1. Two part question from the Appleby paper: The authors state that \"we found t
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Question
1. Two part question from the Appleby paper: The authors state that "we found that transient synaptic activation of NMDARs in hippocampal neurons leads to an increase in native GluA1-containing, but not GluA2-containing AMPAR surface expression, and that this effect is dependent on CaMKII activation." We can assume that the mechanism by which CaMKII is being activated is due to an influx of Ca2+ via NMDA receptor activation.
a. If blockade of the NMDA receptors on the hippocampal neurons had not affected CaMKII autophosphorylation, what might the next logical experiment have been to determine the mechanism for CaMKII activation.
b. Why would increasing the proportion of GluA1 subunits in the AMPA receptors contribute to LTP?
Explanation / Answer
Part-a: The next logical experiment is "FURA-2-AM- dye labeled calcium imaging" to determine the mechanism for CaMKII activation followed by induced cell death due to high intracellular calcium. This calcium imaging along with flow cytometry in the presence of "oxygen deprivation condition" and oxygenated conditions can be a good detector of blockade of the NMDA receptors (in the presence of MK-801, a NMDA receptor blocker) on the hippocampal neurons had not affected CaMKII autophosphorylation
The morphological examination of NMDA receptors in the hippocampal neurons can be done via the labeling of NR1 subunit, through immunohistochemistry because NR1 is obligaotry subunits of NMDA receptors
Part-b:
The higher the proportion of GluA1 subunits in the AMPA receptors contribute to LTP (long term potentiation) because glutamate the excitatory neurotransmitter that promote "Na+" influx into the cells followed by downstream signal transduction events for gene expression to promote "synaptic plasticity" or memory functions
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