Stress-related gene expression in brain and adrenal gland of porcine fetuses and neonates.
This study was conducted to examine stress-induced effects on gene expression of specific markers for HPA axis and neuronal activity in fetuses and neonatal pigs. Brain, pituitary gland, and adrenal gland were obtained to determine the mRNA levels for corticotropin-releasing hormone (CRH), CRH receptor 1 (CRHR1), pro-opiomelanocortin (POMC), ACTH receptor (MC2R), c-jun and c-fos. The suitability of these molecular markers was determined in neonatal pigs which were maternally deprived for two hours. It was found that maternal deprivation caused significantly higher transcript levels of c-fos and CRH in brain accompanied by a down-regulation of CRHR1 mRNA and an up-regulation of c-jun in the pituitary gland. To determine the effect of elevated maternal cortisol levels on gene expression of these molecular markers in fetuses, pregnant sows were treated with 100 IU ACTH (Synacthen Depot) s.c. every two days between Day 49 and Day 75 of gestation (normal gestation length 114 days). Animals were killed 48 hours after the last ACTH administration and fetuses of each sow were isolated. The ACTH treatment of sows significantly increased mRNA expression of c-fos but not of CRH in the fetal brain, and significantly decreased MC2R mRNA expression in the adrenal gland. However, HPA axis seems not to be fully developed in Day 77-fetuses because fetal pituitary CRHR1 and POMC mRNA expression was low in most of the fetuses. Although the expression of endocrine regulatory factors was partially incomplete in fetuses at the beginning of the third-trimester, ACTH dependent activation of c-fos mRNA in brain indicates a stress-related increase of neuronal activity. Based on these results it is assumed that prenatal stress in pigs may also have effects on the activity of the HPA axis in the offspring.
Schwerin
Manfred
M
Research Unit of Molecular Biology, Research Institute for the Biology of Farm Animals Dummerstorf, D-18196 Dummerstorf, Germany.
Kanitz
Ellen
E
Tuchscherer
Margret
M
Brüssow
Klaus-Peter
KP
Nürnberg
Gerd
G
Otten
Winfried
W
D000311:Adrenal Glands / Q000737:chemistry* / Q000196:embryology / Q000254:growth & development; D000324:Adrenocorticotropic Hormone; D000818:Animals; D000831:Animals, Newborn; D001921:Brain / Q000196:embryology / Q000254:growth & development; D001923:Brain Chemistry; D003346:Corticotropin-Releasing Hormone / Q000235:genetics; D005260:Female; D005333:Fetus; D015870:Gene Expression; D016762:Genes, fos / Q000235:genetics; D016758:Genes, jun / Q000235:genetics; D006854:Hydrocortisone / Q000502:physiology; D010902:Pituitary Gland / Q000737:chemistry / Q000196:embryology / Q000254:growth & development; D011247:Pregnancy; D011333:Pro-Opiomelanocortin / Q000235:genetics; D012333:RNA, Messenger / Q000032:analysis; D018043:Receptors, Corticotropin / Q000235:genetics; D018019:Receptors, Corticotropin-Releasing Hormone / Q000235:genetics; D013312:Stress, Physiological / Q000235:genetics / Q000662:veterinary*; D013552:Swine; D013553:Swine Diseases / Q000235:genetics*; D000099052:CRF Receptor, Type 1
D012333:RNA, Messenger; D018043:Receptors, Corticotropin; D018019:Receptors, Corticotropin-Releasing Hormone; D000099052:CRF Receptor, Type 1; D011333:Pro-Opiomelanocortin; D000324:Adrenocorticotropic Hormone; D003346:Corticotropin-Releasing Hormone; D006854:Hydrocortisone