Chronic effects of imipramine and lithium on postsynaptic 5-HT1A and 5-HT1B sites and on presynaptic 5-HT3 sites in rat brain.

Mizuta, Tadashi; Segawa, Tomio

doi:10.1254/jjp.47.107

Cited by 43 publications

(16 citation statements)

References 19 publications

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“…These findings indicate that 5-HT~A receptors may be up-regulated by lithium treatment, resulting in increased biochemical and electrophysiological responses. However, these findings are inconsistent with the present results and those of previous ligand binding studies (Mizuta and Segawa 1988;Odagaki et al 1990) showing down-regulation of 5-HTIA receptors in the rat hippocampus. A further discrepancy exists between the present findings of behavioral and hypothermic responses to 8-OH-DPAT and [3H]8-OH-DPAT binding in rat hippocampus.…”

Section: Discussioncontrasting

confidence: 99%

“…Mizuta and Segawa (1988) and Odagaki et al (1990) reported that chronic lithium treatment caused 5-HT~A receptor downregulation in the rat hippocampus. Our results are consistent with the earlier findings of decreased 5-HT1A receptors in the rat hippocampus after chronic lithium treatment.…”

Section: Discussionmentioning

confidence: 99%

“…It has been proposed that the clinical efficacy of lithium is related to its action on the 5-HT system. It was reported that chronic lithium treatment decreased the density of 5-HT 1 receptors (Maggi and Enna 1980) and 5-HTIA receptors in the rat hippocampus (Mizuta and Segawa 1988;Odagaki et al 1990), and enhanced 5-HT-stimulated cyclic adenosine monophosphate formation ) and the 5-HT behavioral syndrome in rats (Goodwin et al 1986;Yamawaki et al 1986). However, these findings are controversial.…”

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confidence: 98%

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Chronic lithium treatment enhances the postsynaptic 5-HT1A receptor-mediated 5-HT behavioral syndrome induced by 8-OH-DPAT in rats via catecholaminergic systems

Uchitomi

Yamawaki

1993

Psychopharmacology

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The effects of antimanic agents, including lithium, carbamazepine, clonazepam and zotepine, on the postsynaptic 5-HT1A receptor-mediated behavioral and hypothermic responses induced by 8-OH-DPAT in rats, and on [3H]8-OH-DPAT binding to 5-HT1A receptors in the rat hippocampus were examined. Treatment with lithium (3 mEq/kg, IP) for 14 days enhanced forepaw treading, one component of the 5-HT behavioral syndrome induced by 8-OH-DPAT, and this enhancement by lithium was abolished by catecholamine depletion with reserpine or alpha-methyl-p-tyrosine, but not by 5-HT depletion with p-chlorophenylalanine. These data suggest that lithium enhances 5-HT1A-mediated behavior via catecholaminergic systems. In contrast, chronic lithium treatment did not alter the hypothermic response to 8-OH-DPAT in untreated rats, as well as in rats treated with reserpine. These findings strengthen the suggestion that lithium has no direct influence on the postsynaptic 5-HT1A-mediated response. Other antimanic agents had no effect on either forepaw treading or hypothermia induced by 8-OH-DPAT. Radioligand binding studies using [3H]-8-OH-DPAT demonstrated that chronic lithium treatment, but not other antimanic agents, caused 5-HT1A receptor down-regulation in rat hippocampus. A discrepancy therefore exists between 5-HT1A receptor down-regulation and unaltered 5-HT1A-mediated behavioral and hypothermic responses in catecholamine-depleted rats after chronic lithium treatment.

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Section: Discussioncontrasting

confidence: 99%

Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 98%

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Chronic lithium treatment enhances the postsynaptic 5-HT1A receptor-mediated 5-HT behavioral syndrome induced by 8-OH-DPAT in rats via catecholaminergic systems

Uchitomi

Yamawaki

1993

Psychopharmacology

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“…Chronic lithium is reported to increase the 5-HT concentration in the serotonergic synaptic cleft by reducing 5-HT 1 density, particularly the density of presynaptic 5-HT 1B receptors, but it does not appear to affect 5-HT 2A/ 2C receptor density (Friedman and Wang, 1988;Goodwin, 1989;Haddjeri et al, 2000;Januel et al, 2002;Massot et al, 1999;Mizuta and Segawa, 1988;Redrobe and Bourin, 1999). As 5-HT 1B receptors depress presynaptic 5-HT release, lithium's elevation of k* for AA in auditory and visual areas may result from derepressed 5-HT release, elevated 5-HT in the cleft, or an increased 5-HT 2A/2C -mediated activation of PLA 2 (Januel et al, 2002;Redrobe and Bourin, 1999).…”

