scholarly journals Functional and Structural Changes in the Corticospinal Tract of Streptozotocin-Induced Diabetic Rats

2021 ◽  
Vol 22 (18) ◽  
pp. 10123
Author(s):  
Ken Muramatsu ◽  
Satoshi Shimo ◽  
Toru Tamaki ◽  
Masako Ikutomo ◽  
Masatoshi Niwa
Keyword(s):  
Spinal Cord ◽  
Conduction Velocity ◽  
Corticospinal Tract ◽  
Morphological Changes ◽  
Cervical Spinal Cord ◽  
Diabetic Animal ◽  
Lumbar Spinal Cord ◽  
Dorsal Funiculus ◽  
Lumbar Spinal ◽  
G Ratio

This study aimed to reveal functional and morphological changes in the corticospinal tract, a pathway shown to be susceptible to diabetes. Type 1 diabetes was induced in 13-week-old male Wistar rats administered streptozotocin. Twenty-three weeks after streptozotocin injection, diabetic animals and age-matched control animals were used to demonstrate the conduction velocity of the corticospinal tract. Other animals were used for morphometric analyses of the base of the dorsal funiculus of the corticospinal tract in the spinal cord using both optical and electron microscopy. The conduction velocity of the corticospinal tract decreased in the lumbar spinal cord in the diabetic animal, although it did not decrease in the cervical spinal cord. Furthermore, atrophy of the fibers of the base of the dorsal funiculus was observed along their entire length, with an increase in the g-ratio in the lumbar spinal cord in the diabetic animal. This study indicates that the corticospinal tract fibers projecting to the lumbar spinal cord experience a decrease in conduction velocity at the lumbar spinal cord of these axons in diabetic animals, likely caused by a combination of axonal atrophy and an increased g-ratio due to thinning of the myelin sheath.

scholarly journals Caudal-rostral progression of alpha motoneurone degeneration in the SOD1G93A mouse model of amyotrophic lateral sclerosis

2020 ◽  
Author(s):  
Alastair J Kirby ◽  
Thomas Palmer ◽  
Richard Mead ◽  
Ronaldo Ichiyama ◽  
Samit Chakrabarty
Keyword(s):  
Spinal Cord ◽  
Cervical Spinal Cord ◽  
Motor Impairment ◽  
Ventral Horn ◽  
Lumbar Spinal Cord ◽  
List Type ◽  
Spatial Trend ◽  
Transgenic Expression ◽  
Spinal Segments ◽  
Lumbar Spinal

AbstractMice with transgenic expression of human SOD1G93A are a widely used model of ALS, with a caudal-rostral progression of motor impairment. Previous studies have quantified the progression of motoneurone (MN) degeneration based on size, even though alpha (α-) and gamma (γ-) MNs overlap in size. Therefore, using molecular markers and synaptic inputs, we quantified the survival of α-MNs and γ-MNs at the lumbar and cervical spinal segments of 3- and 4-month SOD1G93A mice, to investigate whether there is a caudal-rostral progression of MN death. By 3-months, in the cervical and lumbar spinal cord, there was α-MN degeneration with complete γ-MN sparing. At 3-months the cervical spinal cord had more α-MNs per ventral horn than the lumbar spinal cord, in SOD1G93A mice. A similar spatial trend of degeneration was observed in the corticospinal tract, which remained intact in the cervical spinal cord at 3- and 4-months of age. These findings agree with the corticofugal synaptopathy model, that α-MN and CST of the lumbar spinal cord are more susceptible to degeneration in SOD1G93A mice. Hence, there is spatial and temporal caudal-rostral progression of α-MN and CST degeneration in SOD1G93A mice.HighlightsSOD1G93A mice display a caudal-rostral progression of motor impairment.Lumbar spinal cord of SOD1G93A mice has an enhanced susceptibility to degeneration.SOD1G93A mice exhibit a caudal-rostral progression of α-MN and CST degeneration

scholarly journals Differences between C57BL/6 and BALB/cBy Mice in Mortality and Virus Replication after Intranasal Infection with Neuroadapted Sindbis Virus

