scholarly journals Developmental regulation of α-amino-3-hydroxy-5-methyl-4-isoxazole-propionic acid receptor subunit expression in forebrain and relationship to regional susceptibility to hypoxic/ischemic injury. II. Human cerebral white matter and cortex

2006 ◽  
Vol 497 (1) ◽  
pp. 61-77 ◽  
Author(s):  
Delia M. Talos ◽  
Pamela L. Follett ◽  
Rebecca D. Folkerth ◽  
Rachel E. Fishman ◽  
Felicia L. Trachtenberg ◽  
...  
2008 ◽  
Vol 28 (9) ◽  
pp. 1613-1623 ◽  
Author(s):  
Ursula I Tuor ◽  
Shuzhen Meng ◽  
Min Qiao ◽  
Nicole B Webster ◽  
Shauna M Crowley ◽  
...  

We hypothesized that magnetic resonance magnetization transfer (MT) imaging would be sensitive for detecting cerebral ischemic injury in white matter of neonatal brain. We compared the progression of changes in T2 and the MT ratio (MTR) after cerebral hypoxic-ischemic insults of differing severity in neonatal rats. Magnetization transfer imaging parameters were first optimized, and then MTR and T2 maps were acquired at various times after a mild (rather selective white matter) or substantial insult produced by unilateral cerebral hypoxia—ischemia. Depending on insult severity, time after insult, and region (e.g., subcortical white matter or cortex), cerebral hypoxia—ischemia produced reductions in MTR and an increase in T2. The exception was acutely at 1 to 5 h at which time points MTR was reduced ipsilaterally in white matter, whereas T2 was not affected significantly. Progression of imaging changes differed in rats grouped according to whether gross damage was present after chronic recovery. Behavioral changes were generally associated with chronic reductions in MTR and gross brain damage. Magnetization transfer imaging was capable of early detection of hypoxic-ischemic injury and particularly sensitive for identifying the progression of cerebral injury in white matter. Magnetization transfer ratio has potential for assisting with early diagnosis and treatment assessment for infants affected by perinatal hypoxia—ischemia.


Neuroreport ◽  
2006 ◽  
Vol 17 (12) ◽  
pp. 1337-1341 ◽  
Author(s):  
Gloria Patricia Cardona-Go??mez ◽  
Cesar Arango-Davila ◽  
Juan Carlos Gallego-Go??mez ◽  
Alvaro Barrera-Ocampo ◽  
Hernan Pimienta ◽  
...  

2014 ◽  
Vol 35 (4) ◽  
pp. 543-553 ◽  
Author(s):  
Tahani Huria ◽  
Narasimha Murthy Beeraka ◽  
Badrah Al-Ghamdi ◽  
Robert Fern

Ischemic-type injury to developing white matter is associated with the significant clinical condition cerebral palsy and with the cognitive deficits associated with premature birth. Premyelinated axons are the major cellular component of fetal white matter and loss of axon function underlies the disability, but the cellular mechanisms producing ischemic injury to premyelinated axons have not previously been described. Injury was found to require longer periods of modelled ischemia than at latter developmental points. Ischemia produced initial hyperexcitability in axons followed by loss of function after Na+ and Ca2+ influx. N-methyl-D-aspartate- (NMDA) type glutamate receptor (GluR) agonists potentiated axon injury while antagonists were protective. The NMDA GluR obligatory Nr1 subunit colocalized with markers of small premyelinated axons and expression was found at focal regions of axon injury. Ischemic injury of glial cells present in early developing white matter was NMDA GluR independent. Axons in human postconception week 18 to 23 white matter had a uniform prediameter expansion phenotype and postembedded immuno-gold labelling showed Nr1 subunit expression on the membrane of these axons, demonstrating a shared key neuropathologic feature with the rodent model. Premyelinated central axons therefore express high levels of functional NMDA GluRs that confer sensitivity to ischemic injury.


2019 ◽  
Vol 29 (6) ◽  
pp. 743-749
Author(s):  
Jacqueline Salas ◽  
Nihaal Reddy ◽  
Kathryn A. Carson ◽  
Frances J. Northington ◽  
Thierry A.G.M. Huisman

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