Since zinc oxide (ZnO) nanoparticles (NPs) have been widely applied, the nano community and the general public have paid great attention to the toxicity of ZnO NPs. We detected 20-nm ZnO NPs biotoxicity following nasal exposure utilizing the non-invasive and real-time magnetic resonance imaging (MRI) technique. MR images were scanned in the rat olfactory epithelium (OE) and olfactory bulb (OB) on a 4.7 T scanner following the treatment (as early as 1 day and up to 21 days after), and the histological changes were evaluated. The influence of the size of the ZnO NPs and chemical components was also investigated. Our study revealed that 20-nm ZnO NPs induced obvious structural disruption and inflammation in the OE and OB at the acute stage. The results suggest that the real-time and non-invasive advantages of MRI allow it to observe and assess, directly and dynamically, the potential toxicity of long-term exposure to ZnO NPs in the olfactory system. These findings indicate the size-dependent toxicity of ZnO NPs with respect to the olfactory bulb. Further study is needed to reveal the mechanism behind ZnO NPs’ toxicity.

Visual deprivation leads to structural neuroplasticity in the blind subjects, including gray matter (GM) and white matter (WM) atrophy and alterations in structural connectivity. The rat model of binocular enucleation (BE) is a frequently used animal model for studying brain plasticity induced by early blindness. Yet few neuroimaging studies have been performed on this model to investigate whether or not the BE rats have image phenotypes similar to or comparable to, those observed in the early blind subjects. The current study aimed to assess brain structural plasticity in BE rats using anatomical magnetic resonance imaging (MRI) and diffusion tensor imaging (DTI). The results demonstrated that early BE at postnatal day 4 (P4) caused almost complete degeneration of optic nerve (ON) and optic chiasma (OCH), atrophy in a number of visual and non-visual structures, including optic tract (OT), dorsal lateral geniculate nucleus (DLG) and corpus callosum (CC). The BE rats also exhibited impairments of WM microstructural integrity in the OT, and reduction of structural connectivity between the normal-appearing visual cortex (VC) and somatosensory/motor cortices at 4 months of age, likely as manifestations of deafferentation-induced maldevelopment. The structural neuroplasticity in BE rats observable to structural MRI parallels largely with what has been reported in blind subjects, suggesting that longitudinal neuroimaging studies on animal models of sensory deprivation can provide insights into how the brain changes its wiring and function during development/adaption in response to the lack of sensory stimuli.