摘要
Traditionally, ketamine was considered useful as a dissociative anesthetic. More recently, ketamine has been examined for its effects as a fast-acting antidepressant, for treatment-resistant depression, and as a non-opiate treatment of chronic pain. Unfortunately, ketamine has enjoyed popularity as a recreational drug among both adolescents and young adults. While some research suggests the use of this drug during neurodevelopment is not without consequence, relatively little work has been conducted to examine the chronic effects of ketamine on the adolescent brain at different stages of neural development. Using a rodent model of development, we probed the effects of early adolescent exposure to ketamine. Between postnatal days 22 to 40, a period comprising early to mid-adolescence, rats were exposed to one of two doses of ketamine or saline. Beginning at 90 days of age and drug free for 50 days, a series of neuropsychological assessments were employed to examine general activity, spatial navigation, as well as nonspatial response learning. Contrary to prediction, except for differences in general activity levels, no spatial or nonspatial impairments were found among the drug- and saline-treated animals. The present results are considered in light of ketamine-associated effects found in a related study with older adolescent rats and the role of drug exposure during different points in adolescent brain development.
Traditionally, ketamine was considered useful as a dissociative anesthetic. More recently, ketamine has been examined for its effects as a fast-acting antidepressant, for treatment-resistant depression, and as a non-opiate treatment of chronic pain. Unfortunately, ketamine has enjoyed popularity as a recreational drug among both adolescents and young adults. While some research suggests the use of this drug during neurodevelopment is not without consequence, relatively little work has been conducted to examine the chronic effects of ketamine on the adolescent brain at different stages of neural development. Using a rodent model of development, we probed the effects of early adolescent exposure to ketamine. Between postnatal days 22 to 40, a period comprising early to mid-adolescence, rats were exposed to one of two doses of ketamine or saline. Beginning at 90 days of age and drug free for 50 days, a series of neuropsychological assessments were employed to examine general activity, spatial navigation, as well as nonspatial response learning. Contrary to prediction, except for differences in general activity levels, no spatial or nonspatial impairments were found among the drug- and saline-treated animals. The present results are considered in light of ketamine-associated effects found in a related study with older adolescent rats and the role of drug exposure during different points in adolescent brain development.
