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, 32 (21), 1666-73

Output Properties of the Cortical Hindlimb Motor Area in Spinal Cord-Injured Rats

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Output Properties of the Cortical Hindlimb Motor Area in Spinal Cord-Injured Rats

Shawn B Frost et al. J Neurotrauma.

Abstract

The purpose of this study was to examine neuronal activity levels in the hindlimb area of motor cortex following spinal cord injury (SCI) in rats and compare the results with measurements in normal rats. Fifteen male Fischer-344 rats received a 200 Kdyn contusion injury in the thoracic cord at level T9-T10. After a minimum of 4 weeks following SCI, intracortical microstimulation (ICMS) and single-unit recording techniques were used in both the forelimb and hindlimb motor areas (FLA, HLA) under ketamine anesthesia. Although movements could be evoked using ICMS in the forelimb area with relatively low current levels, no movements or electromyographical responses could be evoked from ICMS in the HLA in any of the injured rats. During the same procedure, electrophysiological recordings were obtained with a single-shank, 16-channel Michigan probe (Neuronexus) to monitor activity. Neural spikes were discriminated using principle component analysis. Neural activity (action potentials) was collected and digitized for a duration of 5 min. Despite the inability to evoke movement from stimulation of cortex, robust single-unit activity could be recorded reliably from hindlimb motor cortex in SCI rats. Activity in the motor cortex of SCI rats was significantly higher compared with uninjured rats, and increased in hindlimb and forelimb motor cortex by similar amounts. These results demonstrate that in a rat model of thoracic SCI, an increase in single-unit cortical activity can be reliably recorded for several weeks post-injury.

Keywords: cortical activity; hindlimb; rat motor cortex; spinal cord injury.

Figures

<b>FIG. 1.</b>
FIG. 1.
Spinal cord contusion injury in the thoracic spinal cord. (A) Schematic diagram of the spinal cord and column showing the location of the injury. (B) Photomicrograph of a Luxol® blue stained sagittal section through the spinal cord at the level of the injury. C, caudal; D, dorsal; L, lumbar vertebrae; R, rostral; SCI, spinal cord injury; T, thoracic vertebrae; V, ventral. Color image is available online at www.liebertpub.com/neu
<b>FIG. 2.</b>
FIG. 2.
ICMS methods. (A) Schematic diagram of a dorsolateral view of the rat brain showing the location of the hindlimb motor area (HLA) relative to the forelimb motor area (FLA) and face representations in primary motor cortex (M1). Circled B, bregma. (B) Hindlimb representation in a normal rat. Circles represent the location of microelectrode penetrations and colors represent the movement evoked by near-threshold stimulation (<60 μA). (C) ICMS map in an SCI rat. The green X in both maps marks the location in which hindlimb movements were evoked in 100% of normal Fischer rats in a previous study. A, anterior; ICMS, intracortical microstimulation; P, posterior; SCI, spinal cord injury. Color image is available online at www.liebertpub.com/neu
<b>FIG. 3.</b>
FIG. 3.
Activity recording. (A) Cresyl stained coronal section at the level of the hindlimb motor representation showing the location and depth of the 16-channel Neuronexus recording probe in HLA (Box). Numbers on left indicate cortical layers. HLA, hindlimb motor area. (B) Schematic diagram showing the site positions on the electrode shank. Color image is available online at www.liebertpub.com/neu
<b>FIG. 4.</b>
FIG. 4.
Action potentials (spikes) measured in the hindlimb motor area of a ketamine-anesthetized spinal cord-injured rat. Top: Overlaid subset of spiking activity profiles recorded from a single-channel dataset. Bottom: Spikes recorded from the same channel displayed over the entire time period of 300 sec.
<b>FIG. 5.</b>
FIG. 5.
Typical spike recordings from each of the 16 channels in a single penetration in the HLA of a (A) normal rat and (B) a SCI rat over a period of 5 min. DEEP, deep recording sites; HLA, hindlimb motor area; MID, middle recording sites; SF, superficial recording sites.
<b>FIG. 6.</b>
FIG. 6.
Average spontaneous spike activity in M1 (combined HLA and FLA) for the entire dataset of 16 channels at all penetration sites in each rat. Error bars are ± SE. FLA, forelimb motor area; HLA, hindlimb motor area; M1, primary motor cortex; SE, standard error.
<b>FIG. 7.</b>
FIG. 7.
Average spontaneous spike activity in M1 in normal and SCI rats. (A) Average spontaneous spike activity in HLA and FLA in normal and SCI rats. Normal: n = 5; SCI: n = 15. (B) Ratio of spike frequency in the HLA and FLA of normal and SCI rats. Error bars are ± SE, * = p < 0.05. FLA, forelimb motor area; HLA, hindlimb motor area; M1, primary motor cortex; SCI spinal cord injury; SE, standard error.
<b>FIG. 8.</b>
FIG. 8.
Average spontaneous spike activity in normal and SCI rats at 4–6 and 7–18 weeks post-injury. Normal: n = 5; week 4–6: n = 9; week 7–18: n = 6. Error bars are ± SE. SCI spinal cord injury; SE, standard error.
<b>FIG. 9.</b>
FIG. 9.
Average spontaneous spike activity in superficial (SF), middle (Mid), and deep electrode sites in normal and SCI rats. Error bars are ± SE. * = p < 0.05; ** = p < 0.0001. SCI spinal cord injury; SE, standard error.

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