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Figure 2 | BMC Neuroscience

Figure 2

From: Death Associated Protein Kinase (DAPK) -mediated neurodegenerative mechanisms in nematode excitotoxicity

Figure 2

The effect of dapk-1 does not correlate with several proposed mechanisms. A) Aldicarb assay measures the overall activity of the common mechanism of synaptic vesicle release. Complexin (cpx-1) mutant is used as example of an oversensitive mutant (where synaptic release is exaggerate), while rab-3 serves as an example of aldicarb resistant mutant (where synaptic release is abnormally low). dapk-1 mutants do not show oversensitivity or resistance, suggesting their level of synaptic release is roughly normal. B) Duration of forward runs during spontaneous mobility is a sensitive reporter of the overall strength of Glu synapses that control this parameter. Even small changes in the activity or number of GluRs typically modify this behavior. dapk-1 mutants are not different from normal counterparts in either a WT background, in an excessive Glu stimulation background (glt-3), or in the sensitized background (nuIs5) used in our excitotoxicity model. These three conditions by themselves do not cause excessive command neuron loss, a loss that might otherwise render the assay uninformative as it is suppressible by dapk-1. C) A mutation in the gene encoding the DANGER-related protein MAB-21 does not affect nematode excitotoxicity. D) A mutation in the gene encoding the nematode homolog of CaMKK does not affect nematode excitotoxicity.

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