Transport of Catecholamines by Native and Reconstituted Rat Heart Synaptic Vesicles

Angelides, Kimon J.

doi:10.1111/j.1471-4159.1980.tb07094.x

Cited by 26 publications

(5 citation statements)

References 29 publications

(30 reference statements)

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“…The monoamine transporter has identical affinities for 5-HT and TBZOH and similar "turnover number" ( Vmax/Bmm) in dopaminergic , serotoninergic, and noradrenergic mouse synaptic vesicles in P3 fractions. Comparable results are reported for bovine caudate nucleus synaptic vesicles ( K , = 2.6 p M , ICs0 = 7 nM; Near and Mahler, 1983), for rat heart noradrenergic synaptic vesicles ( K , = 0.7 p M , Angelides, 1980), and for the mainly adrenergic chromaffin granules ( K , = 0.5 p M , B. Gasnier and D. Scherman, unpublished data; IC,, = 3.5 nM; turnover number = 35, . These data suggest the involvement of a common transporter molecule in monoamine uptake by the various monoaminergic storage vesicles.…”

Section: Discussionsupporting

confidence: 52%

“…Total monoamine concentrations of fractions P2 and P3 were 121 +-42 nM and 79 k 25 nM, respectively (mean of values obtained in the six brain areas). Thus, even if endogenous monoamines were completely free in solution during the uptake experiments, their concentration was low compared to the K , of uptake: K , for 5-HT is 1 p M (Table 2 ) and K , values for catecholamines are higher than that of 5-HT (Phillips, 1974;Kanner et al, 1979;Angelides, 1980;Near and Mahler, 1983). Therefore, endogenous monoamines did not seriously affect uptake measurements.…”

Section: Stability Of [3h]tbzoh Incubated With Membranesmentioning

confidence: 99%

“…Monoaminergic synaptic vesicles of the central and peripheral nervous systems and chromaffin granules of the adrenal medulla take up monoamines by active ATP-induced processes (Carlsson et al, 1962;von Euler, 1972;Philippu, 1976;Toll et al, 1977) that possess common properties: (1) they are secondary uptake systems in which a specific monoamine transporter is activated by the electrochemical proton gradient built up by a proton pump ATPase (Njus and Radda, 1978;Toll and Howard, 1978;Johnson and Scarpa, 1979; Maron et al, 1979;Angelides, 1980;Scherman and Henry, 1980a); (2) the vesicles take up indoleamines and catecholamines with similar efficiency, independently of which monoamine is physiologically present (Phillips, 1974;Da Prada et al, 1975;Angelides, 1980;Near and Mahler, 1983); and (3) active uptake is inhibited by reserpine (Kirshner, 1962;von Euler, 1972;Toll and Howard, 1978;Angelides, 1980). This latter effect of reserpine may be responsible for the depleting effect of the drug on monoamine levels (Carlsson, 1965).…”

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Dihydrotetrabenazine Binding and Monoamine Uptake in Mouse Brain Regions

Scherman

1986

Journal of Neurochemistry

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Binding of [2-3H]dihydrotetrabenazine and uptake of 5-hydroxytryptamine (serotonin) were studied in mouse brain cerebellum, pons-medulla, frontal cortex, hypothalamus, hippocampus, and striatum. Binding of [2-3H]dihydrotetrabenazine to homogenates of these brain areas is stable for several hours and occurs at a homogeneous class of binding sites ( K D = 2.4 nM). Subcellular fractionation and regional distribution of [2-3H]dihydrotetrabenazine binding and serotonin uptake showed that the ligand binds to synaptic vesicles. Dihydrotetrabenazine inhibited serotonin uptake with the same inhibitory constant (IC50 = 2.6 nM) for synaptic vesicles from brain regions containing 3,4-dihydroxyphenylethylamine (dopamine) or serotonin and noradrenaline in different proportions. This constant is similar to the K D of [2-3H]dihydrotetrabenazine, which suggests that the latter ligand labels specifically and with the same affinity the monoamine transporter from various mono-aminergic synaptic vesicles. Therefore the regional differences in central monoamine depletion induced in vivo by tetrabenazine are not due to regional differences in inhibition of vesicular monoamine uptake. Moreover, vesicular monoamine transporters from the central and peripheral nervous systems of various mammals and from bovine adrenal glands have comparable affinity for substrate and inhibitor ( K , values for serotonin and ICso for dihydrotetrabenazine are about 0.8 p M and 3 nM, respectively) and comparable turnover number (10-35 molecules transported per transporter per minute), which suggests the involvement of a common transporter molecule in the process of monoamine uptake by the various monoaminergic storage vesicles. Key Words: Monoamine uptake-Synaptic vesi~les-[2-~H]Dihydrotetrabenazine binding-Tetrabenazine. Scherman D. Dihydrotetrabenazine binding and monoamine uptake in mouse brain regions. 5-HT, 5-hydroxytryptamine (serotonin); TBZ, tetrabenazine; Pierre and Marie Curie, Pans 75005, France. TBZOH, dihydrotetrabenazine. Whittaker V. P., Michaelson I. A., and Kirkland R. J. (1963) The separation of synaptic vesicles from disrupted nerve-ending particles. Biochem. Pharmacol. 12, 300-302. 694-706.

