TRIORTHOCRESYL PHOSPHATE–INDUCED NEURONAL LOSSES IN LUMBAR SPINAL CORD OF HENS—AN IMMUNOHISTOCHEMISTRY AND …

DL Mou, YP Wang, JF Song, ZR Rao… - International journal of …, 2006 - Taylor & Francis
DL Mou, YP Wang, JF Song, ZR Rao, L Duan, G Ju
International journal of neuroscience, 2006Taylor & Francis
To investigate the neuronal losses of hens' spinal cords in the model of organophosphate-
induced delayed neuropathy (OPIDN) and to analyze the impact of apoptosis on the
pathogenesis of OPIDN. Adult hens were challenged with triorthocresyl phosphate (TOCP)
at a single dose (750 mg/kg). Neuronal losses in the 3rd lumbar spinal cord (L3) were
assessed by light-microscopy and electron-microscopy methods at different days post
exposure, respectively. The typical OPIDN signs were seen in the TOCP-exposed hens at …
To investigate the neuronal losses of hens’ spinal cords in the model of organophosphate-induced delayed neuropathy (OPIDN) and to analyze the impact of apoptosis on the pathogenesis of OPIDN. Adult hens were challenged with triorthocresyl phosphate (TOCP) at a single dose (750 mg/kg). Neuronal losses in the 3rd lumbar spinal cord (L3) were assessed by light-microscopy and electron-microscopy methods at different days post exposure, respectively. The typical OPIDN signs were seen in the TOCP-exposed hens at about 9th day. The number of large nerve cells declined gradually. And these cells were verified as neurons by immunostained with neuronal marker NeuN. The expression of FasL reached proximal at about 9th day, decreased from 14th day. Neurons in TOCP exposed groups displayed degenerative morphologies in electronic microscopy. Some neurons showed apoptotic-like ultrastructure profiles at 5th day. The nuclear membrane was complete with chromatin condensed to the margins of nuclear membrane like a crescent-shaped body. Mitochondria morphologic changes appeared early (5 d) following exposure to TOCP, and developed in a time-dependent fashion. Apoptosis might be involved in the development of OPIDN, and play a role in the pathogenesis of OPIDN.
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