Formation of dopamine and noradrenaline in rat vas deferens: comparison with guinea-pig vas deferens. (1/3)

1 The formation of [14C]-3,4-dihydroxyphenylalanine (DOPA) from [14C]-tyrosine, in the presence of the amino acid decarboxylase inhibitor, brocresine (3-hydroxy-4-bromobenzyloxyamine dihydrogen phosphate), was greatly enhanced in rat vasa deferentia depolarized by a KCl-enriched Krebs-Henseleit solution (52 mM KCl) compared with tissues maintained in unmodified Krebs-Henseleit solution. 2 When the conversion of tyrosine was allowed to proceed as far as catecholamine (brocresine absent) no significant difference was observed between the accumulation of [14C]-catecholamines (CA) in depolarized rat vasa deferentia and the accumulation in control (non-depolarized) tissues. 3 Endogenous CA levels in the depolarized rat vasa deferentia fell to 67% of the controls after a 1 h incubation period and to 53% at the end of 2 hours. 4 Chromatographic separation on Amberlite CG-120 columns of the newly synthesized CA and catechol metabolites from the rat vas deferens revealed that a very high proportion was present as dopamine. The percentage distribution after 1 h incubation in control Krebs-Henseleit was: noradrenaline (NA): 30.6 +/- 5.2; dopamine 56.9 +/- 5.9; acid metabolites: 12.8 +/- 1.1; and in KCl-rich Krebs-Henseleit, NA: 32; dopamine: 44.7 and acid metabolites 23.3. In contrast to the newly synthesized (14C-labelled) CA, endogenous dopamine comprises only 10% of the endogenous CA stores in rat vas deferens. 5 The distribution of newly synthesized NA and dopamine in rat vas deferens is strikingly different from that of guinea-pig vas deferens where more than 80% of newly formed amine is present as NA. In the latter tissue depolarization with K+ causes a striking increase in CA biosynthesis.  (+info)

Limited recovery of pineal function after regeneration of preganglionic sympathetic axons: evidence for loss of ganglionic synaptic specificity. (2/3)

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Biphasic actions of L-DOPA on the release of endogenous noradrenaline and dopamine from rat hypothalamic slices. (3/3)

Effects of L-DOPA on the release of endogenous noradrenaline and dopamine from rat hypothalamic slices evoked by electrical field stimulation at 5 Hz were investigated in the absence and presence of p-bromobenzyloxyamine (NSD-1055), a DOPA-decarboxylase inhibitor. In the absence of NSD-1055, L-DOPA produced a facilitation of impulse-evoked release of noradrenaline at 0.1 microM but not at 1 and 10 microM, and had no effect on the spontaneous release. On the other hand, L-DOPA 0.1 to 10 microM dose-dependently increased the spontaneous release of dopamine and the highest concentration only increased the evoked release and tissue content of dopamine. In the presence of NSD-1055 10 microM, the increase in the spontaneous release of dopamine was prevented and L-DOPA produced biphasic regulatory effects on the evoked release of noradrenaline and dopamine, a facilitation at 0.1 microM and an inhibition at 1 microM. The facilitation was antagonized by (-)-propranolol 0.1 microM, but not by the (+)-isomer, whereas the inhibition was antagonized by S-sulpiride 1 nM, but not by the R-isomer. In conclusion, L-DOPA appears to produce biphasic actions on the release of endogenous noradrenaline and dopamine from rat hypothalamic slices, not through its conversion to dopamine but through presynaptic regulatory mechanisms, an inhibition via dopamine receptors at a micromolar concentration and a facilitation via beta-adrenoceptors at the lower concentration.  (+info)

