The M-current is a non-inactivating potassium current that plays a critical role in regulating neuronal excitability. Neuronal M-channels are composed of KCNQ2-5 (Kv 7.2-7.5) subunits (Wang et al. 1998; Shah et al. 2002; Hadley et al. 2003). Recent evidence indicates that KCNQ subunits are expressed in hippocampal CA1 dendrites (Roche et al. 2002; Shah et al. 2002) but their functional role therein is unknown. We have used pharmacological tools to assess if functional M-currents are present in CA1 pyramidal cell dendrites and how they affect dendritic excitability. Whole-cell current-clamp recordings were obtained from the somata and dendrites of visually identified CA1 pyramidal neurones in hippocampal slices obtained from 5-7 week old Sprague-Dawley rats (see Shah et al. 2004). Bath application of the KCNQ channel opener retigabine (10 μM) induced a significant hyperpolarization (3.0 ± 0.3 mV, n=9, p<0.05; mean ± s.e.m) of the somatic resting membrane potential (RMP) and a substantial decrease in the somatic input resistance (RN) when measured positive to -70 mV. Hence, greater current was required to evoke action potentials. Conversely, the KCNQ channel blocker, linopirdine (10 μM) significantly depolarized somatic RMP (8.75 ± 1.9 mV, n=6, p < 0.05), enhanced RN and substantially reduced the current required to induce action potentials. In contrast, retigabine had little effect on dendritic RMP (1.4 ± 0.6 mV, n=8) or RN. Despite this, greater dendritic current injection was required to record action potentials in the dendrite in the presence of retigabine. Linopirdine did depolarize the dendritic RMP (4.3 ± 0.4 mV, n=3) but did not affect dendritic RN. Notwithstanding, more action potentials were recorded in the dendrite in the presence of linopirdine. To test for effects of M-current on subthreshold activity, effects of KCNQ channel modulators were assessed on single and repetitive somatic and dendritic simulated excitatory postsynaptic potentials (αEPSPs). Linopirdine significantly increased the amplitude and decay time constant of single somatic but not dendritic αEPSPs, by 41.8 ± 8.1% (n=6, p < 0.05) and 32.1 ± 12% (n=6, p<0.05) at –60 mV, respectively. It did not, however, modify the summation of a train of 5 αEPSPs evoked at 20 Hz or 40 Hz. Retigabine did not affect the amplitude of somatic or dendritic αEPSPs, but accelerated their decay and significantly reduced somatic αEPSP summation (% reduction = 47.2 ± 3.6%, n=8, p < 0.05, at –60 mV). From these observations it is concluded that M-channels are predominantly expressed in the soma/axon region (see Devaux et al. 2004), but that alterations of somatic M-current can, nonetheless, affect dendritic excitability.