Exploring the effects of β-N-methylamino-L-alanine on the GluN1/GluN2A NMDA receptor in Schmidtea mediteranea.

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Description

β-N-methylamino-L-alanine, known as BMAA, is a neurotoxin produced by several species of cyanobacteria and eukaryotic microorganisms such as diatoms and dinoflagellates. BMAA has been implicated in neurodegenerative diseases such as ALS, Parkinson’s disease, and Alzheimer’s disease. Because it is biomagnified through the food chain, accumulation occurs in its symbionts like cycad seeds and seafood, which can be ingested by humans and potentially result in neurological disease. There is evidence that BMAA is an N-methyl-D-aspartate (NMDA) receptor agonist. NMDA receptors are a family of L-glutamate receptors that play a critical role in learning and memory, and in inducing excitotoxicity in neurons. The role of BMAA in inducing motor neuronal death is not well understood. Schmidtea mediterranea (planarians) produce endogenous glutamate and express genes for glutamate receptors making them a desirable model for investigating the interaction between BMAA and NMDA receptors. Previous work suggested that BMAA exposure induced neuronal damage and, ultimately, death in planarians. The present study examined (1) the localization of NMDA receptors in Schmidtea mediterranea via in situ hybridization (2) the interaction between BMAA and NMDA receptors via RNAi and BMAA exposure trials.

Advisor

Dr. Ryan King, Biology

Publication Date

2023

Keywords

biology, BMAA, neurotoxin

Exploring the effects of β-N-methylamino-L-alanine on the GluN1/GluN2A NMDA receptor in Schmidtea mediteranea.
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