No abstract

Preterm infants are exposed to many stressors while in the neonatal intensive care unit including pain and reduced maternal care. Both stressors can have a profound negative impact on brain development, and the present study sought to investigate some of the biological mechanisms underlying this phenomenon. Rat pups underwent a series of repetitive needle pokes and/or reduced maternal care through a novel tea‐ball infuser encapsulation model during the first four days of life. On postnatal day four, pups were sacrificed and serum was analyzed for corticosterone, while brains were tested for various neurotransmitters and brain metabolites through magnetic resonance spectroscopy. We found that exposure to maternal isolation and neonatal pain produced an increase in serum corticosterone but decreased glutamate levels in the hippocampus and frontal cortex. These alterations in stress responding and neurochemistry in response to the early‐life stressors may help explain some of the negative outcomes seen in preterm infants.

Preterm infants often spend a significant amount of time in the neonatal intensive care unit (NICU) where they are exposed to many stressors including pain and reduced maternal care. These early‐life stressful experiences can have negative consequences on brain maturation during the neonatal period; however, less is known about the long‐term cognitive and affective outcomes. Thus, this study was conducted to investigate the impact of neonatal pain and reduced maternal care on adult behavior and HPA axis reactivity in an animal model. Male and female rats underwent a series of repetitive needle pokes and/or reduced maternal care (through a novel tea ball infuser encapsulation method) during the first 4 days of life and were then assessed in a battery of behavioral tests as adults. We found that early‐life pain enhanced spatial learning independent of the animal's sex, but altered HPA recovery from an acute stressor in females only. Moreover, reduced maternal care altered long‐term spatial memory and reversal learning in males. These findings indicate that neonatal stressors have unique sex‐dependent long‐term biobehavioral effects in rodents. Continued examination of the behavioral consequences of these stressors may help explain varying vulnerability and resiliency in preterm infants who experienced early stress in the NICU.

During adolescence, the brain continues to undergo vital developmental processes. In turn, complex behavioral and cognitive skills emerge. Unfortunately, neurobiological development during adolescence can be influenced by environmental factors such as drug exposure. Engaging in drug use during adolescence has been a long-standing health concern, especially how it predicts or relates to drug using behavior later in life. However, recent findings suggest that other behavioral domains, such as learning and memory, are also vulnerable to adolescent drug use. Moreover, it is becoming increasingly apparent that deficits in learning and memory following adolescent drug use endure into adulthood, well after drug exposure has subsided. Although persistent effects suggest an interaction between drug exposure and ongoing development during adolescence, the exact acute and long-term consequences of adolescent drug exposure on substrates of learning and memory are not fully understood. Thus, this review will summarize human and animal findings on the enduring cognitive deficits due to adolescent drug exposure. Moreover, due to the fact that adolescents are more likely to consume drugs of abuse legally available to adults, this review will focus on alcohol, nicotine, and marijuana. Further, given the critical role of the frontal cortex and hippocampus in various learning and memory domains, the impact adolescent use of the previous listed drugs on the neurobiology within these regions will also be discussed.