The M-current contributes to the maintenance of resting membrane potential and underpins the adaptation properties of dissociated neonatal rat intracardiac ganglion (ICG) neurones. However, studies using rat dissociated ICG neurones have shown that the expression of the hyperpolarization-activated (I_h) and inward rectifier K⁺ (I_K(IR)) currents and ATP-sensitive K⁺ conductance (I_K(ATP)) all show changes during postnatal development (Adams & Cuevas, 2004). We have used a wholemount preparation and intracellular recording techniques to investigate the action of M-current blockers on ICG neurones. Membrane potential (E_m), input resistance (R_in), afterhyperpolarization (AHP) amplitude and duration, and synaptic responses were measured. We studied two time points during postnatal development: neonatal (P2-5) and adult (≥ 42 days) and compared the actions of the wide-spectrum K⁺ channel blocker Ba²⁺ (which at 1mM blocks the M-channel), the selective M-channel blocker linopirdine (10 μM) and the M1 muscarinic antagonist oxotremorine M (oxo-M, 10 μM). Ba²⁺ and linopirdine significantly depolarized E_m by ~6-8 mV in both neonates (n=10, p=0.003; n =3, p=0.04, paired t test) and adult ICG neurons (n=13, p=0.0003; n=4, p=0.01). Oxo-M had no significant effect on E_m. The action of these agents on R_in was inconsistent. Ba²⁺ produced a significant increase in R_in for both neonatal and ICG neurones (to 135 ± 33, and 178% ± 63 SD of control values). Linopirdine had no significant action and oxo-M increased R_in significantly in adult (to 134% ± 37, n=6) but not in neonatal ICG neurones. Ba²⁺ increased the duration of the AHP and oxo-M increased the AHP amplitude in neonatal ICG neurones, linopirdine had no action on AHP parameters. Ba²⁺ and linopridine also switched evoked firing patterns. In control conditions the discharge was predominantly phasic (neonates, 77%; adults, 90%). Ba²⁺ altered discharge to multiply adapting and tonic (100 and 57% for neonates and adults, respectively). Linopirdine caused a similar shift in discharge activity. In contrast, oxo-M had little impact on discharge pattern in either neonate or adult ICG neurones (n=4, 6). The effects of Ba²⁺ and linopirdine on synaptic transmission were also investigated. Trains of 20 stimuli at 5, 10, 20 and 50 Hz were applied to the pre-ganglionic nerve process. Ba²⁺ and linopirdine had no effect on the fraction of successful post-ganglionic action potentials discharged. These M channel antagonists have distinct actions on membrane properties and evoked firing patterns of rat ICG neurones, some of which change with postnatal development. The M channel appears to have little functional role in synaptic transmission in the ICG.