Journal of chemical neuroanatomy · 2022
Rotenone induced olfactory deficit in Parkinson's disease rat model: The protective role of adenosine A2A receptors antagonist.
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Babatunde Bamidele Richard, Adeyeye Timileyin Adewumi, Johnson Victoria Funmilayo, Shallie Philemon Dauda
Аннотация
BACKGROUND: Parkinson's disease is both a motor and non-motor disorder. Despite the non-motor being an intrinsic feature of PD, it has been poorly researched and understood in clinical practices; olfactory deficit is one of the first established non motor symptom and nearly all ∼90 % of sporadic PD cases are associated with olfactory dysfunction and there is inconsistency in various pharmacological approaches. Hence this study aimed to evaluate the impact of caffeine at the A2A receptors of the olfactory bulb of a rotenone rat model of Parkinson's disease.
MATERIALS AND METHODS: About 50 male Adult Wistar Rats were used for this study. The rats were randomly divided into five groups of 10 rats each as follows: Group A (vehicle; ethanol), Group B (rotenone 3 mg/kg, i.p), Group C (caffeine 30 mg/kg, i.p + rotenone 3 mg/kg, i.p), Group D (rotenone 3 mg/kg, i.p + caffeine 30 mg/kg, i.p), Group E (caffeine 30 mg/kg, i.p). The animals were subjected to neurobehavioral assay and sacrificed, and brains were excised, weighed, and processed histologically; appropriate sections were taken and processed. The photomicrographs, Morphometric and Statistical analysis was done using Omax led digital Microscope, Image J Software and Graph Pad Prism 7, respectively.
RESULTS: The results showed a significant decrease in body weight (P < 0.05), relative brain weight, mitral/tufted cells count, and high latency in food-seeking test in Rotenone treated groups. Histopathological presentations include degenerated concentric layers of Olfactory bulb, neuronal degeneration, distorted appearance, degenerated neuropile and vacuolation, all of which were abrogated/reversed following caffeine treatment.
CONCLUSION: In conclusion, this study was able to establish the neuroprotective and therapeutic candidature of caffeine acting via the A2A receptor to ameliorate or reverse the various pathological insults caused by rotenone administration.
MATERIALS AND METHODS: About 50 male Adult Wistar Rats were used for this study. The rats were randomly divided into five groups of 10 rats each as follows: Group A (vehicle; ethanol), Group B (rotenone 3 mg/kg, i.p), Group C (caffeine 30 mg/kg, i.p + rotenone 3 mg/kg, i.p), Group D (rotenone 3 mg/kg, i.p + caffeine 30 mg/kg, i.p), Group E (caffeine 30 mg/kg, i.p). The animals were subjected to neurobehavioral assay and sacrificed, and brains were excised, weighed, and processed histologically; appropriate sections were taken and processed. The photomicrographs, Morphometric and Statistical analysis was done using Omax led digital Microscope, Image J Software and Graph Pad Prism 7, respectively.
RESULTS: The results showed a significant decrease in body weight (P < 0.05), relative brain weight, mitral/tufted cells count, and high latency in food-seeking test in Rotenone treated groups. Histopathological presentations include degenerated concentric layers of Olfactory bulb, neuronal degeneration, distorted appearance, degenerated neuropile and vacuolation, all of which were abrogated/reversed following caffeine treatment.
CONCLUSION: In conclusion, this study was able to establish the neuroprotective and therapeutic candidature of caffeine acting via the A2A receptor to ameliorate or reverse the various pathological insults caused by rotenone administration.