Effects of some atypical antidepressants on β-adrenoceptor binding and adenylate cyclase activity in the rat forebrain

Garcha, G.; Smokcum, Roger W.J.; Stephenson, John; Weeramanthri, Tara B.

doi:10.1016/0014-2999(85)90276-6

Cited by 36 publications

(8 citation statements)

References 30 publications

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“…The discrepancy between behavioral and neurochemical findings in sertralinetreated rats led us to speculate that these changes are not primary or common ones responsible for the antidepressive effect of antidepressants, especially of SSRIs. Some investigations on other representative SSRIs, such as fluoxetine (Baron et al 1988;Goodnough and Baker 1994) or citalopram (Hyttel et al 1984;Garcha et al 1985), also seem to confirm our speculation. Most reports did not demonstrate decrease in density of and 5-HT 2 receptors or in cAMP accumulation by norepinephrine and isoproterenol in the cortex after chronic treatment (Baron et al 1988;Nelson et al 1991;Goodnough and Baker 1994).…”

Section: Discussionsupporting

confidence: 87%

“…Recently, some studies demonstrated that chronic administration of SSRIs such as fluoxetine (Baron et al 1988;Goodnough and Baker 1994) and citalopram (Hyttel et al 1984;Garcha et al 1985) neither reduces density of and 5-HT 2 receptors nor diminishes AC activity in rat brain (Mishra et al 1979;Kopanski et al 1983). Therefore, controversy exists concerning whether down-regulation of monoamine receptors and desensitization of AC activity in the brain are primarily involved in the therapeutic mechanism of antidepressants.…”

Section: Introductionmentioning

confidence: 99%

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Behavioral stimulation without alteration of β and 5-HT receptors and adenylate cyclase activity in rat brain after chronic sertraline administration

et al. 1997

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Effects of chronic treatment with selective 5-HT reuptake inhibitors (SSRIs) on the monoaminergic functions have not been much investigated in compared with tricyclic antidepressants. Therefore, we compared the effects of 3-week treatment with sertraline, a potent SSRI, to those of imipramine (10 mg/kg, IP, twice a day), on monoamine receptors and adenylate cyclase (AC) activity in rat brain. Two-week treatment with both sertraline and imipramine reduced immobility in the water wheel test to the comparable extent. Sertraline treatment did not affect Kd and Bmax of [3H]CGP12177 and [3H]ketanserin bindings or cAMP, accumulation by norepinephrine, isoproternol, 5'-guanylylimidodiphosphate [Gpp(NH)p] and forskolin in the cortical membrane compared with vehicle-treated rats. On the other hand, imipramine treatment decreased Bmax of both bindings and norepinephrine- or isoproternol-stimulated cAMP accumulation. Treatment with either antidepressant induced no apparent changes in [3H]8-OH-DPAT [2-(N, N-dipropylamino)-8-hydroxy-1,2,3,4-tetrahydronaphthalene] binding in the hippocampal membrane. These results suggested that chronic treatment of sertraline induced little effect on monoamine receptors and AC activity in the brain and that the alteration of these functions may not be primarily involved in antidepressive effects of antidepressants, at least of SSRIs.

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Section: Discussionsupporting

confidence: 87%

Section: Introductionmentioning

confidence: 99%

Behavioral stimulation without alteration of β and 5-HT receptors and adenylate cyclase activity in rat brain after chronic sertraline administration

et al. 1997

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“…These studies have indicated that one of the most significant modifications induced by prolonged antidepressant treatment is the desensitization of norepinephrine (NE)-sensitive adenylate cyclase (Vetulani and Sulser, 1975), often paralleled by a reduction in the number of beta-adrenergic receptors (Banerjee et al, 1977). However, only a few second-generation antidepressants share both these effects (Mishra et al, 1980;Garcha et al, 1985), which suggests that if antidepressants that inhibit either NE or serotonin (5HT) uptake have common actions, then these actions are not at the level of the P-adrenoreceptor.…”

