Pharmacological strategies that target GABAergic interneurons that may correct dysfunctional inhibitory feedback within corticolimbic circuits are also being investigated. Specifically, parvalbumin+ cells are now also being explored as a novel approach to repairing DLPFC neural circuitry and improving the cognitive symptom domain in schizophrenia (Clinicaltrials.gov Identifier: NCT03164876). Parvalbumin+ cells innervate multiple pyramidal cells and contain lower mRNA for parvalbumin and GAD67 in those with schizophrenia (124) and reduced expression of the potassium channel KCNS3 gene which encodes the Kv9.3 potassium channel α subunit and is essential for control over its fast-spiking abilities (197). Inhibitory parvalbumin+ interneurons contribute to the cognitive deficits in schizophrenia (115) and in unmedicated patients with the illness. Kv3.1 channels located on parvalbumin+ cells are reduced by disease and then normalized with the use of antipsychotic drugs (198). Dr. Charles Large (Autifony Therapeutics) has recently completed a phase I study of AUT00206, a Kv3.1 channel modulator in healthy volunteers (Clinicaltrials.gov Identifer: NCT02589262) and in collaboration with Dr. Oliver Howes (King's College London), his team are currently recruiting for a continued phase I study to explore its safety, tolerability, pharmacokinetics and treatment effects on relevant biomarkers in patients with schizophrenia (Clinicaltrials.gov Identifier: NCT03164876).