In vivo utilization ofd(?)-3-hydroxybutyrate by chick brain and spinal cord

1990 ◽  
Vol 15 (5) ◽  
pp. 529-533 ◽  
Author(s):  
G. J. Caama�o ◽  
A. Linares ◽  
M. A. S�nchez-Del-Castillo ◽  
J. Iglesias ◽  
E. Garc�a-Pereg�n
Keyword(s):  
Spinal Cord ◽  
Chick Brain ◽  
Brain And Spinal Cord

scholarly journals Recapitulate development to promote axonal regeneration: good or bad approach?

2006 ◽  
Vol 361 (1473) ◽  
pp. 1565-1574 ◽  
Author(s):  
Marie T Filbin
Keyword(s):  
Spinal Cord ◽  
Axonal Regeneration ◽  
Molecular Level ◽  
Signal Transduction Pathway ◽  
Developmental Changes ◽  
Transduction Pathway ◽  
The Past ◽  
Brain And Spinal Cord ◽  
The Brain

In the past decade there has been an explosion in our understanding, at the molecular level, of why axons in the adult, mammalian central nervous system (CNS) do not spontaneously regenerate while their younger counterparts do. Now a number of inhibitors of axonal regeneration have been described, some of the receptors they interact with to transduce the inhibitory signal are known, as are some of the steps in the signal transduction pathway that is responsible for inhibition. In addition, developmental changes in the environment and in the neurons themselves are also now better understood. This knowledge in turn reveals novel, putative sites for drug development and therapeutic intervention after injury to the brain and spinal cord. The challenge now is to determine which of these putative treatments are the most effective and if they would be better applied in combination rather than alone. In this review I will summarize what we have learnt about these molecules and how they signal. Importantly, I will also describe approches that have been shown to block inhibitors and encourage regeneration in vivo . I will also speculate on what the differences are between the neonatal and adult CNS that allow the former to regenerate and the latter not to.

Utilization of ketone bodies by chick brain and spinal cord during embryonic and postnatal development

1993 ◽  
Vol 18 (10) ◽  
pp. 1107-1112 ◽  
Author(s):  
A. Linares ◽  
G. J. Caama�o ◽  
R. Diaz ◽  
F. J. Gonzalez ◽  
E. Garcia-Peregrin
Keyword(s):  
Spinal Cord ◽  
Postnatal Development ◽  
Ketone Bodies ◽  
Chick Brain ◽  
Brain And Spinal Cord

Mechanistic evaluation of tapentadol in reducing the pain perception using in-vivo brain and spinal cord microdialysis in rats

2017 ◽  
Vol 809 ◽  
pp. 224-230 ◽  
Author(s):  
Vijay Benade ◽  
Ramakrishna Nirogi ◽  
Gopinadh Bhyrapuneni ◽  
Saivishal Daripelli ◽  
Ganesh Ayyanki ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Pain Perception ◽  
Brain And Spinal Cord

scholarly journals In Vivo Reprogramming for Brain and Spinal Cord Repair

eNeuro ◽  
2015 ◽  
Vol 2 (5) ◽  
pp. ENEURO.0106-15.2015 ◽  
Author(s):  
Gong Chen ◽  
Marius Wernig ◽  
Benedikt Berninger ◽  
Masato Nakafuku ◽  
Malin Parmar ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Spinal Cord Repair ◽  
Brain And Spinal Cord

β-Mannosidosis: Myelin and oligodendrocyte lesions in brain and spinal cord

1984 ◽  
Vol 42 ◽  
pp. 694-695
Author(s):  
Kathryn L. Lovell ◽  
Margaret Z. Jones
Keyword(s):  
Spinal Cord ◽  
Nervous System ◽  
Genetic Disorder ◽  
Neurological Deficits ◽  
Axonal Spheroids ◽  
South Wales ◽  
Pendular Nystagmus ◽  
Myelin Deficits ◽  
Recessive Defect ◽  
Brain And Spinal Cord

Caprine β-mannosidosis, an autosomal recessive defect of glycoprotein catabolism, is associated with a deficiency of tissue and plasma -mannosidase and with tissue accumulation and urinary excretion of oligosaccharides, including the trisaccharide Man(β1-4)GlcNAc(βl-4)GlcNAc and the disaccharide Man(β1-4)GlcNAc. This genetic disorder is evident at birth, with severe neurological deficits including a marked intention tremor, pendular nystagmus, ataxia and inability to stand. Major pathological characteristics described in Nubian goats in Michigan and in Anglo-Nubian goats in New South Wales include widespread cytoplasmic vacuolation in the nervous system and viscera, axonal spheroids, and severe myelin paucity in the brain but not spinal cord or peripheral nerves. Light microscopic examination revealed marked regional variation in the severity of central nervous system myelin deficits, with some brain areas showing nearly complete absence of myelin and other regions characterized by the presence of 25-50% of the control number of myelin sheaths.

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