP) that is normally inhibited by descending control. This pEPSP is released from inhibition immediately after injury but does not produce a long-lasting reflex because of a lack of motoneuron excitability. With chronic injury the motoneuron excitability is increased markedly, and the pEPSP then triggers sustained motoneuron discharges associated with long-lasting reflexes and muscle spasms.

Monica A. Gorassini - One of the best experts on this subject based on the ideXlab platform.

  • Animal Models of Movement Disorders - CHAPTER L3 – The Spastic Rat with Sacral Spinal Cord Injury
    Animal Models of Movement Disorders, 2005
    Co-Authors: P. J. Harvey, Monica A. Gorassini, David J. Bennett
    Abstract:

    Although the spasticity that follows Spinal Cord injury in humans is common, it has been difficult to study experimentally because Spinal Cord injury in animals produces only comparatively mild spasticity. Spasticity occurs in humans without complete Spinal Cord transections, whereas in animals such as rats and cats, incomplete Spinal Cord injury only leads to mild hyperreflexia. However, these cats have inconvenient and traumatic functional impairments, requiring twice-daily bladder and bowel expression. Bladder infection, pressure sores, and impaired locomotion can lead to significant morbidity and mortality. Thus, the complete Spinal cat is an impractical model, and many groups have used hemisections, partial transections, and contusions to study Spinal Cord injury, even though spasticity is not always prominent. By using Sacral Spinal Cord lesions in rats, a model of spasticity that is convenient to study in the awake state and requires minimal care is developed. Furthermore, the small diameter of the Spinal Cord at this level allows for electrophysiological study of adult spastic motoneurons and reflexes in vitro. This preparation has been central to the understanding of how plateau potentials lead to the intense muscle spasms characteristic of Spinal spasticity. Ongoing experiments are elucidating the underlying currents associated with plateaus and the neuromodulators that are involved in the development of these plateaus in the months following the injury.

  • spastic long lasting reflexes in the awake rat after Sacral Spinal Cord injury
    Journal of Neurophysiology, 2004
    Co-Authors: David J. Bennett, P. J. Harvey, Leo Sanelli, C L Cooke, Monica A. Gorassini
    Abstract:

    Following chronic Sacral Spinal Cord transection in rats the affected tail muscles exhibit marked spasticity, with characteristic long-lasting tail spasms evoked by mild stimulation. The purpose of...

  • Spastic long-lasting reflexes in the awake rat after Sacral Spinal Cord injury
    Journal of neurophysiology, 2004
    Co-Authors: David J. Bennett, P. J. Harvey, Leo Sanelli, C L Cooke, Monica A. Gorassini
    Abstract:

    Following chronic Sacral Spinal Cord transection in rats the affected tail muscles exhibit marked spasticity, with characteristic long-lasting tail spasms evoked by mild stimulation. The purpose of the present paper was to characterize the long-lasting reflex seen in tail muscles in response to electrical stimulation of the tail nerves in the awake spastic rat, including its development with time and relation to spasticity. Before and after Sacral Spinal transection, surface electrodes were placed on the tail for electrical stimulation of the caudal nerve trunk (mixed nerve) and for reCording EMG from segmental tail muscles. In normal and acute Spinal rats caudal nerve trunk stimulation evoked little or no EMG reflex. By 2 wk after injury, the same stimulation evoked long-lasting reflexes that were 1) very low threshold, 2) evoked from rest without prior EMG activity, 3) of polysynaptic latency with >6 ms central delay, 4) about 2 s long, and 5) enhanced by repeated stimulation (windup). These reflexes produced powerful whole tail contractions (spasms) and developed gradually over the weeks after the injury (< or =52 wk tested), in close parallel to the development of spasticity. Pure low-threshold cutaneous stimulation, from electrical stimulation of the tip of the tail, also evoked long-lasting spastic reflexes, not seen in acute Spinal or normal rats. In acute Spinal rats a strong C-fiber stimulation of the tip of the tail (20 x T) could evoke a weak EMG response lasting about 1 s. Interestingly, when this C-fiber stimulation was used as a conditioning stimulation to depolarize the motoneuron pool in acute Spinal rats, a subsequent low-threshold stimulation of the caudal nerve trunk evoked a 300-500 ms long reflex, similar to the onset of the long-lasting reflex in chronic Spinal rats. A similar conditioned reflex was not seen in normal rats. Thus there is an unusually long low-threshold polysynaptic input to the motoneurons (pEPSP) that is normally inhibited by descending control. This pEPSP is released from inhibition immediately after injury but does not produce a long-lasting reflex because of a lack of motoneuron excitability. With chronic injury the motoneuron excitability is increased markedly, and the pEPSP then triggers sustained motoneuron discharges associated with long-lasting reflexes and muscle spasms.

