Topic
Norepinephrine binding
About: Norepinephrine binding is a research topic. Over the lifetime, 41 publications have been published within this topic receiving 1255 citations.
Papers
Journal Article•
TL;DR: Consecutive dosing, at a 1-day interval, with reserpine, guanethidine and 6-hydroxydopamine, in any combination of two in either sequence, produced additive depletion of heart norepinephrine.
Abstract: Some compounds were examined for potency in depleting mouse heart norepinephrine, which was measured 16 hours (or 1 hour for tyramine) after intraperitoneal drug administration. These compounds, in order of increasing ED50's (dose, in mg/kg, required to half deplete heart norepinephrine) were: reserpine, metaraminol, 6-hydroxydopamine (2,4,5-trihydroxyphenethylamine), guanethidine and tyramine.
After administration of equipotent doses of the compounds, heart norepinephrine returned to normal with widely varying rates. Most rapid repletion occurred after tyramine, followed in order by guanethidine, metaraminol, reserpine and 6-hydroxydopamine.
Tyramine, administered 1 hour previously, blocked the longer-lasting depletion of heart norepinephrine by 6-hydroxydopamine, but not by metaraminol, guanethidine and reserpine. Under similar conditions, guanethidine blocked 6-hydroxydopamine and reserpine, but not metaraminol; and metaraminol blocked 6-hydroxydopamine.
A second suboptimal dose of reserpine, guanethidine or metaraminol, administered 1 day after a first dose, produced additional depletion of heart norepinephrine. However, a second dose of 6-hydroxydopamine produced no additional effect unless it was larger than the first dose. Consecutive dosing, at a 1-day interval, with reserpine, guanethidine and 6-hydroxydopamine, in any combination of two in either sequence, produced additive depletion of heart norepinephrine.
The data can be interpreted, within the framework of the two-pool concept of norepinephrine storage, as follows:
1. Reserpine releases norepinephrine by acting upon pool 1; guanethidine, like bretylium, blocks the action of reserpine on this pool, but does not itself release norepinephrine from pool 1.
2. Tyramine, guanethidine and metaraminol, in order of increasing affinity for norepinephrine binding sites, release the amine through pool 2.
3. 6-Hydroxydopamine, although possessing less affinity for binding sites of pool 2 than tyramine, metaraminol and guanethidine, destroys or alters the binding sites in such a way that they must be replaced.
234 citations
TL;DR: Binding of norepinephrine to this subcellular fraction was differentiated from binding to neural vesicles by virtue of a different specificity, a lack of sensitivity to reserpine, the absence of an ATP requirement, and the preservation of norpinephrine binding after chemical sympathectomy.
118 citations
TL;DR: Evidence is presented in support of the hypothesis that the rise in cytosolic calcium ions resulting from changes in calcium and other aspects of cellular metabolism is responsible for many of the alpha-adrenergic actions of catecholamines.
Abstract: Epinephrine and norepinephrine binding sites with the physiological characteristics of alpha-adrenergic receptors have been identified in the plasma membranes of liver and other cells. Interaction of catecholamines with these receptors causes a mobilization of calcium ions from mitochondria and perhaps other intracellular stores in liver cells. In other cells, there may also be influx of extracellular calcium ions. Evidence is presented in support of the hypothesis that the rise in cytosolic calcium ions resulting from these changes is responsible for many of the alpha-adrenergic actions of catecholamines. Possible mechanisms by which activation of alpha-adrenergic receptors causes changes in calcium and other aspects of cellular metabolism are discussed.
118 citations
TL;DR: The results indicate that methamphetamine is neurotoxic to serotonin, dopamine, and norepinephrine neurons.
Abstract: The neurotoxicity of methamphetamine to monoaminergic neurons was examined. Neurotoxicity was assessed by quantitative autoradiography using radioligands specific for binding to norepinephrine, dopamine, and serotonin uptake sites. High-dose administration of methamphetamine led to decreases in binding to uptake sites for the three monoamines. Norepinephrine binding sites were decreased in certain amygdaloid nuclei and in the dorsomedial hypothalamic nucleus. Serotonin binding sites were reduced in widespread brain areas, while dopamine binding sites were reduced in the caudate putamen, olfactory tubercle, and nucleus accumbens. The decreases in binding site density for the three monoamines are limited to terminal field areas; cell body areas are not affected. Our results indicate that methamphetamine is neurotoxic to serotonin, dopamine, and norepinephrine neurons. The neurotoxicity to norepinephrine neurons is in selected brain areas.
78 citations
TL;DR: The distribution of radioactivity in association with sympathetic nerve terminals and intraneuronal organelles 30 min after the administration of tritiated norepinephrine (NE-3H) was studied by electron microscope radioautography with recently developed quantitative methods of analysis reported in the accompanying paper.
Abstract: The distribution of radioactivity in association with sympathetic nerve terminals and intraneuronal organelles 30 min after the administration of tritiated norepinephrine (NE-3H) was studied by electron microscope radioautography with recently developed quantitative methods of analysis reported in the accompanying paper (Salpeter et al., 1969). Nerves from the pineal body and the adrenal capsule were examined. It was found that nerve terminals containing vesicles were heavily labeled. (These terminals were not necessarily in contact with some innervated structure.) There was no selective labeling of either the intraneuronal mitochondria or the relatively small population of large (∼1000 A) dense core granules. Small vesicles (∼500 A), some of which have a dense internal granule, could not be analysed separately because they are closely packed and occupy ∼60% of the volume in terminals. Because of the extensive distribution of these small granular and agranular vesicles in the radioactive terminals, they remain the most likely site for norepinephrine binding. Yet although the vesicles were uniformly distributed within the nerve terminals, it appears that the radioactivity was not. There appeared to be a somewhat higher concentration of radioactivity at the periphery of the nerve terminals than in the center. The usefulness of the method of analysis used in this study for determining the location of bound H3NE pools in the nerve is discussed.
69 citations
Related Topics (5)
Performance Metrics
| Year | Papers |
|---|---|
| 2018 | 1 |
| 1999 | 1 |
| 1993 | 1 |
| 1992 | 2 |
| 1985 | 2 |
| 1984 | 1 |