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Lee, Phil; Kim, Jieun; Choi, In‐Young; Pal, Ranu; Hui, Dongwei; Marcario, Joanne K.; Michaelis, Mary L.; Michaelis, Elias K.
Journal of neurochemistry, 20/May , Letnik: 168, Številka: 5Journal Article
The excitatory neurotransmitter glutamate has a role in neuronal migration and process elongation in the central nervous system (CNS). The effects of chronic glutamate hyperactivity on vesicular and protein transport within CNS neurons, that is, processes necessary for neurite growth, have not been examined previously. In this study, we measured the effects of lifelong hyperactivity of glutamate neurotransmission on axoplasmic transport in CNS neurons. We compared wild‐type (wt) to transgenic (Tg) mice over‐expressing the glutamate dehydrogenase gene Glud1 in CNS neurons and exhibiting increases in glutamate transmitter formation, release, and synaptic activation in brain throughout the lifespan. We found that Glud1 Tg as compared with wt mice exhibited increases in the rate of anterograde axoplasmic transport in neurons of the hippocampus measured in brain slices ex vivo, and in olfactory neurons measured in vivo. We also showed that the in vitro pharmacologic activation of glutamate synapses in wt mice led to moderate increases in axoplasmic transport, while exposure to selective inhibitors of ion channel forming glutamate receptors very significantly suppressed anterograde transport, suggesting a link between synaptic glutamate receptor activation and axoplasmic transport. Finally, axoplasmic transport in olfactory neurons of Tg mice in vivo was partially inhibited following 14‐day intake of ethanol, a known suppressor of axoplasmic transport and of glutamate neurotransmission. The same was true for transport in hippocampal neurons in slices from Glud1 Tg mice exposed to ethanol for 2 h ex vivo. In conclusion, endogenous activity at glutamate synapses regulates and glutamate synaptic hyperactivity increases intraneuronal transport rates in CNS neurons. Lee et al. present an ex vivo and in vivo study of axonal transport in a transgenic mouse model of chronic glutamate neurotransmission hyperactivity, which over‐expresses the glutamate dehydrogenase gene (Glud1) in CNS neurons and exhibits increased glutamate transmitter formation, release, and synaptic activation. Glud1 versus wild‐type mice exhibited an increased rate of anterograde axoplasmic transport in hippocampal neurons in ex vivo and in olfactory neurons in vivo. Pharmacologic experiments in brain slices suggested a link between synaptic glutamate receptor activation and axoplasmic transport. Overall, the study demonstrates that endogenous Glu neurotransmission hyperactivity enhances anterograde axonal transport rates in the CNS neurons.
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