Plasma osmolality dipsogenic thresholds and c-fos expression in the near-term ovine fetus

Citation
Zc. Xu et al., Plasma osmolality dipsogenic thresholds and c-fos expression in the near-term ovine fetus, PEDIAT RES, 49(5), 2001, pp. 678-685
Citations number
39
Categorie Soggetti
Pediatrics,"Medical Research General Topics
Journal title
PEDIATRIC RESEARCH
ISSN journal
00313998 → ACNP
Volume
49
Issue
5
Year of publication
2001
Pages
678 - 685
Database
ISI
SICI code
0031-3998(200105)49:5<678:PODTAC>2.0.ZU;2-F
Abstract
In ovine and human pregnancy, fetal swallowing contributes importantly to a mniotic fluid homeostasis. Fetal dipsogenic responsiveness to short-term pl asma hyperosmolality develops in late gestation, although fetal swallowing is not stimulated in response to long-term plasma osmolality increases (2 t o 3%), which typically stimulate adult drinking behavior. To explore the ne ar-term fetal plasma osmolality threshold for swallowing stimulation, we ex amined the effects of i.v. hypertonic saline-induced subacute increases in plasma hypertonicity on fetal swallowing behavior. Central sites of activat ion were examined by c-fos expression in putative dipsogenic nuclei. The re sults demonstrate that subacute 2 to 3% plasma osmolality increases do not stimulate near-term ovine fetal swallowing. However, fetal swallowing activ ity significantly increased (3 times) after plasma osmolality increased >6% above basal values. Consistent with a specific dipsogenic response, i.v. h ypertonic saline induced c-fos expression in the anterior third ventricle r egion, a putative dipsogenic center, as well as in the fetal hindbrain. The stimulation of fetal swallowing under conditions of higher osmotic stimula tion and the correlation with forebrain c-fos expression indicates that nea r-term fetal osmoregulation mechanisms are functional, although not complet ely mature. Reduced fetal dipsogenic responsiveness may result from altered osmoreceptor sensitivity, downstream neuronal or synaptic immaturity, or p otentially inhibitory actions of stimulated hindbrain nuclei.