التفاصيل البيبلوغرافية
| العنوان: |
[(11)C]flumazenil positron emission tomography analyses of brain gamma-aminobutyric acid type A receptors in Angelman syndrome. |
| المؤلفون: |
Asahina N, Shiga T, Egawa K, Shiraishi H, Kohsaka S, Saitoh S, Asahina, Naoko, Shiga, Tohru, Egawa, Kiyoshi, Shiraishi, Hideaki, Kohsaka, Shinobu, Saitoh, Shinji |
| المصدر: |
Journal of Pediatrics; Apr2008, Vol. 152 Issue 4, p546-3, 4p |
| مستخلص: |
Objective: To evaluate the role of the gamma-aminobutyric acid type A (GABA(A)) receptor in Angelman syndrome (AS). Study Design: We performed [(11)C]flumazenil positron emission tomography (PET) and examined GABA(A) receptor expression in 7 patients with AS of various genotypes (5 with the deletion, 1 with an imprinting defect [ID], and 1 with a UBE3A mutation) and 4 normal control healthy volunteers. Results: Relative to the control subjects, the [(11)C]flumazenil binding potentials (BPs) were significantly higher in the cerebral cortex and cerebellum in the 5 patients with the deletion and in the 1 patient with a UBE3A mutation, and were less frequently or barely increased in adult patients with the deletion and in the patient with IDs. Conclusions: Total GABA(A) receptor expression was increased in patients with AS with various genotypes. We suggest that a developmental dysregulation of the GABA(A) receptor subunits occurs in patients with AS. [ABSTRACT FROM AUTHOR] |
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