Abstract

Neonatal post-hemorrhagic hydrocephalus is associated with cognitive decline and a serious deterioration in the patient's quality of life. The underlying impairments to neurons are not well understood. Here, we used the method described by Cherian et al. to construct a model of hydrocephalus after intra-ventricular hemorrhage and then observed the subsequent pathological changes in the morphology of neurons labeled by enhanced green fluorescent proteins (EGFP) using the in utero electroporation technique. Injection of venous blood into the lateral ventricles of 7-day-old rats in the operation group caused marked enlargement of the ventricles in 60% (9/15) of the rats after 2 weeks and in 53.3% (8/15) of the rats after 3 weeks. Compared with the control group, the length of the neural dendrites in the somatosensory cortex was shortened and the number of both neuron dendrite branches and synapses was significantly decreased. There was no evidence of cerebral cortical neuron death as shown by positive EGFP cell counting which suggest that neurological dysfunction after intra-ventricular hemorrhage-induced hydrocephalus may be related to the shortening of neural dendrites and the decreased number of synapses in somatosensory cortex and thus provides a possible neurological cause for hydrocephalus-induced cognitive decline and motor dysfunction.

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