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The plasticity of hypothalamic magnocellular system following axonal damage by hypophysectomy in developing and adult rats

by Yuan, Qiuju

Abstract (Summary)
(Uncorrected OCR) Abstract Axonal transection provides very useful paradigms to study cellular responses to injury, mechanisms of plasticity and the processes that lead to nerve cell degeneration. The outcome of axonal injury depends on many parameters including the location and nature of the lesion, age of animal and etc. Hypophysectomy axotomizes the magnocellular neurons in the supraoptic (SON) and paraventricular (PVN) nuclei of the hypothalamo-neurohypophyseal system (HNS). In the adult mammal, the HNS shows a remarkable ability to recover function despite substantial neuronal degeneration following hypophysectomy. The mechanisms underlying this recovery are completely unknown, but it has been hypothesized that the neuronal regeneration may be due to, at least in part, upregulation of nitric oxide synthase, increased neuronal activity, or special microenvironment. There is little data regarding how hypophysectomy influences HNS in immature animals. The retrograde reactions induced by axonal injury also involve in the cellular elements of the local microenvironment of those neurons, surrounding nonneuronal cells. These changes are likely to play a critical role in the attempt of the injured neuron to survive and achieve functional repair. Though these various cellular processes have been well documented by many groups over the last few decades, few have directly addressed the perineuronal glial reaction of magnocellular neurons of the HNS and the role of the glial reaction in the post-injury remodeling of the HNS. The present study was undertaken to examine 1) the response of magnocellular neurons of oxytocin (OT) and arginine vasopressin (AVP) neuron to hypophysectomy including survival, regeneration, expression of nitric oxide synthase and c-fos in adult and developing rats; 2) the role of NOS on survival and regeneration after hypophysectomy by use of the NOS blocker, L-NAME; 3) the glial reaction to hypophysectomy in adult and developing rats. In the present study we found that, in contrast to a striking age-dependent alteration in nNOS expression and regeneration, hypophysectomy induced substantial degeneration of magnocellular neurons of HNS in both immature and adult rats and there was no obvious difference in neuronal survival after the same injury between immature and adult rats. Moreover, L-NAME, could inhibit neural regeneration but had no effect on magnocellular neuronal survival. These results suggested that 1) difference in vulnerability to axotomy between immature and mature neurons is not a general feature; 2) induced increase of NOS expression is involved in the regeneration of magnocellular neurons of HNS; 3) the magnocellular neurons are resistant to induced NO. Secondly, we demonstrated that there were qualitative as well as quantitative differences in induced c-fos expression between the newborn and the adult hypophysectomized SON and PVN. Following the hypothesis that the expression c-fos protein is induced by the cellular demands for acceleration of the gene transcription, we suggest that different pattern of c-fos expression between immature and adult rats may regulate different gene expression in response to hypophysectomy. Furthermore, hypophysectomy also induced different responses of astrocytes surrounding the affected neuronal perikaya in immature rats and adult rats. Following hypophysectomy in the adult, reactive astrocytes re-express the immature phenotypes of astrocytes, nestin and vimentin. In contrast to the situation in the adult, hypophysectomy did not induce nestin or vimentin expression in reactive astrocytes in SON and PVN in immature rats. Impacts of hypophysectomy on the astrocyte reactivity are age-dependent.
Bibliographical Information:

Advisor:

School:The University of Hong Kong

School Location:China - Hong Kong SAR

Source Type:Master's Thesis

Keywords:oxytocin vasopressin hypophysectomy nervous system wounds and injuries rats physiology

ISBN:

Date of Publication:01/01/2005

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