Osmotic stimulation causes structural plasticity of neurone-glia relationships of the oxytocin but not vasopressin secreting neurones in the hypothalamic supraoptic nucleus.
A comparative quantitative analysis was carried out on identified supraoptic neurones of male and female Wistar and Long Evans rats under normal conditions and after chronic osmotic stimulation, and in homozygous Brattleboro rats suffering from diabetes insipidus. The neurones were identified by immunocytochemical or morphological means. Osmotic stimulation resulted in significant increases in the number and extent of direct neuronal appositions and in the number of presynaptic terminals contacting two neurosecretory cells simultaneously ("double" synapses). In the supraoptic nuclei of both sexes these increases were restricted to the oxytocin secreting neurones. In Brattleboro homozygous rats treated with vasopressin, the proportion of oxytocinergic neurones in apposition was not modified, but the number of appositions per soma profile decreased as did the incidence of "double" synapses. In nuclei of osmotically stimulated rats, increase in cell volume affected both types of neurosecretory cell and was accompanied by an increase of the absolute extent of glial coverage. However, the extent of glial coverage of the oxytocinergic neurones did not match the hypertrophy of the cells, resulting in a decrease in their relative glial coverage, compared to normal hydrated animals. The increased neuronal appositions, therefore, cannot result simply from a retraction of glial processes. The structural reorganization of the oxytocinergic system observed during chronic osmotic stimulation was as extensive as that observed at lactation. Moreover, the changes were as extensive in Wistar as in Brattleboro lactating rats, although the latter have an added osmotic stimulus. This implies that lactation and osmotic stimulation do not produce additive effects.(ABSTRACT TRUNCATED AT 250 WORDS)
D B
DB
Chapman
D T
DT
Theodosis
C
C
Montagnese
D A
DA
Poulain
J F
JF
Morris
D000818:Animals; D001127:Arginine Vasopressin; D005260:Female; D008297:Male; D009457:Neuroglia / Q000378:metabolism / Q000502:physiology* / Q000648:ultrastructure; D009473:Neuronal Plasticity; D009997:Osmotic Pressure; D010121:Oxytocin / Q000378:metabolism*; D051381:Rats; D011910:Rats, Brattleboro; D011919:Rats, Inbred Strains; D013045:Species Specificity; D013194:Staining and Labeling; D013495:Supraoptic Nucleus / Q000378:metabolism / Q000502:physiology* / Q000648:ultrastructure; D013997:Time Factors; D014667:Vasopressins / Q000378:metabolism* / Q000494:pharmacology
C016671:pitressin tannate; D014667:Vasopressins; D001127:Arginine Vasopressin; D010121:Oxytocin