Disease relevance of Pyramidal Tracts

• Alsin mutations are responsible for a primitive, retrograde degeneration of the upper motor neurons of the pyramidal tracts, leading to a clinical continuum from infantile (IAHSP) to juvenile forms with (ALS2) or without (JPLS) lower motor-neuron involvement [1].
• Limited corticospinal tract involvement in amyotrophic lateral sclerosis subjects with the A4V mutation in the copper/zinc superoxide dismutase gene [2].
• The phenotype of severe congenital hydrocephalus secondary to neural cell adhesion molecule L1 (L1CAM) gene mutations includes the distinct finding of brainstem corticospinal tract hypoplasia [3].
• Two siblings with hemolytic anemia caused by triosephosphate isomerase deficiency developed a progressive neurological syndrome featuring dystonic movements, tremor, pyramidal tract signs, and evidence of spinal motor neuron involvement [4].
• In humans, mutations in the L1 gene are linked with a spectrum of brain disorders, including loss of the corticospinal tract, but the mechanistic basis for these disorders is unknown [5].

Psychiatry related information on Pyramidal Tracts

• We investigated whether the brainstem is affected by the pathologic process of sporadic Creutzfeldt-Jakob disease (sCJD), with particular attention to brainstem atrophy, neuronal loss, pyramidal tract degeneration, and prion protein (PrP) deposition, in 33 patients with sCJD [6].
• Trinucleotide expansions in the gene for the TATA-binding protein (TBP) have recently been described in cerebellar ataxia associated with dementia, pyramidal tract and basal ganglia symptoms [7].

High impact information on Pyramidal Tracts

• AHI1 is most highly expressed in brain, particularly in neurons that give rise to the crossing axons of the corticospinal tract and superior cerebellar peduncles [8].
• Joubert syndrome is a congenital brain malformation of the cerebellar vermis and brainstem with abnormalities of axonal decussation (crossing in the brain) affecting the corticospinal tract and superior cerebellar peduncles [8].
• For example, there is a reduction in mossy fiber tracts in the hippocampus of mice that lack NCAM, a requirement for DCC in the response of commissural neurons to a floor plate-derived chemoattractant, and a loss of corticospinal tracts in humans who carry mutations in the L1 gene [9].
• In contrast, NGF levels were decreased in ALS cerebral motor cortex, where the corticospinal tract originates, but increased in the lateral column of spinal cord, which includes the region of corticospinal tract degeneration in ALS [10].
• When True blue is injected into the pyramidal decussation during the first postnatal week and the animals are allowed to survive until the fourth postnatal week, the distribution of pyramidal tract neurones is as widespread as in the immediate postnatal period and includes the entire visual cortex [11].

Chemical compound and disease context of Pyramidal Tracts

• Three Japanese patients with peroxisomal acyl coenzyme A oxidase deficiency who manifested psychomotor retardation and regression during the late infantile period showed characteristic patterns of demyelination in the ponto- medullary corticospinal tracts and in the cerebellar and cerebral white matter [12].
• Reversible spastic and pyramidal tract signs in a patient with Parkinson's disease on L-dopa [13].
• Alumina cream induced focal motor epilepsy in cats. II. Wakefulness--sleep modulation of pyramidal tract multiple unit activity [14].
• Flow determined from 15 electrodes in adjacent pyramidal tracts (white matter) was less at all levels of CO2; 22.9 +/- 12.3 in hypocapnia, 29.1 +/- 15.9 in normocapnia, and 33.9 +/- 13.9 in hypercapnia [15].
• An isolated defect in folate transport into CSF was identified in a patient suffering from a cerebellar syndrome and pyramidal tract dysfunction [16].

Biological context of Pyramidal Tracts

• Analysis of the clinical features in the patients with SCA7 confirmed that the most frequently associated features are pigmentary maculopathy, pyramidal tract involvement, and slow saccades [17].
• Fukutin protein may play a part in the morphogenesis of certain neuronal structures in the brainstem and the dysplastic structure termed "aberrant pyramidal tract" in previous reports may essentially result from an ectopic migration of pontine nucleus neurons [18].
• By the late second trimester, expression of MBP, PLP and MAG was noted in all locations in the spinal white matter except for the corticospinal tract [19].
• GABA and isoguvacine (a GABAA receptor agonist) were applied to isolated neonatal (seven to 14 days old) dorsal columns during recordings of conducted cuneate-gracilis fasciculi and corticospinal tract action potentials [20].
• After inhalation of 15% CO2, immunoreactions to glutamate and glutamic acid decarboxylase were found in some c-Fos or c-Jun-labeled neurons distributed in the reticular region just dorsal to the pyramidal tract in the rostroventromedial medulla (parapyramidal RVMM) [21].

