Please use this identifier to cite or link to this item: https://scholarbank.nus.edu.sg/handle/10635/177145
Title: NEUROENDOCRINOLOGY OF OREOCHROMIS MOSSAMBICUS
Authors: ISHWAR SINGH
Issue Date: 1991
Citation: ISHWAR SINGH (1991). NEUROENDOCRINOLOGY OF OREOCHROMIS MOSSAMBICUS. ScholarBank@NUS Repository.
Abstract: A stereotaxic atlas of the diencephalon was prepared, and validated, to permit experimental manipulation of predetermined sites in the hypothalamus and preoptic area. Several new subdivisions were recognised in both the preoptic area and the anterior periventricular hypothalamus, in particular. A preliminary study was made of the ultrastructure of the pituitary gland, and the effects of thyroid manipulations. Two different cell-types were identified in the rostral pars distalis which are presumed to correspond to the adrenocorticotrophin- (ACTH-) and prolactin- (PRL-) secreting cells of other teleosts. Four endocrine cell-types were identified in the proximal pars distalis: one which corresponds to the growth hormone- (GH-) secreting cells of other teleosts, two which appear may produce one or more gonadotrophs (GTH), and one which may be thyrotrophic. As in other teleosts, two cell-types could be recognised in the pars intermedia (PI). On the basis of ultrastructural criteria, four different types of axons could be recognised in the neurohypophysis. Lesioning studies suggest that the preoptic area may be involved in the inhibitory control of ACTH, GH and GTH cell activities, based on changes in the ultrastructural appearance of these cells, together with evidence for a stimulation of certain stages of spermatogenesis and a trend for an increase in gonadosomatic index (GS!). Lesions of the anterior tuberal area, on the other hand, indicate that neurones in this area may be involved in the stimulatory control of GTH secretion: such lesions were associated with the cessation of spermatogenesis, a decrease in GSI, as well as indications of decreased GTH cell activity and decreased serum testosterone levels. In addition, there was evidence that lesions of the anterior tuberal area removed an inhibitory control of ACTH and GH cell activities. Lesions of the posterior tuberal area were associated with evidence for activation of the ACTH cells. Implants of oestradiol ( E2) and testosterone ( T) into the preoptic area both led to activation of the GH cells; together with evidence for inhibition of GTH cell activity associated with inhibition of spermatogenesis and a decrease in GSI. E2, but not T, also appeared to stimulate PRL cell activity. When implanted into the anterior hypothalamus (the anterior tuberal and/or periventricular areas), there was evidence that sex steroids may stimulate PRL, ACTH and GTH cell activities. To investigate the role of monoaminergic systems in the regulation of the neuroendocrine centres, a further series of implant experiments was done to test the effects of a dopamine (DA) agonist (bromocriptine); a DA antagonist (metoclopramide); and a monoaminergic neurotoxin (6- hydroxydopamine). Interpretation of these studies is complicated by the possibility that the effects of these drugs may wear off towards the end of the 20-day experimental period: whilst the gonadal axis would appear to be inhibited by implants of metoclopramide or 6- hydroxydopamine into the anterior periventricular area on the basis of serum sex steroids and gonadal size and structure, the GTH cells in the pituitary appeared to be activated. Bearing this possibility in mind, there was evidence that monoaminergic systems may modulate the preoptic control of GTH cell-activity. The distribution of DA, and its metabolite dihydroxyphenylacetic acid (DOPAC) shows that there are pronounced regional differences in the forebrain. Castration, either alone or combined with replacement therapy with either E2 or T, had no effect on the distribution. Lesioning of centres implicated as sources of the pituitary's dopaminergic innervation in other teleosts failed to affect pituitary DA contents.
URI: https://scholarbank.nus.edu.sg/handle/10635/177145
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