Origin, course, and laterality of spinocerebellar axons in the North American Opossum,Didelphis virginiana

Terman, Jonathan R.; Wang, Xian M; Martin, George F.

doi:10.1002/(sici)1097-0185(199808)251:4<528::aid-ar9>3.0.co;2-n

Cited by 15 publications

(9 citation statements)

References 88 publications

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“…There are no previous reports of pTDP-43 pathology in neurons of Clarke’s column, although mild neuronal loss in the posterior thoracic nucleus has been noted in cases with a long duration of disease [26]. Clarke’s column neurons receive proprioceptive afferences from skeletal muscles and project to the cerebellum via the posterior spinocerebellar tract [57]. However, all neurons of lamina VII are also targeted by brain regions involved in motor functioning, including the motor cortex, red nucleus, and periaqueductal gray matter [14, 61].…”

Section: Discussionmentioning

confidence: 99%

TDP-43 pathology and neuronal loss in amyotrophic lateral sclerosis spinal cord

et al. 2014

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We examined the phosphorylated 43-kDa TAR DNA-binding protein (pTDP-43) inclusions as well as neuronal loss in full-length spinal cords and five selected regions of the central nervous system from 36 patients with amyotrophic lateral sclerosis (ALS) and 10 age-matched normal controls. The most severe neuronal loss and pTDP-43 lesions were seen in lamina IX motor nuclei columns 4, 6, and 8 of lower cervical segments and in columns 9–11 of lumbosacral segments. Severity of pTDP-43 pathology and neuronal loss correlated closely with gray and white matter oligodendroglial involvement and was linked to onset of disease, with severe involvement of columns 4, 6, and 8 of upper extremity onset cases and severe involvement of columns of 9, 10, and 11 in cases with lower extremity onset. Severe TDP-43 lesions and neuronal loss were observed in stage 4 cases and sometimes included Onuf’s nucleus. Notably, three cases displayed pTDP-43 aggregates in the midbrain oculomotor nucleus, which we had not seen previously even in cases with advanced (i.e., stage 4) pathology. pTDP-43 aggregates were observed in neurons of Clarke’s column in 30.6 % of cases but rarely in the intermediolateral nucleus (IML). Gray matter oligodendroglial pTDP-43 inclusions were present in areas devoid of neuronal pTDP-43 aggregates and neuronal loss. Taken together, our findings indicate that (1) the dorsolateral motor nuclei columns of the cervical and lumbosacral anterior horn may be the earliest foci of pTDP-43 pathology in the spinal cord, (2) gray matter oligodendroglial involvement is an early event in the ALS disease process that possibly heralds subsequent involvement of neurons by pTDP-43 pathology, and (3) in some very advanced cases, there is oculomotor nucleus involvement, which may constitute an additional neuropathological stage (designated here as stage 5) of pTDP-43 pathology in ALS.

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Section: Discussionmentioning

confidence: 99%

TDP-43 pathology and neuronal loss in amyotrophic lateral sclerosis spinal cord

et al. 2014

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“…Relatively fewer degenerative changes in the cervical spinal cord can be partially explained by a ''dilutional effect'' of unaffected ascending fibers from thoracic limbs, cervical musculature, and other cranial structures and of unaffected proximal descending fibers from upper motor neuron centers. 27,30,31,35 The predominance of lesions in the thoracic spinal cord, however, cannot be fully explained by normal anatomic changes in tract sizes at different segmental levels.…”

Section: Discussionmentioning

confidence: 99%

Degenerative Myelopathy in 18 Pembroke Welsh Corgi Dogs

et al. 2009

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Abstract. Postmortem examination was performed on 18 Pembroke Welsh Corgi dogs (mean age 12.7 years) with clinical signs and antemortem diagnostic tests compatible with a diagnosis of degenerative myelopathy. Tissue sections from specific spinal cord and brain regions were systematically evaluated in all dogs. Axonal degeneration and loss were graded according to severity and subsequently compared across different spinal cord segments and funiculi. White matter lesions were identified in defined regions of the dorsal, lateral, and ventral funiculi. The dorsolateral portion of the lateral funiculus was the most severely affected region in all cord segments. Spinal cord segment T12 exhibited the most severe axonal loss. Spinal nerve roots, peripheral nerves, and brain sections were within normal limits, with the exception of areas of mild astrogliosis in gray matter of the caudal medulla. Dogs with more severe lesions showed significant progression of axonal degeneration and loss at T12 and at cord segments cranial and caudal to T12. Severity of axonal loss in individual dogs positively correlated with the duration of clinical signs. The distribution of axonal degeneration resembled that reported in German Shepherd Dog degenerative myelopathy but differed with respect to the transverse and longitudinal extent of the lesions within more clearly defined funicular areas. Although these lesion differences might reflect disease longevity, they could also indicate a form of degenerative myelopathy unique to the Pembroke Welsh Corgi dog.

