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Stress rapidly increases alpha 1d adrenergic receptor mRNA in the rat dentate gyrus

  • Serge Campeau
  • , Tara J. Nyhuis
  • , Elisabeth M. Kryskow
  • , Cher V. Masini
  • , Jessica A. Babb
  • , Sarah K. Sasse
  • , Benjamin N. Greenwood
  • , Monika Fleshner
  • , Heidi E.W. Day

Producción científica: Article › revisión exhaustiva

17 Citas (Scopus)

Resumen

The hippocampal formation is a highly plastic brain region that is sensitive to stress. It receives extensive noradrenergic projections, and noradrenaline is released in the hippocampus in response to stressor exposure. The hippocampus expresses particularly high levels of the α1D adrenergic receptor (ADR) and we have previously demonstrated that α1d ADR mRNA expression in the rat hippocampus is modulated by corticosterone. One of the defining features of a stress response is activation of the hypothalamic pituitary adrenal (HPA) axis, resulting in the release of corticosterone from the adrenal glands. However, the effect of stress on hippocampal expression of α1d ADR mRNA has not been determined. In this study, male rats were exposed to inescapable tail shock, loud noise or restraint, and the effect on α1d ADR mRNA expression in the hippocampus was determined by semi-quantitative in situ hybridization. All three stressors resulted in a rapid upregulation of α1d ADR mRNA in the dentate gyrus, with expression peaking at approximately 90 min after the start of the stressor. Physical activity has previously been reported to counteract some of the effects of stress that occur within the dentate gyrus. However, 6 weeks of voluntary wheel running in rats did not prevent the restraint stress-induced increase in α1d ADR mRNA expression in the dentate gyrus. Although the function of the α1D ADR in the dentate gyrus is not known, these data provide further evidence for a close interaction between stress and the noradrenergic system in the hippocampus.

Idioma originalEnglish
Páginas (desde-hasta)109-118
Número de páginas10
PublicaciónBrain Research
Volumen1323
DOI
EstadoPublished - abr 6 2010

Financiación

These studies were supported by R01 MH-067988 (HD), a NARSAD Young Investigator Award (HD) and R01 MH-068283 (MF). The authors would like to thank Dr. Robert Spencer (University of Colorado, Psychology and Neuroscience Department) for the use of his rat restrainers in Experiments 2 and 4.

FinanciadoresNúmero del financiador
National Institute of Mental HealthR01MH068283
National Alliance for Research on Schizophrenia and DepressionR01 MH-068283

    ASJC Scopus subject areas

    • General Neuroscience
    • Molecular Biology
    • Clinical Neurology
    • Developmental Biology

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