Immune-mediated central nervous system (CNS) diseases triggered by Group A ß-haemolytic streptococcal (GABHS) infections include movement disorders associated with psychiatric disturbances. A pathogenic role of GABHS infections has been proposed for a subgroup of paediatric patients affected by tic disorders and/or obsessive-compulsive disorder, which was denominated Paediatric Autoimmune Neuropsychiatric Disorders Associated with Streptococcal Infection (PANDAS). An autoantibody-mediated mechanism has been proposed to mediate the full spectrum of these disorders. Serum anti-neuronal antibodies targeting a group of glycolytic enzymes, pyruvate kinase (PK), enolase and aldolase C, ubiquitously expressed in the CNS, were demonstrated in children with tics and obsessive-compulsive symptoms the onset of which was temporally linked to GABHS infections. PK is a good candidate for the "molecular mimicry" between human brain and GABHS . To explore the influences on neurons of the PK serum autoantibodies from PANDA patients, here we investigate, in mouse brain, the physical association of PK with the Kir6.1 and Kir6.2 subunits of the ATP-sensitive potassium channels. We show that strong anti-PK positive sera recognise the PK/Kir6.1 association in CNS. Our results allow to hypothesize that the anti-PK autoantibodies can perturb the macromolecular protein complex of KATP channels within the CNS and could affect neuronal excitability.