Fig. 6: Genetic ablation of Chrna7 prevents HNK-mediated synaptic and nuclear effects leaving KET-mediated effects unaffected. | Translational Psychiatry

Fig. 6: Genetic ablation of Chrna7 prevents HNK-mediated synaptic and nuclear effects leaving KET-mediated effects unaffected.

From: Hydroxynorketamine, but not ketamine, acts via α7 nicotinic acetylcholine receptor to control presynaptic function and gene expression

Fig. 6

A Representative images showing KCl-induced depolarization-driven Syt1 Ab-uptake IF (magenta) in VGLUT1-positive (green) synapses in DIV18 cortical neurons treated with vehicle, KET or HNK. The cultures were prepared from Chrna7 floxed animals and infected with a virus that expressed control (∆CRE) and or active cre recombinase (CRE) leading to a genetic deletion of α7nAchRs. B Quantification of Syt1 Ab-uptake from experiment in (A). C Representative pseudocolour-gradient images of pSer133CREB nuclear IF in neurons treated with vehicle, KET and HNK, green marks expression of ∆CRE and CRE in cell nuclei. D Quantification of pSer133CREB nuclear IF from C. Significance was assessed using two-way ANOVA with Holm-Šídák’s multiple comparison test and depicted as ****p < 0.0001. Sample size (in bracket) corresponds to the number of independently treated coverslips. Cells originated from two to three independent culture preparations. Scale bar is 5 µm in (A) and 10 µm in (C).

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