2000 ◽  
Vol 74 (13) ◽  
pp. 6156-6161 ◽  
Author(s):  
Dzung C. Thach ◽  
Takashi Kimura ◽  
Diane E. Griffin
Keyword(s):  
Spinal Cord ◽  
Sindbis Virus ◽  
Infectious Virus ◽  
Cervical Spinal Cord ◽  
Neutralizing Antibody ◽  
Virus Antigen ◽  
Ependymal Cells ◽  
Lumbar Spinal Cord ◽  
Mouse Strains ◽  
Lumbar Spinal

ABSTRACT Neuroadapted Sindbis virus (NSV), given intranasally, caused fatal encephalitis in 100% of adult C57BL/6 mice and 0% of BALB/cBy mice. Most C57BL/6 mice developed severe kyphoscoliosis followed by hind-limb paralysis, while BALB/cBy mice did not. In situ hybridization for detecting NSV RNA and immunohistochemistry for detecting NSV antigen indicated that virus delivered by this route infected neurons of the olfactory region and spread caudally without infection of ependymal cells. Virus antigen was more abundant and infectious virus increased more rapidly and reached higher levels in C57BL/6 mice than in BALB/cBy mice. Surprisingly, infectious virus was cleared faster in C57BL/6 mice, and this was associated with more rapid production of neutralizing antibody. However, viral RNA was cleared more slowly in C57BL/6 mice. In both mouse strains, more infectious virus was present in the lumbar spinal cord than in the cervical spinal cord. These data suggest that genetic susceptibility to fatal NSV encephalomyelitis is determined at least in part by the efficiency of viral replication and spread in the central nervous system. The differences identified in this study provide possible phenotypes for mapping genetic loci involved in susceptibility.

The terminations of single, physiologically identified, somatosensory, corticospinal tract axons in the lumbar spinal cord of the cat

1991 ◽  
Vol 66 (5) ◽  
pp. 1738-1749 ◽  
Author(s):  
E. J. Casale ◽  
A. R. Light
Keyword(s):  
Spinal Cord ◽  
Gray Matter ◽  
Corticospinal Tract ◽  
Lumbar Spinal Cord ◽  
Spinal Cord Segment ◽  
Apparent Correlation ◽  
Dorsolateral Funiculus ◽  
The Mean ◽  
Lumbar Spinal ◽  
Area 3B

1. Two hundred and twelve corticospinal axons were identified by stimulation in the hindlimb representation in area 3b of the somatosensory cortex and were recorded in the left dorsolateral funiculus of the spinal cord of the cat. The mean conduction velocity was 38 m/s, range 9-113 m/s. 2. Electrical stimulation of the receptive field evoked discharge in corticospinal axons with a mean latency of 36 ms (range 9-100 ms). 3. One hundred nine of the 212 recorded axons were successfully intra-axonally labeled by iontophoretic injection of horseradish peroxidase, with the mean length of labeled axon being 4.8 mm. Seventy-three of the labeled axons issued no collaterals, and 36 issued at least one labeled collateral into the spinal gray matter along the labeled portion of the parent axon. 4. Most labeled axons issued only one labeled collateral per spinal cord segment. Fourteen collaterals from 10 units were labeled well enough to permit reconstruction of their terminal arborizations. 5. Most terminal collaterals were oriented rostrocaudally and terminated in laminae V, VI, and VII. Most collaterals terminated within large mediolateral extents of the gray matter with no apparent topographic organization. 6. No collaterals terminated in laminae I or II or within the motoneuron pools, and no apparent correlation was found between their anatomic and physiological characteristics.

scholarly journals In Vivo Recording of Nerve Conduction Velocity of Spinal CNS Fibers in the Mouse

2017 ◽  
pp. 545-548
Author(s):  
P. DIBAJ ◽  
E. D. SCHOMBURG
Keyword(s):  
Spinal Cord ◽  
Conduction Velocity ◽  
Nerve Conduction ◽  
Nerve Conduction Velocity ◽  
Compound Action Potential ◽  
Lumbar Spinal Cord ◽  
Measured Distance ◽  
Spinal Cord Level ◽  
Lumbar Spinal

Anesthetic and surgical procedures and an electrophysiological method were developed for recording nerve conduction velocity (NCV) of CNS fibers in the murine spinal cord. Under intravenous anesthesia and artificial ventilation the lumbar spinal cord segments L1 to L4 and dorsal roots L3 to L5 on the left side were exposed by laminectomy. After stimulation of the dorsal root L4, a compound action potential (CAP) was recorded at the ipsilateral left fasciculus gracilis at the spinal cord level L1. The latency from stimulation to the CAP together with the measured distance between the electrodes was used for the determination of the NCV. NCV of the fastest fibers in the fasciculus gracilis was observed to be approximately 28 m/s. Reversible decrease of the NCV was measured, in vivo, under general hypothermia. The technique described serves for in vivo electrophysiological investigations of spinal central fibers in wildtype and mutant mice.

