Targeted therapies for the treatment of CRC in the future. Group A b-hemolytic streptococcal infection can lead in susceptible individuals to the development of delayed nonsuppurative sequelae autoimmune disorders, such as acute poststreptococcal glomerulonephritis, streptococcal reactive arthritis and acute rheumatic fever. The autoimmune response can also target the central nervous system, leading to neurological and psychiatric disorders, such as Sydenham’s chorea, pediatric autoimmune neuropsychiatric disorders associated with streptococcus, obsessive-compulsive disorder, and Tourette’s syndrome. SC is the main neurological manifestation of ARF, appearing weeks to months after GAS infection, and is characterized by involuntary movements and neuropsychiatric disturbances, including obsessivecompulsive symptoms, tics, and emotional lability. Although the exact mechanism of pathogenesis in GAS-related neuropsychiatric disorders is not yet clear, it has been hypothesized that GAS infection induces the production of antibodies against GAS and neuronal determinants, through the process of molecular mimicry. It has been demonstrated that anti-GAS antibodies can bind to different brain determinants, and may consequently lead to increased altered neurotransmitter release, resulting in neuropsychiatric symptoms. There is some evidence suggesting that continued (+)-JQ1 Epigenetic Reader Domain inhibitor antibiotic treatment throughout childhood may prevent or decrease recurrences of SC and other GAS-related neuropsychiatric disorders. Yet current data are too scant to reach firm conclusions. Moreover, it is currently not clear whether the prophylactic action of antibiotics is achieved by preventing GAS reinfections or by the effects of antibiotics on other bacteria or if the effects may be directly on the brain. The aim of the present study was to assess the effects of antibiotic treatment in an animal model of GAS-related neuropsychiatric disorders. In this model, exposure of male Lewis rats to GAS antigen leads to a syndrome which resembles behavioral, pharmacological, immunological and neural characteristics of GAS-related neuropsychiatric disorders. More specifically, GAS-exposed rats show increased compulsive-like behavior and motor disturbances, which are attenuated by pharmacological agents used to treat the corresponding symptoms in human patients ; Immunologically, IgG in sera obtained from GASexposed rats demonstrates strong immunoreactivity to neural tissue, to D1 and D2 dopamine receptors and to 5-HT2a and 5-HT2c serotonin receptors, and activates calcium/ calmodulin dependent protein kinase II signaling, as has been found for IgG in sera obtained from SC and PANDAS patients ; Finally, dopamine and glutamate levels are altered in the frontal cortex and basal ganglia of GAS-exposed rats. The present study used our rat model to assess the behavioral and biochemical effects of treatment with the b-lactam antibiotic ampicillin. Rats were exposed to GAS extract or to adjuvants only, and treated with ampicillin. Additional groups of GAS-exposed and Control rats received regular drinking water. Motor abilities and compulsive- and depressive-like behaviors as well as the level of D1 and D2.