Effect of Chronic Alcohol Intake on Vasopressin and Oxytocin-containing Neurons in the Paraventricular and Supraoptic Nucleus of the Rat Hypothalamus.
10.11637/kjpa.2006.19.4.313
- Author:
Yoon Young CHUNG
1
;
Young Lan PARK
;
Jong Joong KIM
Author Information
1. Department of Anatomy, College of Medicine, Chosun University, Korea. jjbkim@chosun.ac.kr
- Publication Type:Original Article
- Keywords:
Chronic alcohol intake;
Vasopressin;
Oxytocin;
Supraoptic nucleus;
Paraventricular nucleus
- MeSH:
Animals;
Brain;
Cell Size;
Hypothalamus*;
Neurons*;
Oxytocin;
Paraventricular Hypothalamic Nucleus;
Rats*;
Supraoptic Nucleus*;
Vasopressins*
- From:Korean Journal of Physical Anthropology
2006;19(4):313-324
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
Chronic alcohol intake can profoundly modify the neuronal activity and the morphologic structure of hypothalamic nucleus in the rat brain. The aim of the present study is to observe the effects of chronic alcohol intake on expression of vasopressin and oxytocin in the paraventricular and supraoptic nucleus in the rat hypothalamus. Experimental rats (n=14) were divided into control group and chronic alcohol group. Chronic alcohol group was induced via daily liquid alcohol intake for 6 months beginning at 8 weeks of age. As a result, the number of vasopressin and oxytocin-containing neurons was decreased in the paraventricular and supraoptic nucleus in chronic alcohol group. Especially, the number of vasopressin-containing neurons of chronic alcohol group was significantly decreased in the paraventricular nucleus. Chronic alcohol intake produced significant changes in the volume of the cell bodies and their nucleus in neurons of the paraventricular and supraoptic nucleus. Particularly, the size of nucleus of vasopressin-containing neurons in chronic alcohol group was larger than in control group. These results show that chronic alcohol intake may affect the synthesis of vasopressin and oxytocin in the neurons of hypothalamic nuclei. Whereas, chronic alcohol intake induces an enlargement of the cell size of surviving neuron to compensate.
