SEASONAL-CHANGES OF THE LEYDIG-CELLS OF VISCACHA (LAGOSTOMUS-MAXIMUS MAXIMUS) - A LIGHT AND ELECTRON-MICROSCOPY STUDY

Citation
E. Munoz et al., SEASONAL-CHANGES OF THE LEYDIG-CELLS OF VISCACHA (LAGOSTOMUS-MAXIMUS MAXIMUS) - A LIGHT AND ELECTRON-MICROSCOPY STUDY, Tissue & cell, 29(1), 1997, pp. 119-128
Citations number
41
Categorie Soggetti
Cell Biology
Journal title
ISSN journal
00408166
Volume
29
Issue
1
Year of publication
1997
Pages
119 - 128
Database
ISI
SICI code
0040-8166(1997)29:1<119:SOTLOV>2.0.ZU;2-N
Abstract
The Leydig cells of viscacha (seasonal rodent) show cytoplasmic hypert rophy and regional distribution during the breeding period (summer-aut umn), The dominant organelles are smooth endoplasmic reticulum (SER) a nd mitochondria. A moderately well-developed Golgi, abundant lipid inc lusions, dense bodies like lysosomes in different stages, and centriol es are observed. Extensive or focal desmosome and gap-like junctions b etween neighbouring Leydig cells are present. These cells exhibit an e vident hypotrophy and an increase in the number of dense bodies during the gonadal regression in winter (July and August). Cells in differen t stages of involution are observed in this period. Their nuclei are i rregular and heterochromatic. The cytoplasm contains few mitochondria. The vesicular SER is scarse. Irregular and large intercellular spaces with microvilli and amorphous material are present. The junctional co mplexes are absent. The nuclear and cytoplasmic volume and development of SER and mitochondria increase during the recovery period (spring). The lipid inclusions decrease. Dilatations of the intercellular space with microvilli and limited by focal desmosome-like junctions are obs erved. In conclusion, the Leydig cells of Lagostomus maximus maximus s how deep changes alongside the reproductive cycle. The photoperiod var iations, through pineal hypothalamus pituitary axis and the hormone me latonin, are probably responsible for them. Moreover, the fall of seru m and tubular testosterone would be one of the factors responsible for gonadal regression.