Immunohistochemical investigation of neuronal injury in cerebral cortex of cobra-envenomed rats

Abstract

ABSTRACT. The immunohistochemical expression of neuron-specific enolase, NSE (a cytoplasmic glycolytic enzyme of the neurons), synaptophysin, SYN (a major membrane glycoprotein of synaptic vesicles), and Bcl-2 (anti-apoptotic protein) were determined in cerebral cortex of rats envenomed with neurotoxic venom from Egyptian cobra. Male rats were intramuscularly (IM) injected with a single injection of either physiological saline solution or ½ LD 50 or LD 50 of cobra venom and sacrificed 24, 48, or 72 hr after envenoming.Formalin-fixed paraffin sections were immunohistochemically studied by avidin-biotinperoxidase complex method. Neuron histological structure and isolation of genomic DNA were also detected. The results showed a dose and time-dependent increase in NSE and SYN immunoreactivity in cerebral cortex of envenomed rats except in 72 hr high dose envenoming, where decreased SYN was observed. On the other hand, low dose venom induced high Bcl-2 expression 24 hr after envenoming, while the high dose decreased Bcl-2 protein expression. Temporal and spatial Bcl-2 expression was accompanied by DNA fragmentation in cerebral cortex of all envenomed rats, although no serious histological alterations were noticed. These results suggest that cobra venom may lead to neuronal injury and impairment of axonal transport as ascertained by alterations in NSE and SYN immunoreactivity. It could also indicate that venom alters the molecular machinery of apoptosis by inhibiting Bcl-2 expression; however, some vulnerable cells have the ability to overcome this by increasing Bcl-2 protein. These immunohistochemical investigations can be used as tools for detecting neuronal abnormalities even before the occurrence of any histological alterations in case of cerebral cortex neurotoxicity.

Jobelyn® Supplement Lowered Neuronal Degeneration: Significance of Altered p53 and ɤ-Enolase Protein Expressions in Prefrontal Cortex of Rat Exposed to Ethanol

“…NSE (ɤ-enolase) is a biochemical marker for pathogenic processes and ongoing neuronal degeneration [24] . NSE overexpression, as seen in the alcohol group of this study, has been previously correlated with an overall histological evidence of neuronal damage [22,25,26] . Furthermore, neurons or cells with sustained overexpression of NSE proteins are apt to lysis, which leads to cell death.…”

“…In this study, we observed a significant distortion in the cytoarchitecture organization of the PFC in the alcohol group; especially in the molecular, outer granular, and outer pyramidal layers. Furthermore, most neuronal perikarya show a rounded profile as against the characteristic polygonal profile consistent with normal neurons [22] . The neuropil of rats that received alcohol without Jobelyn supplement showed mild vacuolation and aggregation of inflammatory cells, which are classic indicators of cellular stress [23] .…”

Dendritic and Synaptic Degeneration in Pyramidal Neurons of the Sensorimotor Cortex in Neonatal Mice With Kaolin-Induced Hydrocephalus

“…Although immunoreactivity was delayed in appearance and also diminished in the hydrocephalic brains compared to control, staining increased with age and was more intense in the deeper layers of the cortex. The decreased synaptophysin reactivity in the experimental mice is also suggestive of synaptic pathology (Eastwood et al, 2000), which might take place as the process of deterioration of tissue continues (Tanaka et al, 2000), may mirror deformities of either post-transcription of synaptophysin and decrease in the number of axonal connections of cerebral cortical neurons (Rahmy and Hassona, 2004).…”