Bojidar Stankov
University of Texas Health Science Center at San Antonio
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Life Sciences | 1990
Bojidar Stankov; Russel J. Reiter
Great progress has been made in the identification of melatonin binding sites, commonly identified as melatonin receptors by many authors, in recent years. The bulk of these studies have investigated the sites using either autoradiographic and biochemical techniques with the majority of the experiments being done on the rat, Djungarian and Syrian hamster, and sheep, although human tissue has also been employed. Many of the studies have identified melatonin binding in the central nervous system with either tritium- or iodine-labelled ligands. The latter ligand seems to provide the most reproducible and consistent data. Of the central neural tissues examined, the suprachiasmatic nuclei are most frequently mentioned as a location for melatonin binding sites although binding seems to be widespread in the brain. The other tissue that has been prominently mentioned as a site for melatonin binding is the pars tuberalis of the anterior pituitary gland. There may be time-dependent variations in melatonin binding densities in both neural and pituitary gland tissue. Very few attempts have been made to identify melatonin binding outside of the central nervous system despite the widespread actions of melatonin. Preliminary experiments have been carried out on the intracellular second messengers which mediate the actions of melatonin.
Archive | 1991
Bojidar Stankov; Valeria Lucini; Francesco Scaglione; Bruno Cozzi; Marco Righi; Gianfranco Canti; G. Demartini; Franco Fraschini
After a decade of controversy over the reliability of identification and quantification of the melatonin binding sites, a highly potent melatonin analogue (2-iodomelatonin) was synthesized (Vakkuri et al., 1984). In the years that followed the introduction of the iodinated melatonin the field has developed rapidly (for reviews see Morgan and Williams, 1989; Stankov and Reiter, 1990).
Archive | 1995
Franco Fraschini; Russel J. Reiter; Bojidar Stankov
D. P. Cardinali, D. A. Golombek, R. E. Rosenstein, B. A. Kanterewicz, M. Fiszman Department of Physiology, Faculty of Medicine, University of Buenos Aires, CC 243, 1425 Buenos Aires, Argentina In the last years, considerable efforts have been devoted to examine the participation of brain -y-aminobutyric acid (GABA) neurons in circadian phenomena. The importance of gabaergic neurons in circadian organization of brain function is underlined by the fact that almost every single neuron in the suprachiasmatic nucleus contains GABA. In addition, drugs affecting GABA function, like benzodiazepines (BZP) or melatonin, are effective to phase-shift circadian rhythms. Several data point out to a melatonin interaction with GABA-containing neurons in the CNS. Melatonin injection decreases brain GABA concentration, modifies GABA-BZP binding to brain membranes, and increases GABA turnover rate, GABA-induced chloride influx in rat hypothalamus, and the electrophysiological effects of GABA in rabbit cerebral cortex. As other GABA-positive ligands, melatonin inhibited cage-convulsant (TBPS) binding to rat brain membranes. Under long photoperiods, a significant rhythm of GABA turnover was detected in the areas studied (cerebral cortex, preoptic-medial basal hypothalamus, cerebellum and pineal gland) of Syrian hamsters, with maxima at night Under short photoperiods the synchronization in turnover rate among the remaining regions was lost This effect was attributed to the different melatonin secretory patterns under both lighting environments. In a number of studies carried out to define the participation of gabaergic mechanisms in behavioral effects of melatonin in rodents, we found that: (1) The administration of the central-type BZP antagonist f1umazenil blunted the analgesic response to melatonin in mice, indicating that time-dependent melatonin analgesia was sensitive to central-type BZP antagonism. (2) Flumazenil although unable by itself to modify locomotor activity or induced seizures in rodents, significantly attenuated the inhibitory effects of melatonin. (3) The anxiolytic and pro-exploratory melatonin properties assessed in rats in a plus-maze indicated maximal effects of melatonin at night, with absence of effects at noon and a weak activity at the The PiMal Gland and Its HomwMs Edited by F. Fraschini et ai., Plenum Press, New York, 1995 119 beginning of the light phase, an effect blunted by administration of flumazenil. (4) In Syrian hamsters, flumazenil inhibited melatonin-induced re-entrainment of locomotor activity and body temperature rhythms of Syrian hamsters after phase-advancing the L: D cycle. Collectively, the results are compatible with the view that melatonin activity on circadian rhythmicity was sensitive to central-type BZP antagonism. Melatonin and BZP seem to have in common an activity on central gabaergic neurons participating in circadian organization.
Archive | 1992
Gabriele Biella; Franco Fraschini; Bojidar Stankov; Strambi Luigi Ferini
Archive | 1994
Franco Fraschini; Bojidar Stankov; Margherita Borgonovo; Carlo Introini; Aldo Laguzzi; Ermanno Duranti; T. Moni heir Maria
Archive | 1993
Gabriele Biella; Franco Fraschini; Bojidar Stankov; Luigi F. Strambi
Archive | 1995
Franco I.F.L.O. S.A.S. Fraschini; Russel J. Reiter; Bojidar Stankov; Nato Advanced Study
Archive | 1991
Franco Fraschini; Bojidar Stankov; Luigi Di Bella; Ermanno Duranti; Aldo Lagguzzi
Archive | 1993
Margherita Borgonovo; Carlo Introini; Franco Fraschini; Bojidar Stankov
Archive | 1993
Margherita Borgonovo; Carlo Introini; Franco Fraschini; Bojidar Stankov
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University of Texas Health Science Center at San Antonio
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