Nicotinic stimulation produces multiple forms of increased glutamatergic synaptic transmission - PubMed (original) (raw)

The nicotine-induced seconds-scale increase in mEPSC frequency has the pharmacology of α7-containing nAChRs and requires external calcium. A, A specific inhibitor of α7-containing nAChRs, 5 n

m

MLA, completely blocked the nicotine-induced currents (0.5 m

m

nic, solid bars) and prevented the mEPSCs that followed the nicotinic currents. B, Nicotinic currents were inhibited completely by 0.5 n

m

MLA (solid bar), but those currents recovered after being washed. The time course for inhibition and recovery of the nicotinic currents is shown (n = 4 neurons, ± SEM). The peak nAChR currents before MLA treatment were normalized to one to average currents from different neurons. C, In a solution containing 5 m

m

Ca2+, the frequency of mEPSCs increased after nicotinic currents were activated (0.5 m

m

,solid bar). In the same cell when the Ca2+ was absent (0 m

m

Ca2+), nicotine applications (solid bar) did not increase mEPSC frequency. D, In Ca2+-free and 5 m

m

Ca2+ solutions, the frequency of mEPSCs was measured in the same neurons (n = 4) immediately after nicotine-induced currents. The frequency of mEPSCs before nicotine was applied was normalized to one to combine results from different neurons. The frequency of mEPSCs increased only after nicotinic currents that were activated in the Ca2+-containing solution.