Section: Introductionmentioning

confidence: 99%

EFFECT OF SOME TRICYCLIC AND NONTRICYCLIC ANTIDEPRESSANTS ON [³H]IMIPRAMINE BINDING AND SEROTONIN UPTAKE IN RAT CEREBRAL CORTEX AFTER PROLONGED TREATMENT

Brunello

Riva

Volterra

et al. 1987

Fundamemntal Clinical Pharma

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Chronic administration of different antidepressant drugs reduced the number of [3H]imipramine [( 3H]IMI) binding sites in rat cerebral cortex. In the same experimental conditions, fluvoxamine and dothiepin, as well as desmethylimipramine, induced an increase in the maximal velocity of high affinity serotonin (5HT) uptake in cortical slices, whereas citalopram and viloxazine were ineffective in this regard. Our results indicate that even if 5HT uptake and [3H]IMI binding sites are located on the same nerve terminals, they are differently modulated. Increased Vmax of the 5HT uptake process could be due to a rebound phenomenon after withdrawal from drugs that acutely inhibit 5HT uptake. The effect on [3H]IMI sites might be explained through either the agonist properties of the drugs towards these sites or the involvement of mechanisms still unknown.

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“…1982, Delini-Stulaetal. 1983), but even in this respect controversial find ings have been recently published (Garcha et al 1985). The beta-receptor down-regu lating effects of imipramine have not been reproduced in a study by Antkiewicz-Michaluk (1985) and Costa et al (1986) failed to show a decrease of beta-receptor density (Bmax) or of the formation of NA-stimulated cyclic AMP after chronic maprotiline treatment.…”

Section: Delayed Effects Of Antidepressant Drugsmentioning

confidence: 98%

New Pharmacological Findings in Depression

Delini‐Stula¹

1986

Psychopathology

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The last decade of psychopharmacological research in depression is characterised by the development of structurally novel and biochemically selective-acting drugs and by the shift of interest from the acute to long-term treatment effects of antidepressants on catecholaminergic transmission. Of particular importance in this respect are the findings demonstrating adaptative changes occurring at receptor levels which have led to alternative theoretical formulations about the origin of depression and the mode of action of antidepressants. However in spite of the progress in this field of research the mechanism of therapeutic action of antidepressants remains unknown. Examples of drugs not affecting NA and 5-HT uptake or release and producing no adaptative changes of adrenergic receptors (trimipramine, levoxaprotiline) indicate that antidepressant-like activity can be achieved by mechanisms which still remain to be elucidated.

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Effects of some atypical antidepressants on β-adrenoceptor binding and adenylate cyclase activity in the rat forebrain

Cited by 36 publications

References 30 publications

Behavioral stimulation without alteration of β and 5-HT receptors and adenylate cyclase activity in rat brain after chronic sertraline administration

Behavioral stimulation without alteration of β and 5-HT receptors and adenylate cyclase activity in rat brain after chronic sertraline administration

EFFECT OF SOME TRICYCLIC AND NONTRICYCLIC ANTIDEPRESSANTS ON [³H]IMIPRAMINE BINDING AND SEROTONIN UPTAKE IN RAT CEREBRAL CORTEX AFTER PROLONGED TREATMENT

New Pharmacological Findings in Depression

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Effects of some atypical antidepressants on β-adrenoceptor binding and adenylate cyclase activity in the rat forebrain

Cited by 36 publications

References 30 publications

Behavioral stimulation without alteration of β and 5-HT receptors and adenylate cyclase activity in rat brain after chronic sertraline administration

Behavioral stimulation without alteration of β and 5-HT receptors and adenylate cyclase activity in rat brain after chronic sertraline administration

EFFECT OF SOME TRICYCLIC AND NONTRICYCLIC ANTIDEPRESSANTS ON [3H]IMIPRAMINE BINDING AND SEROTONIN UPTAKE IN RAT CEREBRAL CORTEX AFTER PROLONGED TREATMENT

New Pharmacological Findings in Depression

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EFFECT OF SOME TRICYCLIC AND NONTRICYCLIC ANTIDEPRESSANTS ON [³H]IMIPRAMINE BINDING AND SEROTONIN UPTAKE IN RAT CEREBRAL CORTEX AFTER PROLONGED TREATMENT