Citation

Pitcher JB, Riley AM, Doeltgen SH, Kurylowicz L, Rothwell JC, McAllister SM, Smith AE, Clow A, Kennaway DJ, Ridding MC. J. Neurosci. 2012; 32(46): 16410-16416.

Affiliation

Robinson Institute, School of Paediatrics and Reproductive Health, University of Adelaide, Adelaide 5005, Australia, UCL Institute of Neurology, Queen Square, London WC1N 3BG, United Kingdom, and Department of Psychology, University of Westminster, London W1BN 2UW, United Kingdom.

Copyright

(Copyright © 2012, Society for Neuroscience)

DOI

10.1523/JNEUROSCI.3079-12.2012

PMID

23152623

Abstract

Preterm-born children commonly experience motor, cognitive, and learning difficulties that may be accompanied by altered brain microstructure, connectivity, and neurochemistry. However, the mechanisms linking the altered neurophysiology with the behavioral outcomes are unknown. Here we provide the first physiological evidence that human adolescents born preterm at or before 37 weeks of completed gestation have a significantly reduced capacity for cortical neuroplasticity, the key overall mechanism underlying learning and memory. We examined motor cortex neuroplasticity in three groups of adolescents who were born after gestations of ≤32 completed weeks (early preterm), 33-37 weeks (late preterm), and 38-41 weeks (term) using a noninvasive transcranial magnetic brain stimulation technique to induce long-term depression (LTD)-like neuroplasticity. Compared with term-born adolescents, both early and late preterm adolescents had reduced LTD-like neuroplasticity in response to brain stimulation that was also associated with low salivary cortisol levels. We also compared neuroplasticity in term-born adolescents with that in term-born young adults, finding that the motor cortex retains a relatively enhanced neuroplastic capacity in adolescence. These findings provide a possible mechanistic link between the altered brain physiology of preterm birth and the subsequent associated behavioral deficits, particularly in learning and memory. They also suggest that altered hypothalamic-pituitary-adrenal axis function due to preterm birth may be a significant modulator of this altered neuroplasticity. This latter finding may offer options in the development of possible therapeutic interventions.

Language: en