Neurobiology of speech and language has previously been studied in the KE family, in which half of the members have severe impairment in both speech and language. The gene responsible for the phenotype was mapped to chromosome 7q31 and identified as the FOXP2 gene, coding for a transcription factor containing a polyglutamine tract and a forkhead DNA-binding domain. Because of linkage studies implicating 7q31 in autism, where language impairment is a component of the disorder, and in specific language impairment, FOXP2 has also been considered as a potential susceptibility locus for the language deficits in autism and͞or specific language impairment. In this study, we characterized mice with a disruption in the murine

The present study was conducted to determine whether cognitive impairments in adult rats treated with cocaine during adolescence demonstrated in previous investigations extend to tests of object discrimination learning. Accordingly, 30-day-old male Long-Evans rats were injected subcutaneously with either 10 or 20 mg/kg cocaine or received control injections of saline for 7-8 consecutive days. An extended abstinence period was then introduced (mean = 70.7 ± 9.8 days) before subjects, who were now young adults (mean = 106.3 ± 10.2 days old), were assessed for acquisition of a two-choice object discrimination task. Using a correctional learning procedure conducted in a water maze, subjects were trained (eight trials per day for 10 days) to approach one of two multi-dimentional 'junk' objects. Although all animals acquired the discrimination to a reasonable extent, cocaine-treated subjects exhibited lower percentages of correct choices over the course of training (10 mg/kg = 59.6 ± 7.2% and 20 mg/kg = 59.4 ± 4.9%) relative to the saline control group (67.5 ± 4.9%). Further analyses revealed that saline-treated subjects acquired proficient discrimination performance earlier during the course of training, achieving an approximate 72% performance rate after only 3 days of training. This was in contrast to the two cocaine-treated groups needing 7 days of training to achieve comparable levels of performance. In addition, saline-treated subjects required significantly fewer trials (20.8 ± 8.9) than either cocaine-treated group (10 mg/kg = 52.2 ± 11.9 and 20 mg/kg = 63.3 ± 8.7) to reach an 87.5% correct response criterion (i.e. 7-correct-out-of-8-consecutive-trials) and performed at a higher above-chance level (13.5%) than either cocaine-treated group (3.6% and 5.3% for the 10 and 20 mg/kg cocaine groups, respectively). These findings demonstrate the existence of cognitive impairments in adulthood subsequent to cocaine exposure during adolescence despite a prolonged drug-free interval. Speculation regarding the neurobiological basis for this effect, especially with regard to alterations to prefrontal circuitry, is provided.