Figure 1.

Direct excitation of medial prefrontal layer VI pyramidal neurons by acetylcholine is dependent on the nicotinic receptor α5 subunit. A, The peak inward current response to 10 s bath application of 1 mm acetylcholine was significantly greater in neurons from wild-type mice expressing the α5 subunit (WT) compared with neurons from mice in which the α5 subunit had been genetically deleted (α5^−/−) (two-tailed unpaired t test, *p < 0.0001). Values are mean ± 1 SEM. B, Voltage-clamp traces showing typical responses in one neuron each from a WT and an α5^−/− mouse. For neurons of both genotypes, inward current responses to acetylcholine were resistant to 10 min pretreatment with TTX (2 μm) to block action potentials and were significantly reduced by 10 min pretreatment with the α4β2* nicotinic receptor competitive inhibitor DHβE (3 μm), indicating that responses were mediated by α4β2* receptors located directly on the recorded neurons.