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|Title:||Localization of insulin-like immunoreactive neurons in the hypothalamic paraventricular and supraoptic nuclei of streptozotocin-induced diabetic rats|
|Source:||Dheen, S.T.,Tay, S.S.W.,Wong, W.C. (1994). Localization of insulin-like immunoreactive neurons in the hypothalamic paraventricular and supraoptic nuclei of streptozotocin-induced diabetic rats. Journal of Brain Research 35 (4) : 487-494. ScholarBank@NUS Repository.|
|Abstract:||Insulin-like immunoreactive (ILIR) neurons were localized in the hypothalamic paraventricular nucleus (PVN) and supraoptic nucleus (SON) of normal as well as streptozotocin-induced diabetic rats at different time intervals ranging from 1 to 12 months post-diabetes. Insulin-like immunoreactivity was localized in the cytoplasm and nucleoplasm of the neuronal somata in the PVN and SON of control rats but the nucleolus appeared unlabelled. In the neuropil of PVN and SON, the reaction product was mainly localized in the dendrites and axonal profiles. The overall intensity of labelling was light and diffuse. In streptozotocin-induced diabetic rats, also the PVN and SON contained ILIR neuronal somata, dendrites and axonal profiles. However, these ILIR neuronal profiles displayed abnormality at all the time intervals studied. At 1-6 months post-diabetes, the ILIR somata and dendrites appeared to be hypertrophied and they contained dilated endoplasmic reticulum. Both ILIR myelinated as well as non-myelinated axons were also present in the neuropil. Numerous unlabelled axon terminals showing swollen agranular as well as dense-cored spherical vesicles were also present in the neuropil and they were presynaptic to labelled dendrites. At 9-12 months post-diabetes, some of the ILIR neuronal profiles appeared to be degenerating. The ILIR somata showed distended rER, membranous bodies and autophagic vacuoles. Highly vacuolated ILIR dendritic processes were also present in the neuropil. It is hypothesized that streptozotocin-induced diabetes produced a state of hypoinsulinemia or hyperglycemia which in turn sensitized the PVN and SON resulting in hyperactivity of the ILIR neurons and the prolonged stimulus could have possibly produced the neuronal degeneration seen at later survival periods.|
|Source Title:||Journal of Brain Research|
|Appears in Collections:||Staff Publications|
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