Increase in Serotonin 1A Receptors in the Dentate Gyrus as Revealed by Autoradiographic Analysis Following Repeated Electroconvulsive Shock But Not Imipramine Treatment

Hayakawa, Hiroshi; Shimizu, Masami; Nishida, Akira; Motohashi, Nobutaka; Yamawaki, Shigeto

doi:10.1159/000119413

Cited by 24 publications

(10 citation statements)

References 8 publications

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“…The absence of change in 5-HT 1A R binding after ECT observed in this study is consistent with animal studies that reported unaltered 5-HT 1A R binding and mRNA after chronic ECS in the cerebral cortex (Burnet et al 1999 ;Stockmeier et al 1992) and dorsal raphe (Burnet et al 1999 ;Hayakawa et al 1994).…”

Section: Discussionsupporting

confidence: 92%

Effect of electroconvulsive therapy on 5-HT1A receptor binding in patients with depression: a PET study with [11C]WAY 100635

Saijo

Takano²,

Suhara³

et al. 2010

Int. J. Neuropsychopharm.

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In our previous positron emission tomography (PET) study, we demonstrated that ECT decreased dopamine D2 receptor in major depressive disorder (MDD). Although many animal studies have focused on the effect of ECT on serotonergic neurotransmission, no human study has directly examined the effect of ECT on brain serotonin [5-hydroxytryptamine (5-HT)] 1A receptors (5-HT1ARs). Using PET with [11C]WAY 100635, we aimed to evaluate the effect of ECT on 5-HT1ARs in patients with MDD. Nine patients underwent PET scans before and after a series of 6-7 bilateral ECTs. Region-of-interest analysis was performed based on the simplified reference tissue model. There were no significant changes in 5-HT1AR binding in patients between before and after ECT. ECT did not alter [11C]WAY 100635 binding even after recovery from depressive episode. Although the present finding does not exclude the involvement of brain 5-HT1A systems in the antidepressant action of ECT, it may indicate the involvement of other neurotransmission mechanisms.

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Section: Discussionsupporting

confidence: 92%

Effect of electroconvulsive therapy on 5-HT1A receptor binding in patients with depression: a PET study with [11C]WAY 100635

Saijo

Takano²,

Suhara³

et al. 2010

Int. J. Neuropsychopharm.

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“…In contrast, chronic administration of antidepressant drugs induces functional hypersensitivity of postsynaptic 5-HT 1A receptors, at least as detected electrophysiologically in the hippocampus (Bijak et al 1996(Bijak et al , 2001Beck et al 1997;Haddjeri et al 1998). However, most receptor studies have shown no change in the [ 3 H]8-OH-DPAT binding in the rat hippocampus following prolonged treatment with antidepressants (Watanabe et al 1993;Hayakawa et al 1994;Bijak et al 1996). Comparing the effects of glucocorticoids and antidepressant drugs on hippocampal 5-HT 1A receptor function, and considering changes in 5-HT 1A receptors in depressed patients, it may be concluded that both functional desensitization and a decrease in the expression of 5-HT 1A receptors induced by glucocorticoids may account considerably for their "pro-depressive" activity.…”

Section: Discussionmentioning

confidence: 99%

Prolonged corticosterone treatment alters the responsiveness of 5-HT 1A receptors to 8-OH-DPAT in rat CA1 hippocampal neurons

