Figure 6.

Increased cytosolic calcium ([Ca²⁺]_i ) in response to nicotinic receptor activation is greatly attenuated by methyllycaconitine, but not α-conotoxin MII in retinal ganglion cell (RGC)-committed precursors. The effect of pharmacological inhibition of the α4β2 and α6β2 nicotinic acetylcholine receptors (AChRs) with methyllycaconitine (MLA, 100 nmoles/l) and of the α3β2 nicotinic AChR with α-conotoxin MII (α-CT, 100 nmoles/l) on the rise in [Ca²⁺]_i triggered by nicotine (2 mM) was assessed. A: Methyllycaconitine caused a substantial reduction in the [Ca²⁺]_i rise (n=99 cells from 3 experiments) in comparison to stimulation with nicotine alone (n=113 cells from 3 experiments , ***p<0.001). B: α-conotoxin MII did not significantly affect the rise in [Ca²⁺]_i after stimulation with nicotine (n=254 cells from 4 experiments) in comparison to stimulation with nicotine alone (n=290 cells from 4 experiments).