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Dendritic Morphology Changes in Neurons From the Ventral Hippocampus, Amygdala and Nucleus Accumbens in Rats With Neonatal Lesions Into the Prefrontal Cortex

机译:新生皮损大鼠前额叶皮层大鼠海马,杏仁核和伏隔核神经元的树突形态学变化

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Neonatal prefrontal cortex (nPFC) lesions in rats could be a potential animal model to study the early neurodevelopmental abnormalities associated with the behavioral and morphological brain changes observed in schizophrenia. Morphological alterations in pyramidal neurons from the ventral hippocampus (VH) have been observed in post-mortem schizophrenic brains, mainly because of decreased dendritic arbor and spine density. We assessed the effects of nPFC-lesions on the dendritic morphology of neurons from the VH, basolateral-amygdala (BLA) and the nucleus accumbens (NAcc) in rats. nPFC lesions were made on postnatal day 7 (PD7), after dendritic morphology was studied by the Golgi-Cox stain procedure followed by Sholl analysis at PD35 (prepubertal) and PD60 (adult) ages. We also evaluated the effects of PFC-lesions on locomotor activity caused by a novel environment. Adult animals with nPFC lesions showed a decreased spine density in pyramidal neurons from the VH and in medium spiny cells from the NAcc. An increased locomotion was observed in a novel environment for adult animals with a PFC-lesion. Our results indicate that PFC-lesions alter the neuronal dendrite morphology of the NAcc and the VH, suggesting a disconnection between these limbic structures. The locomotion paradigms suggest that dopaminergic transmission is altered in the PFC lesion model. This could help to understand the consequences of an earlier PFC dysfunction in schizophrenia. To evaluate possible dendritic changes in neonatal prefrontal cortex lesions in schizophrenia-related regions including nucleus accumbens, ventral hippocampus and basolateral amygdala, we used the Golgi-Cox stain samples at PD35 and PD70. Our results suggest that neonatal prefrontal cortex damage alters dendritic parameters in limbic regions, and this has potential implications for schizophrenia. Synapse 69:314-325, 2015. (c) 2015 Wiley Periodicals, Inc.
机译:大鼠的新生前额叶皮层(nPFC)损伤可能是研究与精神分裂症中观察到的行为和形态学大脑变化相关的早期神经发育异常的潜在动物模型。在死后精神分裂症患者的大脑中已观察到腹侧海马(VH)锥体神经元的形态学改变,这主要是由于树突状乔木和脊柱密度降低。我们评估了nPFC病变对大鼠VH,基底外侧杏仁核(BLA)和伏隔核(NAcc)的神经元树突形态的影响。在通过高尔基-柯克斯(Golgi-Cox)染色程序研究树突形态之后,在PD35(青春期前)和PD60(成人)年龄研究树突形态,然后在出生后第7天(PD7)制作nPFC病变。我们还评估了PFC病变对由新环境引起的运动活动的影响。患有nPFC损伤的成年动物在VH的锥体神经元和NAcc的中棘细胞中显示出较低的脊柱密度。在具有PFC病变的成年动物的新环境中,观察到运动增加。我们的结果表明,PFC病变改变了NAcc和VH的神经元树突形态,表明这些边缘结构之间存在断连。运动范例表明在PFC病变模型中多巴胺能传递发生了改变。这可能有助于了解精神分裂症中早期PFC功能障碍的后果。为了评估精神分裂症相关区域(包括伏隔核,腹侧海马和基底外侧杏仁核)在新生儿前额叶皮层病变中可能的树突状变化,我们在PD35和PD70处使用了高尔基-柯克斯染色样本。我们的结果表明,新生儿前额叶皮层损伤会改变边缘区的树突状参数,这对精神分裂症具有潜在的影响。突触69:314-325,2015.(c)2015 Wiley Periodicals,Inc.

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