The perirhinal cortex (PrhC) is critical for object recognition memory; however, information regarding the molecular mechanisms underlying this type of memory following repeated exposure to drugs of abuse during adolescence is unknown. To this end, adolescent or adult rats were exposed to cocaine from postnatal day (PND) 28 to PND 42 or PND 63 to PND 77, respectively. Two weeks later, rats were subjected to the cognitive test named Novel Object Recognition (NOR) test. We found that adolescent, but not adult, cocaine exposure caused a significant impairment in the NOR test, independently from changes in the stress response system. In adolescent saline-treated rats, NOR test up-regulated BDNF and its downstream signaling whereas a downregulation of the same pathway was observed in cocaine-treated rats together with a reduction of Arc/Arg3.1 and PSD95 expression, indicating reduced pro-cognitive structural adaptations in the PrhC. Of note, cocaine-treated adult rats correctly performed in the NOR test indicating intact recognition memory mechanisms, despite a significant cocaine-induced reduction of BDNF levels in the PrhC, suggesting that recognition memory is heavily dependent on BDNF during adolescence whereas during adulthood other mechanisms come into play.

周围神经皮层（PrhC）对于物体识别记忆至关重要。然而，有关青春期反复接触滥用药物后这种记忆基础的分子机制的信息尚不清楚。为此，青春期或成年大鼠分别从产后日（PND）28至PND 42或PND 63至PND 77暴露于可卡因。两周后，对大鼠进行名为“新对象识别”（NOR）测试的认知测试。我们发现，青少年（而非成人）可卡因暴露与压力反应系统的变化无关，在NOR测试中引起了显着损害。在青春期盐水治疗的大鼠中，NOR测试可上调BDNF及其下游信号传导，而在可卡因治疗的大鼠中则观察到同一途径的下调以及Arc / Arg3的降低。1和PSD95的表达，表明PrhC中减少的前认知结构适应。值得注意的是，尽管可卡因诱导的PrhC中BDNF水平显着降低，但可卡因治疗的成年大鼠在NOR测试中正确执行，表明其识别记忆机制完整，这表明青春期期间识别记忆严重依赖于BDNF，而成年期间其他机制参加进来。