Temporal sequence of changes in central noradrenergic system of rat after prolonged antidepressant treatment: Receptor desensitization and neurotransmitter interactions

Racagni, Giorgio; Mocchetti, Italo; Calderini, G.; Battistella, A.; Brunello, Nicoletta

doi:10.1016/0028-3908(83)90191-0

Cited by 73 publications

(24 citation statements)

References 54 publications

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“…Additionally, it was claimed that long-term administration of tricyclic antidepressants, such as imipramine or desimipramine, would down-regulate the maximal number of 3H-IMI binding sites, but this latter effect was not confirmed in all subsequent studies. Contrary to earlier reports Briley et al, 1982;Racagni et al, 1983;Raisman et aL, 1980), Plenge and Mellerup (1982), Lee et al (1983) and Perry et al (1983)described no change in the maximal number of 3H-IMI binding sites after a long-term treatment with IMI in rats, and Kinnier (1980) reported that such a drug effect is limited to the rat hippocampal region.…”

Section: Introductioncontrasting

confidence: 66%

“…In addition, a lower Kd value for 3H-CN-IMI than for 3H-IMI was observed in the present study. With both ligands we have found higher Bmax values than had previously been reported for untreated rats (Kinnier et al, 1980;Racagni et al, 1983;Raisman et al, 1980). Whether the tissue preparation could be responsible for such quantitative differences, which has also been shown to dramatically influence the maximal number of 3H-IMI binding sites in human thrombocytes (Friedlet al, 1983) and/or whether the amount of tissue used per sample could cause the differences, as suggested by Plenge and Mellerup (1982), remains to be determined.…”

Section: Discussioncontrasting

confidence: 38%

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3H-imipramine and3H-cyano-imipramine binding in rat brain tissue: Effect of long-term antidepressant administration

Gentsch¹,

Lichtsteiner²,

Feer³

1984

J. Neural Transmission

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3H-imipramine and 3H-cyano-imipramine binding was determined in brain homogenates of rats which had been treated for 21 days with imipramine or desimipramine. When compared to control animals, long-term administration of these antidepressants did not induce any alteration in the maximal number of 3H-imipramine or 3H-cyano-imipramine binding sites. However, a transient increase in the apparent dissociation constant was observed. Such findings are discussed in respect to previous studies, which have been highly contraversial.

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Section: Introductioncontrasting

confidence: 66%

Section: Discussioncontrasting

confidence: 38%

3H-imipramine and3H-cyano-imipramine binding in rat brain tissue: Effect of long-term antidepressant administration

Gentsch¹,

Lichtsteiner²,

Feer³

1984

J. Neural Transmission

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“…However, this capacity does not discount that endogenous GnRH neurons contain extensive interneuronal contacts; the preovulatory GnRH surge is probably initiated by these cell-to-cell contacts. Several neural peptides and transmitters have been implicated in regulation of the GnRH/LH axis [65][66][67][68][69][70][71][72]. Peptides in or proximal to GnRH cells include galanin, neuropeptide Y (NPY), delta sleep-inducing peptide, and endorphins [73][74][75].…”

Section: Rabbitsmentioning

confidence: 99%

Coital and Estrogen Signals: A Contrast in the Preovulatory Neuroendocrine Networks of Rabbits and Rhesus Monkeys1

Spies

Pau

Yang

1997

Biology of Reproduction

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Certain brain peptides and catecholamines function in activating the hypothalamohypophysial-ovarian axis in both rabbits and rhesus monkeys. The natural stimulus for a surge release of GnRH is coitus in rabbits, whereas the initial excitatory signal is ovarian steroids in monkeys. Despite this contrast in initial signals, specific neurochemicals may serve as common stimuli for GnRH secretion in both species. Evidence is presented that one such substance is norepinephrine (NE), which is released from the mediobasal hypothalamus before, or simultaneously with, GnRH, although the latency in time between stimulus (coitus/estrogen) and response (GnRH/LH release) is very different. Moreover, both stimuli activate NE gene expression in cells located in the brainstem. We suggest that the brainstem is an extra-hypothalamic site where preovulatory signals for GnRH surges are developed in both rabbits and primates.

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“…The antidepressive effectiveness of tricyclic antidepressants were once ascribed to the in hibitory activity of monoamine reuptake to nerve terminals, but more recently attributed to desensitization of the i9-adrenergic receptor-adenylate cyclase system induced by long-term treatment with the agents (12). It has been reported that other antidepressant manipulations such as treatment with monoamine oxidase inhibitors and consecutive electroconvulsive shocks also produce the same changes (2-4).…”

Section: Discussionmentioning

confidence: 99%

Effects of Lithium on the .BETA.-Adrenergic Receptor-Adenylate Cyclase System in Rat Cerebral Cortical Membranes.

et al. 1991

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ABSTRACT-The effects of lithium on the fl-adrenoceptor-adenylate cyclase system in cerebral cortical membranes of rats were investigated. Lithium chloride inhibited adenylate cyclase activity in a concentration-dependent manner in vitro. However, relatively high concentrations of lithium were needed for this inhibition; and at 1 mM, no significant reduction in adenylate cyclase activity was seen under any condition. Administration of lithium carbonate for 21 days decreased the maximum number of[3H]dihydroalprenolol binding sites without changing the apparent dissociation con stant. Activation of adenylate cyclase by (-)-isoproterenol in the presence of 1 PM guanyl-5'-ylimidodiphosphate (Gpp(NH)p) was significantly attenuated in lithium treated rats compared with the controls. Lithium treatment reduced the Gpp(NH)p stimulated adenylate cyclase activity in the presence of 10,uM (-)-isoproterenol, but not in the absence of this fl-adrenergic receptor agonist. Basal activity or adenylate cyclase activity stimulated by forskolin or manganese was not affected, whereas the activity stimulated by sodium fluoride was significantly attenuated by long-term lithium treatment. These results indicate that chronic lithium treatment induces sub sensitivity in the ,8-adrenoceptor-adenylate cyclase system, for which down-regulation of 9-adrenergic receptors is chiefly responsible.

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Temporal sequence of changes in central noradrenergic system of rat after prolonged antidepressant treatment: Receptor desensitization and neurotransmitter interactions

Cited by 73 publications

References 54 publications

3H-imipramine and3H-cyano-imipramine binding in rat brain tissue: Effect of long-term antidepressant administration

3H-imipramine and3H-cyano-imipramine binding in rat brain tissue: Effect of long-term antidepressant administration

Coital and Estrogen Signals: A Contrast in the Preovulatory Neuroendocrine Networks of Rabbits and Rhesus Monkeys1

Effects of Lithium on the .BETA.-Adrenergic Receptor-Adenylate Cyclase System in Rat Cerebral Cortical Membranes.

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