Section: Discussionmentioning

confidence: 99%

Chronic Lithium Administration to Rats Selectively Modifies 5-HT2A/2C Receptor-Mediated Brain Signaling Via Arachidonic Acid

Basselin

Chang

Seemann

et al. 2004

Neuropsychopharmacol

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The effects of chronic lithium administration on regional brain incorporation coefficients k* of arachidonic acid (AA), a marker of phospholipase A 2 (PLA 2 ) activation, were determined in unanesthetized rats administered i.p. saline or 1 mg/kg i.p. (7)-1-(2,5-dimethoxy-4-iodophenyl)-2-aminopropane hydrochloride (DOI), a 5-HT 2A/2C receptor agonist. After injecting [1-14 C]AA intravenously, k* (brain radioactivity/integrated plasma radioactivity) was measured in each of 94 brain regions by quantitative autoradiography. Studies were performed in rats fed a LiCl or a control diet for 6 weeks. In the control diet rats, DOI significantly increased k* in widespread brain areas containing 5-HT 2A/2C receptors. In the LiCl-fed rats, the significant positive k* response to DOI did not differ from that in control diet rats in most brain regions, except in auditory and visual areas, where the response was absent. LiCl did not change the head turning response to DOI seen in control rats. In summary, LiCl feeding blocked PLA 2 -mediated signal involving AA in response to DOI in visual and auditory regions, but not generally elsewhere. These selective effects may be related to lithium's therapeutic efficacy in patients with bipolar disorder, particularly its ability to ameliorate hallucinations in that disease.

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“…Although other systems are also relevant (Banerjee et al, 1977;Koch et al, 2002;Newton et al, 2004;Tiraboschi et al, 2004), some evidence suggests that a component of the delay in response to ADT could be attributable to the time dependent desensitization of 5-HT1A receptors. Serotonin 1A-mediated responses in animals (Goodwin et al, 1986(Goodwin et al, , 1987cGreen, 1987Green, , 1988Hensler et al, 1991;Le Poul et al, 1997;Li et al, 1994;Martin et al, 1992;Mizuta and Segawa, 1988;Sleight et al, 1988), and in humans (Lesch et al, 1990;Rausch et al, 1990) have been shown to undergo adaptive changes with chronic ADT that are not seen with acute ADT. However, no one has explored whether adaptation in 5-HT1A receptor-mediated responses could account for lack of therapeutic effect to a given antidepressant.…”

Section: Introductionmentioning

confidence: 99%

Temperature Regulation in Depression: Functional 5HT1A Receptor Adaptation Differentiates Antidepressant Response

Rausch

Johnson

Kasik

et al. 2006

Neuropsychopharmacol

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Observations in humans and animals have indicated that chronic, but not acute, antidepressant treatment (ADT) can desensitize 5-HT1A receptor-mediated responses, such as hypothermia. We hypothesized that 5-HT1A desensitization would be necessary for an antidepressant response (ADR) to occur. To test this hypothesis, we examined 5HT1A-agonist ipsapirone (IPS)-induced hypothermia in 28 depressed patients being treated with fixed doses of nortriptyline (75 mg) at 3-day and 3-week treatment points. Decreases in 24-item Hamilton scores (412) were used to dichotomize the response data into ADR groups of 13 responders (ADR + ) and 15 nonresponders (ADRÀ). A two-way repeated measures analysis of variance indicated significant temperature differences in the area under the curve between response groups across time from 3-day to 3-week intervals (df ¼ 1, 26, F ¼ 6.6, po0.02). In comparison to 3 days treatment, at 3 weeks, the ADR + patients showed blunted hypothermic responses to IPS. ADRÀ did not show this effect, implicating ADR + patients to be less responsive to 5HT1A-receptor stimulation after 3 weeks treatment. Similar effects were not found for 5HT1A postsynaptically mediated ACTH and cortisol responses. These results indicate that to achieve ADR, serotonergic neurotransmission needs to be altered as reflected by the change in 5-HT1a receptor responsiveness documented herein.

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Chronic effects of imipramine and lithium on postsynaptic 5-HT1A and 5-HT1B sites and on presynaptic 5-HT3 sites in rat brain.

Cited by 43 publications

References 19 publications

Chronic lithium treatment enhances the postsynaptic 5-HT1A receptor-mediated 5-HT behavioral syndrome induced by 8-OH-DPAT in rats via catecholaminergic systems

Chronic lithium treatment enhances the postsynaptic 5-HT1A receptor-mediated 5-HT behavioral syndrome induced by 8-OH-DPAT in rats via catecholaminergic systems

Chronic Lithium Administration to Rats Selectively Modifies 5-HT2A/2C Receptor-Mediated Brain Signaling Via Arachidonic Acid

Temperature Regulation in Depression: Functional 5HT1A Receptor Adaptation Differentiates Antidepressant Response

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