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“…In the motor field, corollary discharge is a mechanism by which copies of descending motor signals are sent back to the proprioceptive sensory pathways to distinguish self-generated movements from externally generated ones (Sperry, 1950; von Holst and Mittelstaedt, 1950; Crapse and Sommer, 2008). In mammals, to the best of our knowledge, there has been no evidence of corollary discharge occurring at the level of MNs themselves, although retrograde labeling studies of spinocerebellar neurons have reported cerebellar-projecting neurons whose cell bodies reside in the MN lamina IX of the spinal cord (Matsushita and Hosoya, 1979; Matsushita et al, 1979; Terman et al, 1998). In addition, Cooper and Sherrington in their initial description of ascending projections from the spinal cord observed “large cells” in the ventral horn that degenerated upon cutting their ascending axons (Cooper and Sherrington, 1940).…”

Section: Introductionmentioning

confidence: 99%

Motor neurons involved in fine motor control are labeled by tracingAtoh1-lineage neurons in the spinal cord

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et al. 2020

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27Motor neurons (MNs) innervating the digit muscles of the intrinsic hand and foot (IH and IF) 28 control fine motor movements. Previous studies suggest that the IH and IF MN pools have a unique 29 developmental history in comparison to limb MN pools. Consistent with having this unique 30 development, we find that the IH and IF MN pools are labeled postnatally using a CRE knock-in mouse 31 line of Atoh1, a developmentally expressed basic helix-loop-helix (bHLH) transcription factor, while 32 limb-innervating MN pools are not. Approximately 60% of the IH and IF MN pools are labeled and are a 33 mixture of alpha and gamma-MNs. In addition, because Atoh1 is known developmentally to specify 34 many cerebellar-projecting neurons, we tested the hypothesis that IH and IF MNs can send axon 35 collaterals to the cerebellum as a mechanism of corollary discharge. Using intersectional genetic, viral 36 labeling, and retrograde labeling strategies, we were unable to provide evidence in support of this idea. 37As a secondary finding of our viral labeling experiments, we report here that injection of both AAV and 38 Lentiviruses in the periphery can cross the blood-brain barrier to infect Purkinje cells within the central 39 nervous system. Altogether, though, we find that labeling of the IH and IF motor neurons using the 40 Atoh1 CRE knock-in mouse suggests that IH and IF MNs have a unique developmental history and that 41 this mouse strain might be a useful tool to target these specific sets of neurons allowing for functional 42 studies of fine motor control. 43 Significance Statement 44 Motor neurons (MNs) of the intrinsic hand and foot (IH and IF) are labeled postnatally using a 45 CRE knock-in mouse line of the basic helix-loop-helix (bHLH) transcription factor Atoh1 indicating a 46 unique developmental history. We tested whether IH and IF MNs send axon collaterals rostrally to the the periphery can cross the blood-brain barrier and infect Purkinje cells within the central nervous 50 system. Fine motor skills, such as writing or sewing, require exquisite control of the motor neurons 53 (MNs) innervating the digits of the hand. Over vertebrate evolution, unique molecular pathways are 54 involved in the elaboration of digits (Shubin et al., 1997). Correspondingly, the MNs innervating the 55 distal digits have unique developmental programs compared to the neighboring MNs of the lateral 56 motor column (LMC) that innervate limb muscles (Mendelsohn et al., 2017). Precisely how digit-57 innervating MNs adopt their unique identities is unclear. Insight into the development and connectivity 58 of digit-innervating MNs could reveal distinct functions of these MNs in fine motor behavior.59 Developmentally, all MNs derive from a progenitor domain expressing the basic helix-loop-helix 60 (bHLH) oligodendrocyte transcription factor 2 (Olig2) in the ventral neural tube (Lu et al., 2002). 61Unexpectedly, we found that the digit-innervating MNs were labeled using CRE-loxP lineage tracing of 62 the bHLH transcription factor atonal homol...

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Origin, course, and laterality of spinocerebellar axons in the North American Opossum,Didelphis virginiana

Cited by 15 publications

References 88 publications

TDP-43 pathology and neuronal loss in amyotrophic lateral sclerosis spinal cord

TDP-43 pathology and neuronal loss in amyotrophic lateral sclerosis spinal cord

Degenerative Myelopathy in 18 Pembroke Welsh Corgi Dogs

Motor neurons involved in fine motor control are labeled by tracingAtoh1-lineage neurons in the spinal cord

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