Action of mianserin and zimelidine on the norepinephrine receptor coupled adenylate cyclase system in brain: Subsensitivity without reduction in β-adrenergic receptor binding

Mishra, R.; Janowsky, Aaron; Sulser, Fridolin

doi:10.1016/0028-3908(80)90009-x

Cited by 174 publications

(32 citation statements)

References 20 publications

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“…Mianserin was found not to have this effect, confirming an earlier investigation (Mishra et al, 1980). The binding of the ml-receptor-specific ligand [3H]-prazosin was not affected by chronic treatment with amitriptyline.…”

Section: Discussionsupporting

confidence: 85%

“…Mianserin has not been implicated in cardiac disorders in man and does not cause down-regulation of cerebral cortical P-adrenoceptors as monitored by ligand-binding measurements (Mishra et al, 1980). Cardiac and cerebral cortical P-adrenoceptors may be assessed using the radio-ligand [3HJ-dihydroalprenolol ([3H]-DHA) (Alexander et al, 1975;Bylund & Snyder, 1976).…”

Section: Introductionmentioning

confidence: 99%

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Effects of chronic administration of amitriptyline or mianserin on rat cardiac and central adrenoceptors

Choudhury¹,

O’Donnell²

1985

British J Pharmacology

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1 Rats were administered either amitriptyline (20mg kg-, i.p.) or mianserin (10mg kg-', i.p.) for 21 consecutive days and the a-and P-adrenoceptor characteristics of cardiac ventricles, cerebral cortex and hippocampus examined by ligand-binding procedure.2 Chronic administration of amitriptyline significantly reduced the maximum density of P-receptors in the cerebral cortex without significantly altering cardiac a-or P-receptors; mianserin treatment had no significant effect on any of the receptors studied.

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Section: Discussionsupporting

confidence: 85%

Section: Introductionmentioning

confidence: 99%

Effects of chronic administration of amitriptyline or mianserin on rat cardiac and central adrenoceptors

Choudhury¹,

O’Donnell²

1985

British J Pharmacology

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“…Gi-proteins represent the most widespread modulatory signaling pathway in neurones (Holtz et al 1986) and one of their principal effect is the inhibition of adenylate cyclase activity (Sprang 1997). It has been reported that chronic treatment with several antidepressant drugs reduced the cAMP production stimulated by forskolin or noradrenaline (Mishra et al 1980;Okada et al 1986;Newman et al 1993), further supporting the hypothesis of the involvement of this transduction system in the mechanism of action of amitriptyline and clomipramine.…”

Section: Discussionmentioning

confidence: 92%

Role of Gi Proteins in the Antidepressant-like Effect of Amitriptyline and Clomipramine

Galeotti

Bartolini

Ghelardini

2002

Neuropsychopharmacology

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The effect of the i.c.v. administration of pertussis toxin (PTX) and antisense oligodeoxynucleotides directed against the ␣ subunit of different Gi-proteins (anti-For the past several decades, antidepressant drugs have been widely used in the treatment of clinical depression and other psychiatric disorders. Several distinct pharmacological compounds show therapeutic efficacy. These include monoamine oxidase inhibitors, tricyclic compounds, selective serotonin and norepinephrine reuptake inhibitors, as well as some atypical drugs. Numerous studies have examined the effects of antidepressants on neurotransmitter metabolism, turnover, and receptor sensitivity and several theories on their mechanism of action have been proposed. These include the inhibition of monoamine transporter activity in presynaptic membranes (Schildkraut 1965), downregulation of ␤ -adrenoceptors (Mazzola-Pomietto et al. 1994), alteration at cholinergic, dopaminergic or GABAergic receptors (Henringer and Charney 1987). However, the molecular mechanism of action underlying the therapeutic effect of antidepressants is still unclear.Despite their diversity, these treatments subserve the same final clinical effect. Therefore, the possibility that these diverse agents converge on a single postreceptorial target evoked a great research interest. Since most neurotransmitter receptors and neuromodulators are coupled to intracellular effectors through G-proteins (Birnbaumer 1990), recent studies searching for a com-

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“…Thus, chronic administration of the antidepressant drugs mianserin and zimelidine causes a decrease in the sensitivity of the cyclic AMP response to NA in the cortex of rats without any modification of the density of ,3-adrenergic receptors (Mishra et al, 1980). Chlorimipramine and fluroxetine, potent inhibitors of 5-HT uptake, presumably enhance the extracellular concentration of 5-HT, but do not affect 5-HT binding in the brain (Wirz-Justice et al, 1978;Maggi et al, 1980b).…”

Section: Modulation Ofreceptor Sensitivitymentioning

confidence: 95%

Biochemical pharmacology of paradoxical sleep.

Gaillard¹

1983

Brit J Clinical Pharma

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1 The role of noradrenergic cells in the regulation of paradoxical sleep is still controversial, and experimental data have given rise to contradictory interpretations.2 Early investigations focused primarily on chemical neurotransmissions. However, the process of information transmission between cells involves many other factors, and the cell surface is an important site for transduction of messages into modifications of the activity of postsynaptic cells.3 a-adrenoceptors are believed to play an important role in the control of wakefulness and paradoxical sleep. Experimental evidence suggests that physiological modulation of receptor sensitivity, possibly by specific neuro-modulators, may be a key mechanism in synaptic transmission. 4 In the investigation of the mechanisms involved in paradoxical sleep regulation, lesions of the locus coeruleus have given equivocal results. Collateral inhibition, probably mediated by a2-adrenoceptors, appears to be a powerful mechanism. The exact temporal relationship between noradrenergic cell activation and paradoxical sleep production is not established, but 5-HT appears to be involved. Differences between paradoxical sleep and waking may be related to a physiological modulation of a2-adrenoceptor sensitivity.

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Action of mianserin and zimelidine on the norepinephrine receptor coupled adenylate cyclase system in brain: Subsensitivity without reduction in β-adrenergic receptor binding

Cited by 174 publications

References 20 publications

Effects of chronic administration of amitriptyline or mianserin on rat cardiac and central adrenoceptors

Effects of chronic administration of amitriptyline or mianserin on rat cardiac and central adrenoceptors

Role of Gi Proteins in the Antidepressant-like Effect of Amitriptyline and Clomipramine

Biochemical pharmacology of paradoxical sleep.

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