Differential effects of prenatal stress on the morphological maturation of hippocampal neurons.
The present study was designed to clarify an intensity-dependent effect of prenatal stress on the morphological development of hippocampal neurons in rats. In addition, the involvement of receptors for glucocorticoids, i.e. mineralocorticoid receptors and glucocorticoid receptors, in stress-induced changes in the morphology of hippocampal neurons was examined by an in vitro pharmacological approach. The effects of mild prenatal stress on neurogenesis and long-term potentiation in the hippocampus were also investigated in adult offspring. Prenatal stress affected the morphological development of the hippocampus in an intensity-dependent manner. Short-lasting, mild prenatal stress enhanced neonatal neurogenesis and differentiation of processes of hippocampal neurons, whereas long-lasting, severe stress impaired their morphology. Mineralocorticoid receptor was found to mediate enhancement of neurogenesis and differentiation of processes of cultured hippocampal neurons. In contrast, glucocorticoid receptor was involved in the suppression of their morphology. Short-lasting, mild prenatal stress, which has previously been shown to enhance learning performance in adult offspring, facilitated neurogenesis and long-term potentiation in the adult hippocampus. These findings suggest that prenatal stress has enhancing and suppressing effects on the development of hippocampal neurons depending on intensity, and that mineralocorticoid receptors and glucocorticoid receptors contribute to stress-induced morphological changes.
Fujioka
A
A
Department of Emergency and Critical Care Medicine, Yamaguchi University School of Medicine, 1-1-1 Minami-Kogushi, Ube, Yamaguchi 755-8505, Japan; Department of Neuroscience, Yamaguchi University School of Medicine, 1-1-1 Minami-Kogushi, Ube, Yamaguchi 755-8505, Japan.
Fujioka
T
T
Department of Emergency and Critical Care Medicine, Yamaguchi University School of Medicine, 1-1-1 Minami-Kogushi, Ube, Yamaguchi 755-8505, Japan; Department of Neuroscience, Yamaguchi University School of Medicine, 1-1-1 Minami-Kogushi, Ube, Yamaguchi 755-8505, Japan; Department of Clinical Research, Sanyo National Hospital, 685 Higashi-kiwa, Ube, Yamaguchi 755-0241, Japan. Electronic address: tfujioka@yamaguchi-u.ac.jp.
Ishida
Y
Y
Department of Neuroscience, Yamaguchi University School of Medicine, 1-1-1 Minami-Kogushi, Ube, Yamaguchi 755-8505, Japan.
Maekawa
T
T
Department of Emergency and Critical Care Medicine, Yamaguchi University School of Medicine, 1-1-1 Minami-Kogushi, Ube, Yamaguchi 755-8505, Japan.
Nakamura
S
S
Department of Neuroscience, Yamaguchi University School of Medicine, 1-1-1 Minami-Kogushi, Ube, Yamaguchi 755-8505, Japan. Electronic address: snaka@yamaguchi-u.ac.jp.
D000818:Animals; D001973:Bromodeoxyuridine / Q000378:metabolism; D002454:Cell Differentiation / Q000502:physiology*; D048429:Cell Size / Q000187:drug effects; D002478:Cells, Cultured; D004558:Electric Stimulation / Q000379:methods; D004622:Embryo, Mammalian; D005260:Female; D005938:Glucocorticoids / Q000494:pharmacology; D006624:Hippocampus / Q000196:embryology / Q000473:pathology* / Q000503:physiopathology; D007150:Immunohistochemistry / Q000379:methods; D017774:Long-Term Potentiation / Q000187:drug effects / Q000502:physiology / Q000528:radiation effects; D008869:Microtubule-Associated Proteins / Q000378:metabolism; D009474:Neurons / Q000187:drug effects / Q000473:pathology* / Q000502:physiology / Q000648:ultrastructure; D010751:Phosphopyruvate Hydratase / Q000378:metabolism; D011247:Pregnancy; D011297:Prenatal Exposure Delayed Effects / Q000473:pathology*; D051381:Rats; D017207:Rats, Sprague-Dawley; D016622:Silver Staining / Q000379:methods; D013312:Stress, Physiological / Q000473:pathology*; D013997:Time Factors; D014404:Tubulin / Q000378:metabolism
D005938:Glucocorticoids; C489787:MAP2 protein, rat; D008869:Microtubule-Associated Proteins; D014404:Tubulin; D010751:Phosphopyruvate Hydratase; D001973:Bromodeoxyuridine