Histological Patterns of Neurodegeneration of Frontal Cortex Neurons in Datura stramonium Treated Wistar Rats

Abstract

Aim: Datura stramonium (DS) is a known hallucinogen and depressant of the central nervous system, but it is commonly used in alcoholic beverages to increase intoxication. Pharmacological, physiological and ultra-structural studies have demonstrated the neurotoxicity of this drug inanimals and humans at high doses. The present study investigated the histological patterns of neurodegeneration of frontal cortex (FC) neurons in Wistar rats treated with high doses of DS seed extract. Materials and methods: Ethanolic extract of DS dried seeds was diluted in normal saline and administered to male and female Wistar rats weighing 200 g - 250 g. The animals were first placed in three groups which were further sub-divided into four sub-groups. The treated sub-groups received intraperitoneal administration (i.p.) of 750 mg/kg of diluted DS seed extract once daily in group 1, twice daily (1500 mg/kg/day) in group 2 and thrice daily (2250 mg/kg/day) in group 3. The treatment was carried out for 4 weeks while the control groups received normal saline during the same period. The rats were euthanized and sections of the frontal cortices of the brain were histologically processed from all groups. Silver impregnation stain for degenerating axons and neurons was used to elucidate the pattern of degeneration induced by DS seed extract on the neurons of the FC. Results: The results of intraperitoneal administration of DS extract showed no changes in groups 1 & 2 treated rats while group 3 showed a significant pattern of histological changes like axonal atrophy, vacuolization and neuronal deaths in the frontal cortices neurons compared to the controls. Conclusion: DS may have a specific pattern of neurodegeneration at higher doses of administration. This could provide a useful model in understanding how DS intoxication can affect frontal cortex neurons with an implication of neurological disorders, mental diseases and behavioural deficits.