Fine structural evidence of degeneration in supraoptic nucleus and subfornical organ of rats with lesions in the anteroventral third ventricle

Abstract

Lesions of the tissue surrounding the anteroventral third ventricle (AV3V) alter mechanisms controlling body fluid homeostasis and hemodynamics. A period of adipsia and impaired antidiuresis follows AV3V destruction, which causes lesioned animals to become severely dehydrated. In lesioned rats, mechanisms maintaining water balance appear to be refractory to antigiostensin and osmotic stimuli. To further investigate the neural basis for the observed alterations in body fluid balance, the supraoptic nucleus (SON) and subfornical organ (SFO) of rats with adipsia-producing lesions in the AV3V were examined by electron microscopy. In SONS of lesioned rats, degenerating fibers and terminals were present. Degenerating axonal terminals were seen in both axodendritic and axoaxonal synapses on magnocellular neurosecretory cells. These affected terminals in the SONsof lesioned rats may arise from osmoreceptors and angiotensin receptors which have somas or fibers in the lesioned area. Some fibers containing neurosecretory granulated vesicles also underwent degeneration. Neuronal somas displaying retrograde degenerative changes were present in SFOs after AV3V lesions. Degenerating fibers, some of which may be fibers of passage through the SFO, were common. However, little evidence of degenerative changes was seen in axon terminals in the SFOs. The evidence that lesions in the AV3V damaged an efferent projection field of the SFO is discussed in light of reports that AV3V lesions destroy responses in which the SFO is believed to participate.