Hypotheses concerning the mechanism of action of antidepressant drugs

J, Maj; Przegaliński, Edmund; Mogilnicka, E

doi:10.1007/3540133275_1

Cited by 54 publications

(39 citation statements)

References 238 publications

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“…In early studies with the non-selective ligand [3H] WB4101 or [3H] dihydroergocryptine no changes in binding to those receptors were observed (see Charney et al, 1981 ;Maj et al, 1984). Later on, when [3H] prazosin (a selective al-adrenoceptor antagonist) was used as a ligand an increase in the density of ~-adrenoceptors was demonstrated.…”

Section: Introductionmentioning

confidence: 93%

Effect of repeated treatment with antidepressant drugs and electroconvulsive shock (ECS) on [3H] prazosin binding to different rat brain structures

Nowak

Przegaliński

1988

J. Neural Transmission

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The influence of acute and repeated treatment with imipramine, amitriptyline, mianserin, citalopram and ECS on alpha 1-adrenoceptors in different structures of the rat brain (cerebral cortex, hippocampus and thalamus) was measured using [3H] prazosin as a ligand. Repeated, but not acute, treatment with all the above antidepressant drugs and ECS induced an increase in the density of alpha 1-adrenoceptors in the cerebral cortex. On the other hand, no changes were found in the hippocampus and thalamus, with an exception of the increased number of [3H] prazosin binding sites in the thalamus after imipramine. The results suggest that the up-regulation of alpha 1-adrenoceptors following repeated antidepressant treatment is not a general phenomenon within the central nervous system.

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Section: Introductionmentioning

confidence: 93%

Effect of repeated treatment with antidepressant drugs and electroconvulsive shock (ECS) on [3H] prazosin binding to different rat brain structures

Nowak

Przegaliński

1988

J. Neural Transmission

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“…These drugs act as amine uptake inhibitors or alter the functions of adrenergic, serotonergic, and dopaminergic receptors (Maj et al, 1984). Recently, it has been reported that ␤ 1 -adrenergic receptor mRNA and ligand binding are regulated by chronic antidepressant treatment (Hosoda and Duman, 1993).…”

Section: Introductionmentioning

confidence: 99%

Differential inhibition of catecholamine secretion by amitriptyline through blockage of nicotinic receptors, sodium channels, and calcium channels in bovine adrenal chromaffin cells

Park

Shin

Suh

et al. 1998

Synapse

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We investigated the effects of amitriptyline, a tricyclic antidepressant, on [3H]norepinephrine ([3H]NE) secretion and ion flux in bovine adrenal chromaffin cells. Amitriptyline inhibited [3H]NE secretion induced by 1,1-dimethyl-4-phenylpiperazinium iodide (DMPP) and 70 mM K+. The half maximal inhibitory concentration (IC50) was 2 microM and 9 microM, respectively. Amitriptyline also inhibited the elevation of cytosolic calcium ([Ca2+]i) induced by DMPP and 70 mM K+ with IC50 values of 1.1 microM and 35 microM, respectively. The rises in cytosolic sodium ([Na+]i) and [Ca2+]i induced by the Na+ channel activator veratridine were also inhibited by amitriptyline with IC50 values of 7 microM and 30 microM, respectively. These results suggest that amitriptyline at micromolar concentrations inhibits both voltage-sensitive calcium (VSCCs) and sodium channels (VSSCs). Furthermore, submicromolar concentrations of amitriptyline significantly inhibited DMPP-induced [3H]NE secretion and [Ca2+]i rise, but not veratridine- or 70 mM K+-induced responses, suggesting that nicotinic acetylcholine receptors (nAChR) as well as VSCCs and VSSCs can be targeted by amitriptyline. DMPP-induced [Na+]i rise was much more sensitive to amitriptyline than the veratridine-induced rise, suggesting that the influx of Na+ and Ca2+, through the nAChR itself is blocked by amitriptyline. Receptor binding competition analysis showed that binding of [3H]nicotine to chromaffin cells was significantly affected by amitriptyline at submicromolar concentrations. The data suggest that amitriptyline inhibits catecholamine secretion by blocking nAChR, VSSC, and VSCC.

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“…Maprotiline is an antidepressant compound with an atypical tetracyclic structure, which can strongly inhibit the re-uptake of noradrenaline in the brain and peripheral tissues, but not of serotonin. 33 In the competition experiment, it was shown that hNETmediated 125 I-MIBG uptake was specifically inhibited by maprotiline in a dose-dependent manner. Compared with the inhibiting effect in the control of SK-N-SK cells, 125 I-MIBG uptake in HepG2 cells was specially inhibited to the level as in wild-type cells, indicating that the hNET gene products were functionally active.…”

Section: Discussionmentioning

confidence: 99%

In vitro and in vivo studies of adenovirus-mediated human norepinephrine transporter gene transduction to hepatocellular carcinoma

Huang

et al. 2010

Cancer Gene Ther

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The clinical value of 131 I-MIBG for targeted imaging and targeted radiotherapy is limited to neural crest-derived tumors expressing human norepinephrine transporters (hNET) protein. To extend 131 I-MIBG-targeted therapy to other nonexpressed hNET tumors, this study investigated the hNET expression in vitro and in vivo in HepG2 hepatoma mediated by recombinant adenovirus encoding the hNET gene (Ad-hNET). For this purpose, the HepG2 cells showed a 4.87-fold increase in 125 I-MIBG uptake after infection with Ad-hNET, and the uptake of 125 I-MIBG could be specifically inhibited by maprotiline. Immunohistological analysis, in vivo biological study and 131 I-MIBG scintigraphic imaging also revealed the high expression of hNET protein in hepatoma. This in vitro and in vivo studies demonstrate the feasibility of hNET gene transfer, meditated by adenovirus vector, could extend to tumors other than those derived from the neural crest, which provides a sound foundation for further investigation of hepatocellular carcinomatargeted radiotherapy mediated by adenovirus transfection with hNET gene.

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Hypotheses concerning the mechanism of action of antidepressant drugs

Cited by 54 publications

References 238 publications

Effect of repeated treatment with antidepressant drugs and electroconvulsive shock (ECS) on [3H] prazosin binding to different rat brain structures

Effect of repeated treatment with antidepressant drugs and electroconvulsive shock (ECS) on [3H] prazosin binding to different rat brain structures

Differential inhibition of catecholamine secretion by amitriptyline through blockage of nicotinic receptors, sodium channels, and calcium channels in bovine adrenal chromaffin cells

In vitro and in vivo studies of adenovirus-mediated human norepinephrine transporter gene transduction to hepatocellular carcinoma

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