Ultrastructural Changes in the Hypothalamic Paraventricular Nucleus of the Streptozotocin-Induced Diabetic Rat

Abstract

This study describes the ultrastructural and morphometric changes in the hypothalamic paraventricular nucleus (PVN) of the streptozotocin-induced diabetic rat. During the acute phase (3 days after induction of diabetes), dendrites were swollen and appeared to have a watery cytoplasm. The affected dendrites were postsynaptic to seemingly normal axon terminals. During the intermediate phase (1-9 months after induction of diabetes), the neuronal somata contained numerous vacuoles of various sizes which were probably formed from dilated rough endoplasmic reticulum. Several unidentifiable vacuolated profiles were also seen in the neuropil. During the late phase (12 months after induction of diabetes) electron-dense dendrites and axon terminals were readily encountered in the neuropil. Most of the electron-dense dendrites were postsynaptic to normal as well as electron-dense axon terminals. Some of the electron-dense axon terminals formed axosomatic synapses with seemingly normal somata. Perivascular glial cells in the neuropil were in the process of phagocytosis. At 1-12 months of diabetes, the sizes of the somata and nuclei of PVN neurons were significantly increased in comparison with age-matched control rats.

Depressed basal hypothalamic neuronal activity in type-1 diabetic mice is correlated with proinflammatory secretion of HMBG1

“…Finally, increases in PVN neuronal excitation in response to glucose may be acutely adaptive, but chronic activation may produce detrimental effects. Our previous findings [26] and other work [15, 40] showing neuronal degeneration following long-term diabetes are consistent with this observation. Thus, it is possible that reduced basal hypothalamic activity in the present report could have resulted from the loss of neurons over time.…”

Changes in peptidergic nerves in the atrioventricular valves of streptozotocin-induced diabetic rats: A confocal microscopy study

“…It is well established that the animals become hyperglycemic and hypoinsulinemic from the selective destruction of the pancreatic ␤-cells within 24 hr after the administration of a diabetogenic agent (Rakieten et al, 1963). The present study of long-term diabetic rats demonstrates that changes of peptidergic nerves represent the characteristic alteration of the autonomic innervation of the chronically diabetic atrioventricular valve, and is similar to the marked lesions of the PNS (Sharma et al, 1974) and CNS (Tay and Wong, 1990;Dheen et al, 1994) in experimentally induced diabetic animals. Although the mechanism for the changes is unknown, it has been proposed that diabetes mellitus may lead to metabolic dysfunctions in the neuron, resulting in a loss of axonal transport (Jakobsen and Sidenius, 1980;Mendell et al, 1981;Tay and Wong, 1990).…”

Morphoquantitative effects of acute diabetes on the myenteric neurons of the proximal colon of adult rats

“…The smaller neuronal area was caused primarily by a reduction in the cytoplasmic area of the cell body. There are reports of changes in the nuclear and/or cytoplasmic areas in other regions of the nervous system in diabetics 9,33,34 , which were attributed to changed rates of transcription and translation of biomolecules and of electrical activity. The role of cellular dehydration to the reduced size also has to be taken into account.…”