Tian Simon Y, Wang Jun-Feng, Bezchlibnyk Yarema B, Young L Trevor
The Vivian Rakoff Mood Disorders Laboratory, Centre for Addiction and Mental Health, Toronto, Ontario, Canada.
Neurosci Lett. 2007 Jan 10;411(2):123-7. doi: 10.1016/j.neulet.2006.10.031. Epub 2006 Nov 13.
Impairment of neuroplasticity is considered to play a role in the pathogenesis of psychiatric disorders. To further characterize the impairment of neuroplasticity in psychiatric disorders, expression of the neuronal plasticity marker 43 kDa growth-associated protein (GAP-43) was detected in postmortem hippocampal sub-regions from psychiatric patients including major depressive disorder, bipolar disorder and schizophrenia subjects, and matched control subjects. We found that GAP-43 protein levels in the hippocampal hilar region were significantly lower in bipolar disorder and schizophrenia subjects than in control subjects. We also found that GAP-43 protein levels in the inner molecular layer of the dentate gyrus and the stratum radiatum of CA2 region were reduced in a trend in bipolar disorder and schizophrenia subjects when compared with control subjects. These results suggest that impairment of neuroplasticity may occur in the hippocampus of bipolar disorder and schizophrenia patients.
神经可塑性受损被认为在精神疾病的发病机制中起作用。为了进一步表征精神疾病中神经可塑性的受损情况,在包括重度抑郁症、双相情感障碍和精神分裂症患者以及匹配的对照受试者的死后海马亚区域中检测了神经元可塑性标志物43 kDa生长相关蛋白(GAP - 43)的表达。我们发现,双相情感障碍和精神分裂症患者海马门区的GAP - 43蛋白水平显著低于对照受试者。我们还发现,与对照受试者相比,双相情感障碍和精神分裂症患者齿状回内分子层和CA2区辐射层的GAP - 43蛋白水平呈下降趋势。这些结果表明,双相情感障碍和精神分裂症患者的海马体可能发生神经可塑性受损。