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001-es BibID:	BIBFORM073595
Első szerző:	Tóth E. Béla (orvos)
Cím:	Physiological role of salsolinol : its hypophysiotrophic function in the regulation of pituitary prolactin secretion / Béla E. Tóth, Ibolya Bodnár, Krisztián G. Homicskó, Ferenc Fülöp, Márton I. K. Fekete, György M. Nagy
Dátum:	2002
ISSN:	0892-0362
Megjegyzések:	We have recently observed that 1-methyl-6,7-dihydroxy-1,2,3,4-tetrahydroisoquinoline (salsolinol) produced by hypothalamic neurons can selectively release prolactin from the anterior lobe (AL) of the pituitary gland. Moreover, high affinity binding sites for SAL have been detected in areas, like median eminence (ME) and the neuro-intermediate lobe (NIL) that are known terminal fields of the tuberoinfundibular DAergic (TIDA) and tuberohypophysial (THDA)/periventricular (PHDA) DAergic systems of the hypothalamus, respectively. However, the in situ biosynthesis and the mechanism of action of SAL are still enigmatic, these observations clearly suggest that sites other than the AL might be targets of SAL action. Based on our recent observations it may be relevant to postulate that an "autosynaptocrine" regulatory mechanism functioning at the level of the DAergic terminals localized in both the ME and NIL, may play a role in the hypophyseotrophic regulation of PRL secretion. Furthermore, SAL may be a key player in these processes. The complete and precise mapping of these intra-terminal mechanisms should help us to understand the tonic DAerg regulation of PRL secretion. Moreover, it may also give insight into the role of pre-synaptic processes that most likely have distinct and significant functional as well as pathological roles in other brain areas using DAergic neurotransmission, like striatonigral and mesolimbic systems.
Tárgyszavak:	Orvostudományok Gyógyszerészeti tudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:	Neurotoxicology and Teratology 24 : 5 (2002), p. 655-666. -
További szerzők:	Bodnár Ibolya Homicskó Krisztián Gy. Fülöp Ferenc Fekete I. K. Márton Nagy György M.
Internet cím:	Szerző által megadott URL DOI Intézményi repozitóriumban (DEA) tárolt változat
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