In LHX6 knockout mice, the tangential migration of GABA neuron progenitors from the MGE to the cortex was delayed and the subsequent radial migration of these progenitors within the cortical plate appeared to be disturbed, resulting in an abnormal cortical distribution of GABA neurons. The knockout mice also exhibited severely reduced numbers of PV and SST neurons, indicating that LHX6 is important for the phenotypic differentiation of these neurons. Furthermore, the persistent expression of LHX6 after development suggests its role in the maintenance of physiological and morphological properties of mature PV and SST neurons. We recently reported decreased LHX6 mRNA levels in the PFC of subjects with schizophrenia. Interestingly, a subset of schizophrenia subjects was identified by the presence of consistent deficits in LHX6, GAD67, PV and SST mRNAs, suggesting that LHX6 deficits may affect development and/or maintenance of GABAergic phenotype in PV and SST neurons in these subjects. Identifying genes that are regulated by LHX6 may help MLN4924 inform molecular mechanisms of the alterations in PV and SST neurons in schizophrenia. KCNS3 mRNA, which is expressed selectively by the majority of PV neurons in the PFC, encodes Kv9.3 voltage-gated K+ channel modulatory a-subunit. Modulatory a-subunits do not assemble into homomeric channels, but selectively associate with delayed rectifier Kv2 subunits to form functional heteromeric channels. In heterologous expression systems, Kv9.3 subunits coassemble with Kv2.1 subunits, with a 1:3 subunit stoichiometry, Kv2.1/Kv9.3 channels. Kv2.1 immunoreactivity has been detected in the soma and dendrites of most cortical neurons, including PV neurons. Therefore, KCNS3 mRNA expression in PV neurons indicates the presence of heteromeric Kv2.1/Kv9.3 channels in the soma and dendrites of these neurons. Compared with homomeric Kv2.1 channels, Kv2.1/Kv9.3 channels have modified characteristics, such as larger single channel conductance, faster activation, slower deactivation and inactivation, and shifted steady-state activation and inactivation curves towards more negative values by those generated by excitatory synaptic inputs. Interestingly, a recent electrophysiological and modeling study demonstrated that voltage-dependent K+ currents activated by excitatory postsynaptic potentials in PV neuron dendrites shorten both the time course of EPSPs and the time window for the summation of multiple EPSPs produced by excitatory synaptic inputs at spatially separated dendritic sites. Therefore, the presence of Kv9.3 subunits might contribute to the fast excitatory synaptic transmission and precise detection of coincident synaptic inputs in PV neurons. Kv3 channels, which are essential for the ability of PV neurons to fire a train of short-duration action potentials at high frequencies, were also implicated in fast EPSPs and narrow time window of EPSP summation in PV neurons. However, Kv3 channels are activated only by membrane potentials more positive than approximately 210 mV that can be attained during action potentials, but not synaptic EPSPs. Therefore, Kv3 channels are unlikely to play a central role in regulating time course and summation of EPSPs in PV neurons. PV neurons play an essential role in the generation of cortical gamma oscillations that are important for cognitive processes. Because fast excitatory synaptic transmission and precise coincident detection in PV neurons have been implicated in the generation of gamma oscillations, our finding of selective KCNS3 expression in PV neurons suggests that KCNS3 encoded Kv9.3 subunits might contribute to the generation of gam.