Abstract:
:Phenylketonuria is the most common, inherited aminoacidopathy associated with brain injury. To date, no study has focused on the neuropathology of the genetic mouse model of phenylketonuria, BTBR-Pah(enu2). We examined dendritic spines and synapses in the CA1 and prefrontal cortex among the wild-type, heterozygous, and BTBR-Pah(enu2) mice. A reduced density of dendritic spines, a shortened length of the presynaptic active zone, a widened synaptic cleft, and decreased thickness of postsynaptic density were revealed in BTBR-Pah(enu2) mice. Meanwhile, the phosphorylation at Thr286 of Ca(2+)/calmodulin-dependent protein kinase IIα was alerted in BTBR-Pah(enu2) mice. These findings revealed that phenylketonuria-related brain impairment is accompanied with abnormalities of dendritic spines and synapses. The dysfunction of Ca(2+)/calmodulin-dependent protein kinase IIα may result in an impaired synaptic function.
journal_name
Neuroreportjournal_title
Neuroreportauthors
Liang L,Gu X,Lu L,Li D,Zhang Xdoi
10.1097/WNR.0b013e3283495accsubject
Has Abstractpub_date
2011-08-24 00:00:00pages
617-22issue
12eissn
0959-4965issn
1473-558Xjournal_volume
22pub_type
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