Residual performance impairments in adult rats trained on an object discrimination task subsequent to cocaine administration during adolescence.

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.