Fig. 2.

In young postnatal mice, excitation of CA1 pyramidal neurons by ACh is mediated by postsynaptic α4β2* nicotinic receptors. All recordings were made using mice aged postnatal day 5–10 in the continuous presence of 200 nM atropine to block muscarinic acetylcholine receptors and 10 nM MLA to block α7 subunit-containing nicotinic acetylcholine receptors. A: current responses were not desensitized by repeated application of 1 mM ACh for 15 s (paired t-test, P = 0.8). B: similarly, current responses to 1 mM ACh (15 s) were not significantly affected by 10-min pretreatment with the following synaptic blockers: 2 μM TTX, 20 μM CNQX, 50 μM APV, and 10 μM bicuculline (P = 0.8). C: current responses to 1 mM ACh (15 s) were significantly reduced by 10-min pretreatment with the α4β2* nicotinic receptor competitive antagonist dihydro-β-erythroidine (DHβE; 3 μM) (*P = 0.002). D: for neurons induced to fire action potentials at 1 Hz by positive current injection, the increase in firing frequency following application of 1 mM ACh (15 s) was significantly reduced by 10-min pretreatment with 3 μM DHβE (*P < 0.0001). All values are means ± SE. Representative voltage-clamp or current-clamp traces are shown at right for 1 neuron from each pharmacological experiment with ACh application marked by gray horizontal bars.