STRUCTURAL REORGANIZATION IN THE SUPRAOPTIC NUCLEUS OF WITHDRAWN RATSFOLLOWING LONG-TERM ALCOHOL-CONSUMPTION

We have recently shown in the supraoptic nucleus (SON) of the rat that prolonged ethanol consumption induces cell degeneration and enlargeme nt of the surviving neurons and of their subcellular organelles. We an alyzed the SON of withdrawn rats to evaluate whether it displays any e vidence of morphological reorganization following abstinence from etha nol, inasmuch as in this condition the ethanol-induced changes in the plasma levels of neurohormones and plasma osmolality are no longer det ectable. A group of 18-month-old withdrawn rats was compared with age- matched, pair-fed control and ethanol-treated rats. To differentiate b etween the effects of withdrawal and the effects of rehydration, a gro up of 18-month-old rehydrated rats was also included in this study and compared with age-matched, pair-fed control and dehydrated rats. We e stimated the volume of SON, and the total number and mean volume of it s neurons. The cross-sectional areas of the vasopressinergic and oxyto cinergic populations were also evaluated. At the ultrastructural level , we determined the volumes and surface areas of the rough endoplasmic reticulum and Golgi apparatus, and the volumes of neurosecretory gran ules and nucleoli. In withdrawn animals, the total number of SON neuro ns was smaller than in controls, although the neuronal volume was grea ter. The number of SON neurons did not differ between withdrawn and et hanol-treated rats, despite the reduced volume of SON in the former an imals. The decrease of SON volume correlated with and was caused by a reduction in the volume of SON neurons and in the size of the organell es involved in neurohormone synthesis. Thus, withdrawal from ethanol s tops the ethanol-induced neuronal degeneration of the SON and partiall y reverses the ethanol-induced enlargement of SON neurons and their or ganelles. We suggest that the larger volume of SON neurons in withdraw n animals relative to controls represents a compensatory mechanism, tr iggered by the reduced number of neurons, to allow the maintenance of adequate levels of circulating neurohormones.