دانلود مقاله ISI انگلیسی شماره 72408
عنوان فارسی مقاله

بیان PSA-NCAM و پروتئین سیناپسی در آمیگدال بیماران اختلال روانی

کد مقاله سال انتشار مقاله انگلیسی ترجمه فارسی تعداد کلمات
72408 2012 9 صفحه PDF سفارش دهید محاسبه نشده
خرید مقاله
پس از پرداخت، فوراً می توانید مقاله را دانلود فرمایید.
عنوان انگلیسی
Expression of PSA-NCAM and synaptic proteins in the amygdala of psychiatric disorder patients
منبع

Publisher : Elsevier - Science Direct (الزویر - ساینس دایرکت)

Journal : Journal of Psychiatric Research, Volume 46, Issue 2, February 2012, Pages 189–197

کلمات کلیدی
افسردگی شدید؛ اختلال دو قطبی؛ اسکیزوفرنی؛ سیناپتوفیزین؛ دکربوکسیلاز گلوتامات؛ تاولی گلوتامات-1؛ شکل پذیری سازه
پیش نمایش مقاله
پیش نمایش مقاله بیان PSA-NCAM و پروتئین سیناپسی در آمیگدال بیماران اختلال روانی

چکیده انگلیسی

Neuroimaging has revealed structural abnormalities in the amygdala of different psychiatric disorders. The polysialylated neural cell adhesion molecule (PSA-NCAM), a molecule related to neuronal structural plasticity, which expression is altered in schizophrenia, major depression and in animal models of these disorders, may participate in these changes. However, PSA-NCAM has not been studied in the human amygdala. To know whether its expression and that of presynaptic markers, was affected in psychiatric disorders, we have analyzed post-mortem sections from the Stanley Neuropathology Consortium, which includes controls, schizophrenia, bipolar and major depression patients. PSA-NCAM was expressed in neuronal somata and neuropil puncta, many of which corresponded to interneurons. Depressed patients showed decreases in PSA-NCAM expression in the basolateral and basomedial amygdala; synaptophysin and GAD67 were also decreased, while VGLUT-1 was increased, in different nuclei. Increases in PSA-NCAM expression were found in the lateral nucleus of bipolar patients; synaptophysin and GAD67 were reduced, and VGLUT-1 increased, in their basolateral and lateral nuclei. The expression of synaptophysin and GAD67 was downregulated in the basolateral nucleus of schizophrenics. These results indicate that inhibitory and excitatory amygdaloid circuits are affected in these disorders and that abnormal PSA-NCAM expression in depressive and bipolar patients may underlie these alterations.

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