Lipomeningocele associated with diplomyelia in a dog

2018 ◽  
Vol 46 (05) ◽  
pp. 323-329 ◽  
Author(s):  
Nele Ondreka ◽  
Sara Malberg ◽  
Emma Laws ◽  
Martin Schmidt ◽  
Sabine Schulze
Keyword(s):  
Spinal Cord ◽  
Neurological Status ◽  
Split Cord Malformation ◽  
Lumbar Spinal Cord ◽  
Histopathological Diagnosis ◽  
Type I ◽  
Thoracic Spinal Cord ◽  
Thoracic Spinal ◽  
Subcutaneous Mass ◽  
Lumbar Spinal

SummaryA 2-year-old male neutered mixed breed dog with a body weight of 30 kg was presented for evaluation of a soft subcutaneous mass on the dorsal midline at the level of the caudal thoracic spine. A further clinical sign was intermittent pain on palpation of the area of the subcutaneous mass. The owner also described a prolonged phase of urination with repeated interruption and re-initiation of voiding. The findings of the neurological examination were consistent with a lesion localization between the 3rd thoracic and 3rd lumbar spinal cord segments. Magnetic resonance imaging revealed a spina bifida with a lipomeningocele and diplomyelia (split cord malformation type I) at the level of thoracic vertebra 11 and 12 and secondary syringomyelia above the aforementioned defects in the caudal thoracic spinal cord. Surgical resection of the lipomeningocele via a hemilaminectomy was performed. After initial deterioration of the neurological status postsurgery with paraplegia and absent deep pain sensation the dog improved within 2 weeks to non-ambulatory paraparesis with voluntary urination. Six weeks postoperatively the dog was ambulatory, according to the owner. Two years after surgery the owner recorded that the dog showed a normal gait, a normal urination and no pain. Histopathological diagnosis of the biopsied material revealed a lipomeningocele which confirmed the radiological diagnosis.

Aging process of the human lumbar spinal cord: A morphometric analysis

1996 ◽  
Vol 16 (2) ◽  
pp. 106-111 ◽  
Author(s):  
Ming Zhou ◽  
Noboru Goto ◽  
Chen Zhang ◽  
Wei Tang
Keyword(s):  
Spinal Cord ◽  
Morphometric Analysis ◽  
Aging Process ◽  
Lumbar Spinal Cord ◽  
Lumbar Spinal

scholarly journals Multi-pronged neuromodulation intervention engages the residual motor circuitry to facilitate walking in a rat model of spinal cord injury

2021 ◽  
Vol 12 (1) ◽  
Author(s):  
Marco Bonizzato ◽  
Nicholas D. James ◽  
Galyna Pidpruzhnykova ◽  
Natalia Pavlova ◽  
Polina Shkorbatova ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Spinal Cord Injury ◽  
Rat Model ◽  
Stress Responses ◽  
Learning Algorithm ◽  
Lumbar Spinal Cord ◽  
Cord Injury ◽  
Potential Synergy ◽  
Lumbar Spinal ◽  
Deep Brain

AbstractA spinal cord injury usually spares some components of the locomotor circuitry. Deep brain stimulation (DBS) of the midbrain locomotor region and epidural electrical stimulation of the lumbar spinal cord (EES) are being used to tap into this spared circuitry to enable locomotion in humans with spinal cord injury. While appealing, the potential synergy between DBS and EES remains unknown. Here, we report the synergistic facilitation of locomotion when DBS is combined with EES in a rat model of severe contusion spinal cord injury leading to leg paralysis. However, this synergy requires high amplitudes of DBS, which triggers forced locomotion associated with stress responses. To suppress these undesired responses, we link DBS to the intention to walk, decoded from cortical activity using a robust, rapidly calibrated unsupervised learning algorithm. This contingency amplifies the supraspinal descending command while empowering the rats into volitional walking. However, the resulting improvements may not outweigh the complex technological framework necessary to establish viable therapeutic conditions.

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