Figure 14. Removal of both the soma and dendrite results in a loss of the bump as recorded at the axon hillock. There is an increase in response to noise injection owing to the high input resistance of the hillock (in the absence of the conductance load of the soma and dendrite). These results indicate that the generation of a biphasic action potential requires the propagation of the action potential from the axon into a conductance load and capacitance, such as the soma and dendrite, that is also capable of generating an action potential. ...
Abstract: The objective of this study was to apply the radioimmunoassay for 6-sulphatoxymelatonin (aMT6s) to rat urine, and use it to study the source of aMT6s. The radioimmunoassay was found to have acceptable within- and between-assay variation, excellent specificity, and good parallelism between the standard and unknown. Because urine is highly contaminated we assessed whether preliminary purification was required and established that it was unnecessary. Using this assay a 24-hr rhythm in 6-sulphatoxymelatonin output was seen in pools of urine harvested at 3-hr intervals from Wistar rats on LD 12:12. The nocturnal rise in aMT6s was abolished by constant light. In contrast pinealectomy lowered aMT6s output significantly throughout both dark and light. This study confirms previous studies indicating that the pineal is the major source of 6-sulphatoxymelatonin. It is concluded that urinary 6-sulphatoxymelatonin as measured by radioimmunoassay is a valid measure of pineal gland activity in the ...
TY - JOUR. T1 - Neuropeptide Y and optic chiasm stimulation of affect suprachiasmatic nucleus circadian function in vitro. AU - Shibata, Shigenobu. AU - Moore, Robert Y.. PY - 1993/6/25. Y1 - 1993/6/25. N2 - The retinohypothalamic tract (RHT) is a direct pathway from the retina to the suprachiasmatic nucleus (SCN). Electrical stimulation of the optic nerve or optic chiasm activates the RHT and produces shifts in phase of a circadian rhythm in SCN neuron activity in rat hypothalamic slices in vitro. The phase response curve (PRC) for this effect is very similar to that obtained from administration of light pulses to intact animals maintained in constant darkness. The effect of optic chiasm stimulation is blocked by tetrodotoxin. In addition to the RHT, there is a second entraining pathway, the geniculohypothalamic tract, which arises from neuropeptide Y (NPY)-containing neurons of the intergeniculate leaflet of the lateral geniculate complex. In contrast to optic chiasm stimulation, NPY produces ...
... brocresine MeSH D02.755.239.190 --- bromcresol green MeSH D02.755.239.195 --- bromcresol purple MeSH D02.755.239.216 --- ...
Brocresine (INN) Brocrinat (INN) Brodalumab (USAN, INN) Brodimoprim (INN) Brodspec Brofaromine (INN) Brofed Brofezil (INN) ...
alpha-Fluoromethylhistidine • Brocresine • کتیچین • Cyanidanol-۳ • McN-A-۱۲۹۳ • ۳-methoxy-۵٬۷,۳'۴'-tetrahydroxyflavan • ...
α-FMH • Brocresine • Catechin • Cyanidanol-3 • McN-A-1293 • ME • Meciadanol • Naringenin • Thiazol-4-yimethoxyamine • ...
α-FMH • Brocresine • Catechin • Cyanidanol-3 • McN-A-1293 • ME • Meciadanol • Naringenin • Thiazol-4-yimethoxyamine • ...
... brocresine MeSH D02.755.239.190 --- bromcresol green MeSH D02.755.239.195 --- bromcresol purple MeSH D02.755.239.216 --- ...
Brocresine (INN) Brocrinat (INN) Brodalumab (USAN, INN) Brodimoprim (INN) Brodspec Brofaromine (INN) Brofed Brofezil (INN) ...
... brocresine, brocrinat, brodimoprim, brofaromine, brofezil, brofoxine, brolaconazole, brolamfetamine, bromacrylide, bromadoline ...
alpha-Fluoromethylhistidine • Brocresine • کتیچین • Cyanidanol-۳ • McN-A-۱۲۹۳ • ۳-methoxy-۵٬۷,۳۴-tetrahydroxyflavan • ...
α-FMH • Brocresine • Catechin • Cyanidanol-3 • McN-A-1293 • ME • Meciadanol • Naringenin • Thiazol-4-yimethoxyamine • ...
Z1.639.160 Brocresine D2.755.239.180 D2.455.426.559.389.657.239.180 Bromcresol Green D2.755.239.190 D2.455.426.559.389.657. ...
... brocresine, or m-hydroxybenzylhydrazine); [0098] (xxi) N-methyl-D-aspartate (NMDA) receptor antagonists, such as memantine ( ...
α-FMH • Brocresine • Catechin • Cyanidanol-3 • McN-A-1293 • ME • Meciadanol • Naringenin • Thiazol-4-yimethoxyamine • ...
This graph shows the total number of publications written about "Tritolyl Phosphates" by people in this website by year, and whether "Tritolyl Phosphates" was a major or minor topic of these publications ...
Antidynasty regarding nembutal, an zoometric squalls hyphal adopting with respect to a brocresine. https://keritesrendszerek. ...

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