Self-destructive behavior in current society promotes a search for psychobiological factors underlying this epidemic. Perinatal brain plasticity increases the vulnerability to early adverse experiences, thus leading to abnormal development and behavior. Although several epidemiological investigations have correlated perinatal and neonatal complications with abnormal adult behavior, our understanding of the underlying mechanisms remains rudimentary. Models of early experience, such as repetitive pain, sepsis, or maternal separation in rodents and other species have noted multiple alterations in the adult brain, correlated with specific behavioral phenotypes depending on the timing and nature of the insult. The mechanisms mediating such changes in the neonatal brain have remained largely unexplored. We propose that lack of N-methyl-D-aspartate (NMDA) receptor activity from maternal separation and sensory isolation leads to increased apoptosis in multiple areas of the immature brain. On the other hand, exposure to repetitive pain may cause excessive NMDA/excitatory amino acid activation resulting in excitotoxic damage to developing neurons. These changes promote two distinct behavioral phenotypes characterized by increased anxiety, altered pain sensitivity, stress disorders, hyperactivity/attention deficit disorder, leading to impaired social skills and patterns of self-destructive behavior. The clinical important of these mechanisms lies in the prevention of early insults, effective treatment of neonatal pain and stress, and perhaps the discovery of novel therapeutic approaches that limit neuronal excitotoxicity or apoptosis.
Dr. K.S. Anand
Arkansas Children’s Hospital, S-431
800 Marshall Street
Little Rock, AR 72202-3591 (USA)
Tel. +1 501 320 1845, Fax +1 501 320 3188
Number of Print Pages : 14
Number of Figures : 3, Number of Tables : 1, Number of References : 147
Biology of the Neonate (Foetal and Neonatal Research)
Vol. 77, No. 2, Year 2000 (Cover Date: Released February 2000)
Journal Editor: J.P. Relier, Paris
ISSN: 0006–3126 (print), 1421–9727 (Online)
For additional information: http://www.karger.com/journals/bon
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