SCG neurons possess nicotinic ACh receptors (nAChRs) comprising a3 (with b4 and/or b2) or a7 subunits. We previously demonstrated, by immuno-electron microscopy, a significant decrease in postsynaptic apparatus immunopositive for a3 subunit in the SCG of dystrophin-lacking mdx mice compared with the WT, but not in that for a7 subunit. This suggested that dystrophin is necessary for stabilizing the a3-nAChRs at synapses. We report a functional characterization of the nicotinic response in WT and mdx mouse SCG neurons, with patch clamp recordings. Inward currents were elicited either by non-selective agonists, such as acetylcholine and nicotine, and by the selective a7 agonist PHA-543613. We show that the same dose of non-selective agonists elicited a smaller current response in mdx mouse neurons respect to the wild-type neurons (40 ± 13 %, for nic; 25 ± 11 %, for ACh), while currents induced by PHA were similar, consistently with a significant difference in current decay, with a fast desensitizing component when agonists were applied onto mdx neurons. Moreover, while on WT neurons currents elicited by nic/ACh were slightly sensitive to low doses of methyllycaconitine, with partial block of the current to 74 ±4% of the control, mdx mouse neurons displayed a stronger sensitivity to MLA (46±3%). The present results suggest a substantial decrease in the nicotinc current response on neurons lacking dystrophin.