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- ItemSomente MetadadadosDECREASED MUSCARINIC RECEPTOR-BINDING in RAT-BRAIN AFTER PARADOXICAL SLEEP-DEPRIVATION - AN AUTORADIOGRAPHIC STUDY(Elsevier B.V., 1994-05-09) Nunes, G. P.; Tufik, S.; Nobrega, J. N.; CLARKE INST PSYCHIAT; Universidade Federal de São Paulo (UNIFESP)Previous work demonstrated that paradoxical sleep deprivation (PSD) leads to a decrease in yawning behavior elicited by cholinergic agonists, suggesting that a downregulation of cholinergic muscarinic receptors may occur after PSD. More recent work using intracerebral injections of muscarinic agonists has suggested a critical role for M2 receptors in paradoxical sleep. in this study [H-3]AF-DX 384 was used to investigate the effects of PSD on M2-type cholinergic receptors throughout the brain using quantitative autoradiography. After 96 h of paradoxical sleep deprivation, [3H]AF-DX 384 binding was generally reduced throughout the brain, and significantly so in the olfactory tubercle (-20%), n. accumbens (-23%), frontal caudate-putamen (-16%), islands of Callejas (-20%), piriform cortex (-24%), lateral (-26%) and medial (-24%) septum, anteromedial (-19%), ventrolateral (-22%), and lateral geniculate (-15%) nuclei of thalamus, deep layers of the superior colliculus (-15%), entorhinal cortex (-12%) and subiculum (-23%). [H-3]AF-DX 384 binding was reduced in pontine structures, but not to a higher degree than in other brain areas. the observed downregulation of M2-type muscarinic receptors after PSD may be causally related to the previously reported decrease in cholinergically induced behaviors after PSD.
- ItemSomente MetadadadosEFFECT OF THE NEONATAL STEROID-HORMONE TREATMENT OF RATS ON ADULT HORMONE LEVELS AND THE REACTIVITY OF SEMINAL-VESICLES TO PARASYMPATHOMIMETIC DRUGS(Assoc Bras Divulg Cientifica, 1992-01-01) Barros, C. M.; Picarelli, Z. P.; Hayashi, Hisakazu [UNIFESP]; Abreu, L. C.; Universidade Federal de São Paulo (UNIFESP)1. Seminal vesicle reactivity to cholinergic agents, plasma testosterone, luteinizing hormone (LH) and follicle stimulating hormone (FSH) concentrations and seminal vesicle testosterone concentrations were determined in adult male rats treated during the first 6 h of life with 1.0 ml peanut oil (oil-treated), 1.0 mg testosterone propionate (TP-treated) or 1.2 mg 19-nor-testosterone homofarnesate (19-NT-treated).2. At 90-100 days of age, the neonatally treated animals presented atrophied accessory genital organs and increased (TP-treated, N = 10) or unchanged (19-NT-treated, N = 11) pD2 values for acetylcholine (vehicle: 5.18 +/- 0.06, N = 10; TP-treated: 5.26 +/- 0.06, N = 10; 19-NT-treated: 5.14 +/- 0.09, N = 11), and acetyl-beta-methylcholine (vehicle: 5.19 +/- 0.07; TP-treated: 5.43 +/- 0.06; 19-NT-treated: 5.25 +/- 0.07). The relative intrinsic activity, alpha, of acetyl-beta-methylcholine increased after both hormonal treatments (vehicle: 0.85 +/- 0.03; TP-treated: 0.95 +/- 0.02; 19-NT-treated: 0.92 +/- 0.03).3. No variation in mean adult plasma testosterone concentration was observed after neonatal treatment with either TP of 19-NT (vehicle: 752.93 +/- 273.66, N = 8; TP-treated: 459.05 +/- 88.32, N = 8; 19-NT-treated: 836.86 +/- 113.08, N = 7). However, testosterone content of seminal vesicles of adult rats was decreased in the animals treated with TP (N = 5) and 19-NT (N = 6) compared to controls.4. These results indicate a specific effect of neonatal hormone treatment on androgen metabolism which is demonstrable in the adult.
- ItemSomente MetadadadosIN VITRO DENERVATION OF THE RAT VAS-DEFERENS THROUGH HYPOTHERMIC STORAGE(Stockton Press, 1992-10-01) Jurkiewicz, Neide Hyppolito [UNIFESP]; Garcia, Antonio G.; Jurkiewicz, Aron [UNIFESP]; Universidade Federal de São Paulo (UNIFESP); UNIV AUTONOMA MADRID1 The rat vas deferens was excised, stored at 4-6-degrees-C and tested after 24, 48, 72 or 96 h for its contractile activity and for the presence of innervation.2 The maximal contractile capacity of the vas, tested through cumulative concentrations of barium chloride (3 x 10(-2) m) was progressively reduced from about 110 mm to about 63 mm after 72 h, without further decay after 96 h. Spontaneous rhythmic contractions were practically absent.3 A loss of endogenous pools of catecholamines was indicated by four parameters: (a) a decline of about 80% after 24 h and of more than 95% after 48 h of the contractile effect of the indirect sympathomimetic agonist tyramine; (b) a fall of about 20%, 50% and 85% on the concentration of noradrenaline, respectively after 24, 48 and 72 h; (c) a fall of about 25% and 90% after respectively 24 and 48 h, of the activity of dopamine-beta-hydroxylase (DBH); (d) a decline of noradrenaline-induced histofluorescence on cross sections of the vas.4 A loss of neuronal uptake capacity was indicated by: (a) a progressive variation of the apparent affinity for adrenaline, expressed as pD2 values, that increased by about 1.5 log units (corresponding to a 30 fold potentiation) after 72 h, and (b) a reduction of the ability of cocaine to potentiate the contractile effects of adrenaline.5 The pD2 values for barium chloride, 5-hydroxytryptamine (5-HT) and histamine were not significantly changed, while the corresponding value for acetylcholine was slightly but significantly reduced by about 0.8 log units.6 The maximal heights of concentration-response curves for noradrenaline, acetylcholine, histamine and 5-HT were reduced by 42-66% in relation to controls. However, when this reduction was measured in relation to the corresponding barium effect, by means of the relative responsiveness ratio (rho), a small though significant increase was observed for noradrenaline, and a fall for the other drugs.7 It is concluded that: (1) the values for the various biochemical and pharmacological parameters decline at different rates, though revealing altogether that denervation is completed by at least 85% after 72 h of hypothermic storage; (2) two of the results, i.e., the lack of spontaneous rhythmic contractions and the lack of increased contractile effects for acetylcholine, 5-HT and histamine, indicate that in these conditions the vas is devoid of the so-called nonspecific sips of denervation.