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Section: Discussionsupporting

confidence: 52%

Section: Stability Of [3h]tbzoh Incubated With Membranesmentioning

confidence: 99%

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Dihydrotetrabenazine Binding and Monoamine Uptake in Mouse Brain Regions

Scherman

1986

Journal of Neurochemistry

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“…Michaelson & Angel (1980) found that isolated Torpedo vesicles are internally acidic and release endogenous AcCh in the presence of uncouplers. In addition to storage of catecholamines in chromaffin granules and 5-hydroxytryptamine in brain synaptic vesicles, catecholamine storage in brain and heart synaptic vesicles (Toll et al, 1977;Toll & Howard, 1978;Angelides, 1980), 5hydroxytryptamine storage in platelet granules (Rudnick et al, 1980), and peptide storage in neurohypophysis secretory vesicles (Russell & Holz, 1981) are linked to proton gradients.…”

Section: Discussionmentioning

confidence: 99%

Proton gradient linkage to active uptake of [3H]acetylcholine by Torpedo electric organ synaptic vesicles

Anderson¹,

King²,

Parsons³

1982

Biochemistry

135

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It has been confirmed that cholinergic synaptic vesicles isolated from the electric organ of Torpedo californica exhibit adenosine 5'-triphosphate (ATP) dependent active uptake of [3H]acetylcholine. Active uptake can be completely inhibited by low concentrations of the mitochondrial uncouplers carbonyl cyanide p-(trifluoromethoxy)phenylhydrazone, nigericin, gramicidin, valinomycin, and A 23187. Under similar conditions uncouplers stimulate the vesicle adenosinetriphosphatase (ATPase) by from 40 to 80%. ATP-supported uptake of [3H]acetylcholine increases greatly as the external pH is increased from 6.6 to 7.6 and remains approximately constant from pH 7.8 to pH 8.6. The uptake also becomes more selective for [3H]acetylcholine compared to [14C]choline as the pH is increased from 6.6 to 7.6, achieving 12-fold selectively, in a manner similar to the increase in the amount of [3H]acetylcholine taken up. Bicarbonate stimulates both the amount and selectivity of [3H]acetylcholine uptake over the lower pH range, but it has no effect over the higher pH range. Exogenous ammonium ion completely inhibits active [3H]acetylcholine uptake, with lower concentrations of ammonium ion required at higher pH values in a manner consistent with ammonia being the active species. Adenosine 5'-diphosphate and a nonhydrolyzable ATP analogue do not support active [3H]acetylcholine uptake. It is concluded that an ATPase pumps protons into the cholinergic synaptic vesicle to produce an internally acidic and positively charged proton gradient that is linked to [3H]acetylcholine uptake.

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“…It was also evident that the recovery of the neuronal stores of noradrenaline paralleled the recovery of the vesicular uptake process and the delivery of new vesicles to the nerve terminals. However, it was not until 1980 that this action of reserpine was explained in terms of its disruption of the intravesicular/cytoplasmic proton gradient (Angelides, 1980). 6-Hydoxydopamine (6OHDA) was also known to cause long-lasting depletion of noradrenaline and dopamine stores and, in the late 1960s, it was discovered to be a neurotoxin for catecholamine-releasing neurons (Bloom et al, 1969; Thoenen and Tranzer, 1968), which has made it an invaluable research tool ever since.…”

Section: Landmark Developments In Pharmacotherapeuticsmentioning

confidence: 99%

Catecholamines: Knowledge and understanding in the 1960s, now, and in the future

Stanford

Heal

2019

Brain and Neuroscience Advances

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In the 1980s, the development of in vivo microdialysis, highperformance liquid chromatography (HPLC) coupled with electrochemical detection, and fast cyclic voltammetry (see Anderzhanova and Wotjak, 2013; Young, 1993) made it possible to monitor changes in the concentration of extracellular catecholamines of freely moving animals, following an experimental challenge. These approaches are now complemented by a raft of brain imaging techniques, for example: positron emission tomography (PET; see Finnema et al., 2015; Volkow et al., 2007), single-photon emission computed tomography (SPECT), and functional magnetic resonance imaging (fMRI; see Borsook et al., 2006; DeCharms, 2008). However, unlike microdialysis and voltammetry, neuroimaging techniques suffer the limitation that they provide only 'snapshots' of the functional status of the brain of immobilised subjects. A detailed and contemporary account of the state-of-the-science of catecholamine research, 50 years ago, is to be found in

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Transport of Catecholamines by Native and Reconstituted Rat Heart Synaptic Vesicles

Cited by 26 publications

References 29 publications

Dihydrotetrabenazine Binding and Monoamine Uptake in Mouse Brain Regions

Dihydrotetrabenazine Binding and Monoamine Uptake in Mouse Brain Regions

Proton gradient linkage to active uptake of [3H]acetylcholine by Torpedo electric organ synaptic vesicles

Catecholamines: Knowledge and understanding in the 1960s, now, and in the future

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