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

Frost, Shawn B.; Dunham, Caleb; Barbay, Scott; Krizsan-Agbas, Dora; Winter, Michelle K.; Guggenmos, David J.; Nudo, Randolph J.

doi:10.1089/neu.2015.3961

Cited by 29 publications

(38 citation statements)

References 37 publications

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“…The Michigan (or Neuronexus) array commonly consists of a single shank of length 3-5 mm with a thickness of 15-50 lm and multiple substrate integrated microelectrode contacts of 121-1250 lm 2 . Both of these array structures have been used for neural stimulation applications (12,13). For example, the Utah array has been used to explore restoration of tactile and proprioceptive feedback where patterned stimuli are provided as current pulses of 20-80 lA to the human sensory cortex (14).…”

Section: Introductionmentioning

confidence: 99%

Thinking Small: Progress on Microscale Neurostimulation Technology

Pancrazio

Deku

Ghazavi

et al. 2017

Neuromodulation: Technology at the Neural Interface

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Objectives Neural stimulation is well-accepted as an effective therapy for a wide range of neurological disorders. While the scale of clinical devices is relatively large, translational and pilot clinical applications are underway for microelectrode-based systems. Microelectrodes have the advantage of stimulating a relatively small tissue volume which may improve selectivity of therapeutic stimuli. Current microelectrode technology is associated with chronic tissue response which limits utility of these devices for neural recording and stimulation. One approach for addressing the tissue response problem may be to reduce physical dimensions of the device. “Thinking small” is a trend for the electronics industry, and for implantable neural interfaces, the result may be a device that can evade the foreign body response. Materials and Methods This review paper surveys our current understanding pertaining to the relationship between implant size and tissue response and the state-of-the-art in ultra-small microelectrodes. A comprehensive literature search was performed using PubMed, Web of Science (Clarivate Analytics), and Google Scholar. Results The literature review shows recent efforts to create microelectrodes that are extremely thin appear to reduce or even eliminate the chronic tissue response. With high charge capacity coatings, ultra-microelectrodes fabricated from emerging polymers and amorphous silicon carbide appear promising for neurostimulation applications. Conclusion We envision the emergence of robust and manufacturable ultra-microelectrodes that leverage advanced materials where the small cross-sectional geometry enables compliance within tissue. Nevertheless, future testing under in vivo conditions is particularly important for assessing the stability of thin film devices under chronic stimulation.

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Section: Introductionmentioning

confidence: 99%

Thinking Small: Progress on Microscale Neurostimulation Technology

Pancrazio

Deku

Ghazavi

et al. 2017

Neuromodulation: Technology at the Neural Interface

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“…We found a significant . Laminar estimates are based on the depths of electrode sites on a single-shank multi-electrode array relative to the cortical surface 26 . In each rat, single-unit (spike) activity was sampled from 4 to 6 locations within neurophysiologically identified hindlimb motor cortex.…”

Section: Resultsmentioning

confidence: 99%

Distal axotomy enhances retrograde presynaptic excitability onto injured pyramidal neurons via trans-synaptic signaling

Nagendran

Larsen

Bigler

et al. 2016

Preprint

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Injury of CNS nerve tracts remodels circuitry through dendritic spine loss and hyper-excitability, thus influencing recovery. Due to the complexity of the CNS, a mechanistic understanding of injury-induced synaptic remodeling remains unclear. Using microfluidic chambers to separate and injure distal axons, we show that axotomy causes retrograde dendritic spine loss at directly injured pyramidal neurons followed by retrograde presynaptic hyper-excitability. These remodeling events require activity at the site of injury, axon-to-soma signaling, and transcription. Similarly, directly injured corticospinal neurons in vivo also exhibit a specific increase in spiking following axon injury. Axotomy-induced hyperexcitability of cultured neurons coincides with elimination of inhibitory inputs onto injured neurons, including those formed onto dendritic spines. Netrin-1 downregulation occurs following axon injury and exogenous netrin-1 applied after injury normalizes spine density, presynaptic excitability, and inhibitory inputs at injured neurons. Our findings show that intrinsic signaling within damaged neurons regulates synaptic remodeling and involves netrin-1 signaling.

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“…The general location of the craniectomy was guided by previous motor mapping studies in the rat (Frost et al, 2013;Frost et al, 2015). The dura over the cranial opening was incised and the opening was filled with warm, medical grade, sterile, silicone oil (50% Medical Silicone Fluid 12,500, 50% MDM Silicone Fluid 1000, Applied Silicone Corp., Santa Paula, CA) to prevent desiccation during the experiment.…”

Section: Intracortical Microstimulationmentioning

confidence: 99%

“…Understanding the timing of excitation of spinal cord motor neurons via descending pathways and how spinal excitability is altered by spinal cord injury (SCI) is critical for the long-range goal of functional restoration via neuromodulatory and rehabilitative interventions. While animal models of SCI have predominantly focused on cortical control of forelimb muscles, we recently established a reliable model of contusion injury in the lower thoracic spinal cord of the laboratory rat to gain insight into the capacity of spared descending fibers to participate in functional recovery of hindlimb motor behavior (Krizsan-Agbas et al, 2014;Frost et al, 2015).…”

Section: Introductionmentioning

confidence: 99%

Effects of a Contusive Spinal Cord Injury on Spinal Motor Neuron Activity and Conduction Time in Rats

Borrell

Krizsan-Agbas

Nudo

et al. 2020

Preprint

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Objective. The purpose of this study was to determine the effects of spinal cord injury (SCI) on spike activity evoked in the hindlimb spinal cord of the rat from cortical electrical stimulation.Approach. Adult, male, Sprague Dawley rats were randomly assigned to a Healthy or SCI group. SCI rats were given a 175 kDyn dorsal midline contusion injury at the level of the T8 vertebrae. At four weeks post-SCI, intracortical microstimulation (ICMS) was delivered at several sites in the hindlimb motor cortex of anesthetized rats, and evoked neural activity was recorded from corresponding sites throughout the dorsoventral depths of the spinal cord and EMG activity from hindlimb muscles. Main results. In healthy rats, post-ICMS spike histograms showed reliable, evoked spike activity during a short-latency epoch 10-12 ms after the initiation of the ICMS pulse train (short). Longer latency spikes occurred between ~20-60 ms, generally following a Gaussian distribution, rising above baseline at time LON, followed by a peak response (Lp), and then falling below baseline at time LOFF. EMG responses occurred between . In SCI rats, short-latency responses were still present, longlatency responses were disrupted or eliminated, and EMG responses were never evoked. The retention of the short-latency responses indicates that spared descending spinal fibers, most likely via the corticoreticulospinal pathway, can still depolarize spinal cord motor neurons after a dorsal midline contusion injury. Significance. This study provides novel insights into the role of alternate pathways for voluntary control of hindlimb movements after SCI that disrupts the corticospinal tract in the rat.

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

Cited by 29 publications

References 37 publications

Thinking Small: Progress on Microscale Neurostimulation Technology

Thinking Small: Progress on Microscale Neurostimulation Technology

Distal axotomy enhances retrograde presynaptic excitability onto injured pyramidal neurons via trans-synaptic signaling

Effects of a Contusive Spinal Cord Injury on Spinal Motor Neuron Activity and Conduction Time in Rats

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