Czyrak

Maćkowiak

Chocyk

et al. 2002

Naunyn-Schmiedeberg's Archives of Pharmacology

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Hippocampal 5-HT(1A) receptors have been shown to be suppressed by glucocorticoids in a variety of animal studies, however the molecular mechanism and the functional meaning of this effect are still not well understood. The present study was designed to investigate the impact of repeated administration of corticosterone (10 mg/kg s.c. twice daily for 7 days) on the functional consequences of 5-HT(1A) receptor stimulation measured electrophysiologically in hippocampal slices. Additionally, the effects of corticosterone on 5-HT(1A) receptor binding and on receptor mRNA levels in the hippocampus were studied. Prolonged, but not acute treatment with corticosterone attenuated (+/-)-8-hydroxy-2-di- N-propylamino)tetralin hydrobromide (8-OH-DPAT)-induced inhibition of population spikes, and 8-OH-DPAT-induced hyperpolarization in rat CA1 hippocampal neurons. Chronic, but not acute treatment with corticosterone also decreased 5-HT(1A) receptor binding in the CA1 region (in the ventral part only) and the dentate gyrus. A single dose of corticosterone increased [(3)H]8-OHDPAT binding in the dentate gyrus and in the CA3 and CA4 hippocampal regions. Only acute, but not prolonged treatment with corticosterone decreased the level of 5-HT(1A) receptor mRNA in the CA1 region and dentate gyrus of the hippocampus. 5-HT turnover in the hippocampus was not influenced by chronic corticosterone. It is concluded that a chronically elevated level of corticosterone can induce functional desensitization of 5-HT(1A) receptors in the CA1 area of the hippocampus, although this effect is not always followed consequently by decreases in 5-HT(1A) receptor synthesis in this or other areas of the hippocampus.

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“…First, conditions that are associated with diminished granule cell genesis, such as malnutrition (Debassio et al 1996), aging (Kuhn et al 1996;Gould et al 1999), high corticosterone (Cameron and Gould 1994), stress , and NMDA receptor activation (Cameron et al 1995), also decrease the density of 5HT fibers or 5HT1A receptors, or inhibit the release of 5HT in the dentate gyrus (Blatt et al 1994;Chalmers et al 1993;McKittrick et al 1995;Nishimura et al 1995;Meijer and deKloet 1994;Watanabe et al 1993;Tao and Auerbach 1996;Whitton et al 1994;Nyakas et al 1997). Second, experimental manipulations that stimulate granule cell genesis, such as seizures (Parent et al 1997), adrenalectomy (Cameron and Gould 1994), and NMDA receptor antagonist treatment (Cameron et al 1995), also increase the density of 5HT1A receptors or the release of 5HT in the dentate gyrus (Hayakawa et al 1994;Burnet et al 1995;Whitton et al 1994;Kuroda et al 1994). Third, our preliminary evidence indicates that pharmacological manipulations that elevate 5HT levels in the hippocampus (fenfluramine) or stimulate 5TH1A receptors (8-OH-DPAT) increase the rate of proliferation of granule cell precursors (Jacobs et al 1998).…”

Section: Serotoninmentioning

confidence: 99%

Serotonin and Hippocampal Neurogenesis

Gould

1999

Neuropsychopharmacology

299

114

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The role of the molecule serotonin, or 5-hydroxytryptamine, in neurotransmission has been recognized for decades. More recent studies have explored the possibility that serotonin may have structural effects on the brain both during development and in adulthood (Mazer et al. 1997;Yan et al. 1997;Watanabe et al. 1992). These studies have predominantly focused on the role of serotonin in mediating the structure of the adult brain. Our recent studies have identified a new role for serotonin in mediating the structure of the adult brain. We have found that neurogenesis in the adult mammalian dentate gyrus is enhanced by activation of serotonergic receptors (Jacobs et al. 1998).

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Increase in Serotonin 1A Receptors in the Dentate Gyrus as Revealed by Autoradiographic Analysis Following Repeated Electroconvulsive Shock But Not Imipramine Treatment

Cited by 24 publications

References 8 publications

Effect of electroconvulsive therapy on 5-HT1A receptor binding in patients with depression: a PET study with [11C]WAY 100635

Effect of electroconvulsive therapy on 5-HT1A receptor binding in patients with depression: a PET study with [11C]WAY 100635

Prolonged corticosterone treatment alters the responsiveness of 5-HT 1A receptors to 8-OH-DPAT in rat CA1 hippocampal neurons

Serotonin and Hippocampal Neurogenesis

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