ALTERATIONS IN THE HYPOTHALAMIC PARAVENTRICULAR NUCLEUS AND ITS OXYTOCIN NEURONS (PUTATIVE SATIETY CELLS) IN PRADER-WILLI-SYNDROME - A STUDY OF 5 CASES

Citation
Df. Swaab et al., ALTERATIONS IN THE HYPOTHALAMIC PARAVENTRICULAR NUCLEUS AND ITS OXYTOCIN NEURONS (PUTATIVE SATIETY CELLS) IN PRADER-WILLI-SYNDROME - A STUDY OF 5 CASES, The Journal of clinical endocrinology and metabolism, 80(2), 1995, pp. 573-579
Citations number
47
Categorie Soggetti
Endocrynology & Metabolism
ISSN journal
0021972X
Volume
80
Issue
2
Year of publication
1995
Pages
573 - 579
Database
ISI
SICI code
0021-972X(1995)80:2<573:AITHPN>2.0.ZU;2-C
Abstract
Animal experiments have shown that the parvocellular oxytocin (OXT) ne urons of the hypothalamic paraventricular nucleus (PVN) inhibit food i ntake. In the present study, the PVN and its OXT neurons have been inv estigated in an extreme human eating disorder, i.e. the Prader-Willi s yndrome (PWS). PWS patients are characterized by gross obesity, insati able hunger, hypotonia, hypogonadism, and mental retardation. The PVN of 5 PWS patients (2 males and 3 females), varying in age between 22-6 4 yr, and 27 controls (14 males and 13 females) without any primary ne urological or psychiatric diseases was morphometrically investigated a fter conventional staining with thionine and immunocytochemical staini ng for OXT and vasopressin (AVP). The thionine-stained volume of the P VN was 28% smaller in PWS patients (P = 0.028), and the total cell num ber was 38% lower (P = 0.009). The immunoreactivity for OXT and AVP wa s decreased in PWS patients, although the variability within the group s was high. A strong and highly significant decrease (42%; P = 0.016) was found in the number of OXT-expressing neurons of the PWS patients. The volume of the PVN-containing OXT-expressing neurons decreased by 54% (P = 0.028) in PWS. The number of AVP-expressing neurons in the PV N did not change significantly. The OXT neurons of the PVN seem to be good candidates for playing a physiological role in ingestive behavior as ''satiety neurons'' in the human hypothalamus.