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001-es BibID:	BIBFORM073592
Első szerző:	Bodnár Ibolya
Cím:	Brain structures mediating the suckling stimulus-induced release of prolactin / I. Bodnár, Zs. Bánky, B. E. Tóth, G. M. Nagy, B. Halász
Dátum:	2002
ISSN:	0953-8194
Megjegyzések:	Suckling?induced prolactin release is a widely studied neuroendocrine reflex, comprising a neural afferent and a humoral efferent component. The information on the brain structures involved in this reflex is fairly limited. The present studies focused on this question. The following hypothalamic interventions were made in lactating rats and the dams were tested for the suckling?induced prolactin response: (i) unilateral or (ii) bilateral frontal cuts at the level of the anterior and posterior hypothalamus; (iii) administration of 5,7?dihydroxytryptamine or (iv) 6?hydroxydopamine into the hypothalamic paraventricular nucleus (PVN) to destroy serotonergic and catecholaminergic innervation of the cell group, respectively; (v) lesion of the medial subdivision of the PVN; and (vi) horizontal knife cuts below the PVN. Bilateral posterior and bilateral or unilateral anterior frontal cuts caused blockade of the suckling?induced release of prolactin. Likewise, most dams receiving 5,7?dihydroxytryptamine in the PVN did not respond to the suckling stimulus. Immunocytochemistry revealed that, in those rats which did not show a rise in plasma prolactin, there were almost no serotonergic fibres and terminals in the PVN, while in dams which exhibited a response, numerous serotonergic elements were evident. 6?Hydroxydopamine treatment did not cause significant alteration in the prolactin response. Lesion of the medial, largely parvocellular subdivision of the PVN, or horizontal knife cuts below this cell group, blocked the hormone response. The findings demonstrate for the first time that: (i) interruption of the connections between the brain stem and the hypothalamus interferes with the prolactin response to the suckling stimulus; (ii) serotonergic fibres terminating in the hypothalamic PVN are involved in the mediation of the suckling stimulus; and (iii) within the PVN, neurones in the medial, largely parvocellular subdivision of the cell group take part in the transfer of the neural signal, eventually inducing prolactin release.
Tárgyszavak:	Orvostudományok Egészségtudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:	Journal of Neuroendocrinology 14 : 5 (2002), p. 384-396. -
További szerzők:	Bánky Zsuzsanna Tóth E. Béla (1960-) (orvos) Nagy György M. Halász Béla
Internet cím:	Szerző által megadott URL DOI Intézményi repozitóriumban (DEA) tárolt változat
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001-es BibID:	BIBFORM073599
Első szerző:	Horváth Katalin M.
Cím:	Dual role of glucocorticoids in suckling-induced prolactin secretion / Katalin M. Horváth, Zsuzsanna Bánky, Béla E. Tóth, György M. Nagy, Béla Halász
Dátum:	2001
ISSN:	0969-711X
Megjegyzések:	The exact contribution of corticosteroids to the control of prolactin secretion in lactating rats is poorly understood. Therefore, the present studies were focused on the effect of adrenalectomy and dexamethasone treatment on the suckling-induced prolactin release. Animals were adrenalectomized on the 3rd day of lactation and tested on the 7th day of lactation. In adrenalectomized animals, the suckling stimulus failed to induce the characteristic increase in plasma prolactin levels. Dexamethasone pretreatment (400 microg/kg b.w. s.c. 24, 48, 72 h before testing) of adrenalectomized rats restored this prolactin response. The same treatment with dexamethasone given to control animals attenuated the suckling stimulus induced prolactin response. The present findings indicate that corticosteroids are essential for a basic prolactin response of lactating rats.
Tárgyszavak:	Orvostudományok Gyógyszerészeti tudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:	Endocrine. - 15 : 3 (2001), p. 287-290. -
További szerzők:	Bánky Zsuzsanna Tóth E. Béla (1960-) (orvos) Nagy György M. Halász Béla
Internet cím:	Szerző által megadott URL DOI Intézményi repozitóriumban (DEA) tárolt változat
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001-es BibID:	BIBFORM073600
Első szerző:	Horváth Katalin M.
Cím:	Effect of adrenalectomy and dexamethasone treatment on prolactin secretion of lactating rats / Katalin M. Horváth, Zsuzsanna Bánky, Béla E. Tóth, Béla Halász, György M. Nagy
Dátum:	2001
ISSN:	0361-9230
Megjegyzések:	The contribution of corticosteroids to the control of prolactin secretion in lactating rats was investigated. The prolactin response to domperidone (20 ?g/kg b.w., i.v.), a dopamine receptor antagonist and to domperidone plus formalin stress was tested in adrenalectomized and/or dexamethasone-treated continuously nursing rats. Animals were adrenalectomized on the 3rd day of lactation and tested on the 7th day of lactation. Dexamethasone was injected s.c. 24 h before testing (400 ?g/kg b.w.) and on the day of testing (200 ?g/kg b.w.). Domperidone caused a significant rise in plasma prolactin levels. The prolactin response to domperidone was twice as high in solely adrenalectomized dams and in solely dexamethasone-treated rats compared to controls. In adrenalectomized animals treated with dexamethasone, the prolactin response to domperidone was like in controls. Formalin injection to either adrenalectomized plus domperidone-treated animals or to animals injected with dexamethasone plus domperidone, resulted in a statistically significant depletion of plasma prolactin. In controls and in adrenalectomized animals receiving dexamethasone and domperidone, the prolactin response to formalin was very similar, i.e., plasma prolactin levels did not change after the administration of formalin. The present findings suggest that in lactating rats, corticosteroids are involved in the prolactin response to domperidone and to formalin stress.
Tárgyszavak:	Orvostudományok Gyógyszerészeti tudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:	Brain Research Bulletin 56 : 6 (2001), p. 589-592. -
További szerzők:	Bánky Zsuzsanna Tóth E. Béla (1960-) (orvos) Halász Béla Nagy György M.
Internet cím:	DOI Intézményi repozitóriumban (DEA) tárolt változat
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