Horm Metab Res 2006; 38(6): 382-390
DOI: 10.1055/s-2006-944522
Original Basic
© Georg Thieme Verlag KG Stuttgart · New York

Effects of Chronic Alcoholic Disease on Magnocellular and Parvocellular Hypothalamic Neurons in Men

E.  V.  Sivukhina1, 2, 6 , A.  A.  Dolzhikov2 , Iu.  E.  Morozov3 , G.  F.  Jirikowski1 , V.  Grinevich4, 5, 7
  • 1Department of Anatomy II, Friedrich Schiller University, Jena, Germany
  • 2Department of Histology and Embryology, Kursk State Medical University, Kursk, Russia
  • 3Medical Expert Bureau of Medical Legal Examination, Moscow Public Health Department, Moscow, Russia
  • 4Department of Histology and Embryology, Paediatric Faculty, Russian State Medical University, Moscow, Russia
  • 5Group of Neuroimmunoendocrinology, Institute of General Pathology and Pathological Physiology, Russian Academy of Medical Sciences, Moscow, Russia
  • 6Current address: Institute of Biosynthesis of Neural Structures, Centre of Molecular Neurobiology, University of Hamburg, Germany
  • 7Current address: Department of Molecular Neurobiology, Max-Planck-Institute for Medical Research, Heidelberg, Germany
Further Information

Publication History

Received 30 November 2005

Accepted after revision 20 February 2006

Publication Date:
06 July 2006 (online)

Abstract

Although numerous data showing severe morphological impairment of magnocellular and parvocellular hypothalamic neurons due to chronic alcoholic consumption have been gathered from animal experiments, only one study (Harding et al., 1996) was performed on post mortem human brain. This study showed a reduction in the number of vasopressin (VP)-immunoreactive neurons in the supraoptic (SON) and paraventricular (PVN) nuclei, but did not provide any data regarding the effect of chronic alcohol intake on human parvocellular neurons. In order to assess whether the changes observed in the animal model also occur in humans and provide a structural basis for the results of clinical tests, we performed immunohistochemical and morphometric analysis of magnocellular (VP and oxytocin, OT) and parvocellular (corticotropin-releasing hormone, CRH) neurons in post-mortem brains of patients afflicted with chronic alcoholic disease. We analyzed 26-male alcoholics and 22 age-matched controls divided into two age groups - “young” (< 40 yr) and “old” (> 40 yr). Hypothalamic sections were stained for OT, VP, and CRH. The analysis revealed: 1) decrease in VP-immunoreactivity in the SON and PVN as well as OT-immunoreactivity in the SON in alcoholic patients; 2) increase in OT-immunoreactivity in the PVN; 3) increase in CRH-immunoreactivity in parvocellular neurons in the PVN. Furthermore, the proportion of cells containing CRH and VP was increased in alcoholics. These findings indicate that chronic alcohol consumption does indeed impair the morphology of magnocellular neurons. The enhancement of CRH-immunoreactivity and increased co-production of CRH and VP in parvocellular neurons may be due to a decline in glucocorticoid production, implied by the hypoplasic impairment of adrenal cortex we observed in alcoholics during the course of this study.

References

Dr. Valery Grinevich

Department of Molecular Neurobiology

Max-Planck-Institute for Medical Research · Jahnstraße 29 · 69120 Heidelberg · Germany

Phone: +49 (6221) 486-128

Fax: +49 (6221) 486-110 ·

Email: valery.grinevich@mpimf-heidelberg.mpg.de

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