Anatomical context of Pyramidal Tracts

• We have now begun to study the distribution of the neurones of origin of the pyramidal tract during the postnatal development of the rat neocortex using the recently introduced retrogradely transported fluorescent marker, True blue [11].
• Electrophysiologically identified pyramidal tract neurons in the rat cerebral cortex were tested with norepinephrine, acetylcholine, adenosine 3',5'-monophosphate (cyclic AMP), and guanosine 3',5'-monophosphate (cyclic GMP) applied by microiontophoresis [22].
• These projections take a complex route during which they first cross the midline, then form the corticospinal tract, and ultimately connect with motor neurons in the contralateral side of the spinal cord [23].
• AnkyrinB (-/-) mice have reduced L1 in premyelinated axons of long fiber tracts, including the corpus callosum, fimbria, and internal capsule in the brain, and pyramidal tracts and lateral columns of the spinal cord [24].
• Glutamate, a potentially neuroexcitotoxic compound, is thought to be the transmitter of the corticospinal tracts and certain spinal cord interneurons [25].

Associations of Pyramidal Tracts with chemical compounds

• Inosine stimulates extensive axon collateral growth in the rat corticospinal tract after injury [26].
• EphA4 (Sek1) receptor tyrosine kinase is required for the development of the corticospinal tract [27].
• Within the first week after transplantation, the cut corticospinal axons (identified by anterograde transport of biotin dextran) extended caudally along the axis of the corticospinal tract as single, fine, minimally branched sprouts that ended in a simple tip, often preceded by a small varicosity [28].
• Recovery of some flexor and extensor movements of the ipsilateral fingers and toes occurred within 6 h of an incision being made in the upper cervical cord that divided the lateral corticospinal tract unilaterally [29].
• The most marked feature of k maps was their ability to visualize the corticospinal tract, which had elevated k = 3.4-3.8 s(-1) but appeared invisible on f maps [30].

Gene context of Pyramidal Tracts

• In mice, ephrin-B3 functions during development as a midline repellant for axons of the corticospinal tract [31].
• Neither NgR-nor p75(NTR)-deficient mice showed enhanced regeneration of corticospinal tract axons in comparison with wild-type controls after spinal dorsal hemisection [32].
• For instance, the pyramidal tract could be macroscopically detected on S100A6-labeled spinal cord and brainstem sections from SALS patients [33].
• We reported recently that overexpression of neurotrophin-3 (NT-3) by motoneurons in the spinal cord of rats will induce sprouting of corticospinal tract (CST) axons (Zhou et al. [2003] J. Neurosci. 23:1424-1431) [34].
• Infusion of an antibody against Nogo improves behavioral deficits and enhances corticospinal tract regeneration in animals after stroke and spinal cord injury (SCI) [35].

Analytical, diagnostic and therapeutic context of Pyramidal Tracts

• By immunohistochemistry MAP 1B was found to be highly concentrated in developing axonal processes in the cerebellar molecular layer, the corticospinal tract, the mossy fibers in the hippocampus, and the olfactory nerve [36].
• A 35S-labeled mouse GFAP cDNA probe was used for in situ hybridizations of sections of the brain stem obtained 2, 7, and 14 days after unilateral transections of the corticospinal tract in the caudal medulla [37].
• GFAP mRNA levels were already dramatically increased in the injured corticospinal tract by 2 days post axotomy and remained elevated at 14 days [37].
• Film as well as emulsion autoradiography showed a dramatic increase in GFAP mRNA labeling associated with the degenerating corticospinal tract [37].
• Fast transport rates were measured in corticospinal tract axons of male Sprague-Dawley rats by microinjection of tritiated proline into the sensorimotor cortex [38].

References