  • Evidence for plateau potentials in tail motoneurons of awake chronic Spinal rats with spasticity.
    Journal of neurophysiology, 2001
    Co-Authors: David J. Bennett, P. J. Harvey, Monica A. Gorassini
    Abstract:

    Motor units of segmental tail muscles were reCorded in awake rats following acute (1–2 days) and chronic (>30 days) Sacral Spinal Cord transection to determine whether plateau potentials contribute...

  • Spasticity in rats with Sacral Spinal Cord injury.
    Journal of neurotrauma, 1999
    Co-Authors: David J. Bennett, Monica A. Gorassini, Leo Sanelli, Karim Fouad, Y. Han, Jianguo Cheng
    Abstract:

    We have investigated Sacral Spinal Cord lesions in rats with the goal of developing a rat model of muscular spasticity that is minimally disruptive, not interfering with bladder, bowel, or hindlimb locomotor function. Spinal transections were made at the S2 Sacral level and, thus, only affected the tail musculature. After Spinal transection, the muscles of the tail were inactive for 2 weeks. Following this initial period, hypertonia, hyperreflexia, and clonus developed in the tail, and grew more pronounced with time. These changes were assessed in the awake rat, since the tail is readily accessible and easy to manipulate. Muscle stretch or cutaneous stimulation of the tail produced muscle spasms and marked increases in muscle tone, as measured with force and electromyographic reCordings. When the tail was unconstrained, spontaneous or reflex induced flexor and extensor spasms coiled the tail. Movement during the spasms often triggered clonus in the end of the tail. The tail hair and skin were extremely hyperreflexive to light touch, withdrawing quickly at contact, and at times clonus could be entrained by repeated contact of the tail on a surface. Segmental tail muscle reflexes, e.g., Hoffman reflexes (H-reflexes), were measured before and after Spinalization, and increased significantly 2 weeks after transection. These results suggest that Sacral Spinal rats develop symptoms of spasticity in tail muscles with similar characteristics to those seen in limb muscles of humans with Spinal Cord injury, and thus provide a convenient preparation for studying this condition.

Glenn J Giesler - One of the best experts on this subject based on the ideXlab platform.

  • spinothalamic and spinohypothalamic tract neurons in the Sacral Spinal Cord of rats ii responses to cutaneous and visceral stimuli
    Journal of Neurophysiology, 1996
    Co-Authors: James T Katter, Robert J Dado, Ewa Kostarczyk, Glenn J Giesler
    Abstract:

    1. A goal of this study was to determine whether neurons in the Sacral Spinal Cord that project to the diencephalon are involved in the processing and transmission of sensory information that arise...

  • spinothalamic and spinohypothalamic tract neurons in the Sacral Spinal Cord of rats ii responses to cutaneous and visceral stimuli
    Journal of Neurophysiology, 1996
    Co-Authors: James T Katter, Robert J Dado, Ewa Kostarczyk, Glenn J Giesler
    Abstract:

    1. A goal of this study was to determine whether neurons in the Sacral Spinal Cord that project to the diencephalon are involved in the processing and transmission of sensory information that arises in the perineum and pelvis. Therefore, 58 neurons in segments L6-S2 were activated antidromically with currents or = 80 mmHg. More than 90% responded abruptly at stimulus onset, responded continuously throughout the stimulus period, and stopped responding immediately after termination of the stimulus. 6. Thirty-one neurons were tested for their responsiveness to distention of a balloon placed inside the vagina. Eleven (35%) exhibited graded increases in their firing frequencies in response to increasing pressures of vaginal distention (VaD). The thresholds and temporal profiles of the responses to VaD were similar to those for CrD. Twenty-nine neurons were tested with both CrD and VaD. Thirteen (45%) were excited by both stimuli, four (14%) responded to CrD but not VaD, and one (3%) was excited by VaD but not CrD. Neurons excited by CrD, VaD, or both were reCorded throughout the dorsal horn. 7. As a population, WDR neurons, but not LT or HT neurons, encoded increasing pressures of CrD and VaD with graded increases in their firing frequencies. The responses of WDR neurons to CrD differed significantly from those of either LT or HT neurons. Regression analyses of the stimulus-response functions of responsive WDR neurons to CrD and VaD were described by power functions with exponents of 1.6 and 2.4, respectively.(ABSTRACT TRUNCATED)

P. J. Harvey - One of the best experts on this subject based on the ideXlab platform.

  • Animal Models of Movement Disorders - CHAPTER L3 – The Spastic Rat with Sacral Spinal Cord Injury
    Animal Models of Movement Disorders, 2005
    Co-Authors: P. J. Harvey, Monica A. Gorassini, David J. Bennett
    Abstract:

    Although the spasticity that follows Spinal Cord injury in humans is common, it has been difficult to study experimentally because Spinal Cord injury in animals produces only comparatively mild spasticity. Spasticity occurs in humans without complete Spinal Cord transections, whereas in animals such as rats and cats, incomplete Spinal Cord injury only leads to mild hyperreflexia. However, these cats have inconvenient and traumatic functional impairments, requiring twice-daily bladder and bowel expression. Bladder infection, pressure sores, and impaired locomotion can lead to significant morbidity and mortality. Thus, the complete Spinal cat is an impractical model, and many groups have used hemisections, partial transections, and contusions to study Spinal Cord injury, even though spasticity is not always prominent. By using Sacral Spinal Cord lesions in rats, a model of spasticity that is convenient to study in the awake state and requires minimal care is developed. Furthermore, the small diameter of the Spinal Cord at this level allows for electrophysiological study of adult spastic motoneurons and reflexes in vitro. This preparation has been central to the understanding of how plateau potentials lead to the intense muscle spasms characteristic of Spinal spasticity. Ongoing experiments are elucidating the underlying currents associated with plateaus and the neuromodulators that are involved in the development of these plateaus in the months following the injury.

  • spastic long lasting reflexes in the awake rat after Sacral Spinal Cord injury
    Journal of Neurophysiology, 2004
    Co-Authors: David J. Bennett, P. J. Harvey, Leo Sanelli, C L Cooke, Monica A. Gorassini
    Abstract:

    Following chronic Sacral Spinal Cord transection in rats the affected tail muscles exhibit marked spasticity, with characteristic long-lasting tail spasms evoked by mild stimulation. The purpose of...

  • spastic long lasting reflexes of the chronic Spinal rat studied in vitro
    Journal of Neurophysiology, 2004
    Co-Authors: P. J. Harvey, David J. Bennett
    Abstract:

    Over the months following Sacral Spinal Cord transection in adult rats, a pronounced spasticity syndrome emerges in the affected tail musculature, where long-lasting muscle spasms can be evoked by ...

  • Spastic long-lasting reflexes in the awake rat after Sacral Spinal Cord injury
    Journal of neurophysiology, 2004
    Co-Authors: David J. Bennett, P. J. Harvey, Leo Sanelli, C L Cooke, Monica A. Gorassini
    Abstract:

    Following chronic Sacral Spinal Cord transection in rats the affected tail muscles exhibit marked spasticity, with characteristic long-lasting tail spasms evoked by mild stimulation. The purpose of the present paper was to characterize the long-lasting reflex seen in tail muscles in response to electrical stimulation of the tail nerves in the awake spastic rat, including its development with time and relation to spasticity. Before and after Sacral Spinal transection, surface electrodes were placed on the tail for electrical stimulation of the caudal nerve trunk (mixed nerve) and for reCording EMG from segmental tail muscles. In normal and acute Spinal rats caudal nerve trunk stimulation evoked little or no EMG reflex. By 2 wk after injury, the same stimulation evoked long-lasting reflexes that were 1) very low threshold, 2) evoked from rest without prior EMG activity, 3) of polysynaptic latency with >6 ms central delay, 4) about 2 s long, and 5) enhanced by repeated stimulation (windup). These reflexes produced powerful whole tail contractions (spasms) and developed gradually over the weeks after the injury (< or =52 wk tested), in close parallel to the development of spasticity. Pure low-threshold cutaneous stimulation, from electrical stimulation of the tip of the tail, also evoked long-lasting spastic reflexes, not seen in acute Spinal or normal rats. In acute Spinal rats a strong C-fiber stimulation of the tip of the tail (20 x T) could evoke a weak EMG response lasting about 1 s. Interestingly, when this C-fiber stimulation was used as a conditioning stimulation to depolarize the motoneuron pool in acute Spinal rats, a subsequent low-threshold stimulation of the caudal nerve trunk evoked a 300-500 ms long reflex, similar to the onset of the long-lasting reflex in chronic Spinal rats. A similar conditioned reflex was not seen in normal rats. Thus there is an unusually long low-threshold polysynaptic input to the motoneurons (pEPSP) that is normally inhibited by descending control. This pEPSP is released from inhibition immediately after injury but does not produce a long-lasting reflex because of a lack of motoneuron excitability. With chronic injury the motoneuron excitability is increased markedly, and the pEPSP then triggers sustained motoneuron discharges associated with long-lasting reflexes and muscle spasms.

  • Evidence for plateau potentials in tail motoneurons of awake chronic Spinal rats with spasticity.
    Journal of neurophysiology, 2001
    Co-Authors: David J. Bennett, P. J. Harvey, Monica A. Gorassini
    Abstract:

    Motor units of segmental tail muscles were reCorded in awake rats following acute (1–2 days) and chronic (>30 days) Sacral Spinal Cord transection to determine whether plateau potentials contribute...

James T Katter - One of the best experts on this subject based on the ideXlab platform.

  • spinothalamic and spinohypothalamic tract neurons in the Sacral Spinal Cord of rats ii responses to cutaneous and visceral stimuli
    Journal of Neurophysiology, 1996
    Co-Authors: James T Katter, Robert J Dado, Ewa Kostarczyk, Glenn J Giesler
    Abstract:

    1. A goal of this study was to determine whether neurons in the Sacral Spinal Cord that project to the diencephalon are involved in the processing and transmission of sensory information that arise...

  • spinothalamic and spinohypothalamic tract neurons in the Sacral Spinal Cord of rats ii responses to cutaneous and visceral stimuli
    Journal of Neurophysiology, 1996
    Co-Authors: James T Katter, Robert J Dado, Ewa Kostarczyk, Glenn J Giesler
    Abstract:

    1. A goal of this study was to determine whether neurons in the Sacral Spinal Cord that project to the diencephalon are involved in the processing and transmission of sensory information that arises in the perineum and pelvis. Therefore, 58 neurons in segments L6-S2 were activated antidromically with currents or = 80 mmHg. More than 90% responded abruptly at stimulus onset, responded continuously throughout the stimulus period, and stopped responding immediately after termination of the stimulus. 6. Thirty-one neurons were tested for their responsiveness to distention of a balloon placed inside the vagina. Eleven (35%) exhibited graded increases in their firing frequencies in response to increasing pressures of vaginal distention (VaD). The thresholds and temporal profiles of the responses to VaD were similar to those for CrD. Twenty-nine neurons were tested with both CrD and VaD. Thirteen (45%) were excited by both stimuli, four (14%) responded to CrD but not VaD, and one (3%) was excited by VaD but not CrD. Neurons excited by CrD, VaD, or both were reCorded throughout the dorsal horn. 7. As a population, WDR neurons, but not LT or HT neurons, encoded increasing pressures of CrD and VaD with graded increases in their firing frequencies. The responses of WDR neurons to CrD differed significantly from those of either LT or HT neurons. Regression analyses of the stimulus-response functions of responsive WDR neurons to CrD and VaD were described by power functions with exponents of 1.6 and 2.4, respectively.(ABSTRACT TRUNCATED)