Hostname: page-component-cd9895bd7-gbm5v Total loading time: 0 Render date: 2024-12-29T02:41:35.006Z Has data issue: false hasContentIssue false
  • English
  • Français

Effects of combined treatment with clorgyline and selegiline on extracellular noradrenaline and serotonin levels

Published online by Cambridge University Press:  24 June 2014

Yuji Kitaichi ,
Takeshi Inoue ,
Shin Nakagawa ,
Shuken Boku  and
Tsukasa Koyama
Yuji Kitaichi*
Affiliation:
Department of Psychiatry, Hokkaido University Graduate School of Medicine, Sapporo, Japan
Takeshi Inoue
Affiliation:
Department of Psychiatry, Hokkaido University Graduate School of Medicine, Sapporo, Japan
Shin Nakagawa
Affiliation:
Department of Psychiatry, Hokkaido University Graduate School of Medicine, Sapporo, Japan
Shuken Boku
Affiliation:
Department of Psychiatry, Hokkaido University Graduate School of Medicine, Sapporo, Japan
Tsukasa Koyama
Affiliation:
Department of Psychiatry, Hokkaido University Graduate School of Medicine, Sapporo, Japan
*
Yuji Kitaichi, Department of Psychiatry, Hokkaido University Graduate School of Medicine, North 15, West 7, Kita-ku, Sapporo 060-8638, Japan. Tel: +81-11-706-5160; Fax: +81-11-706-5081; E-mail: [email protected]
Get access Rights & Permissions [Opens in a new window]

Extract

Kitaichi Y, Inoue T, Nakagawa S, Boku S, Koyama T. Effects of combined treatment with clorgyline and selegiline on extracellular noradrenaline and serotonin levels.

Objective Combined treatment with clorgyline, an irreversible monoamine oxidase (MAO)-A inhibitor, and selegiline, an irreversible MAO-B inhibitor, reportedly increases extracellular serotonin levels in the raphe nuclei more than clorgyline does alone. However, the effects of combination of these MAO inhibitors on extracellular noradrenaline have not been reported.

Methods Using in vivo microdialysis, we measured extracellular noradrenaline and serotonin levels after administration of clorgyline and/or selegiline in the medial prefrontal cortex of rats.

Results Administration of clorgyline (10 mg/kg) significantly increased both extracellular serotonin and noradrenaline levels. Combined treatment using clorgyline (10 mg/kg) and selegiline (3 mg/kg) increased extracellular serotonin and noradrenaline levels more than each drug alone did.

Conclusions These findings of this study suggest the augmented antidepressant action of the combination of MAO-A inhibition and MAO-B inhibition. The addition of a MAO-A inhibitor to selegiline or increasing dose of selegiline to achieve full MAO-A inhibition might be the promising strategy for the antidepressant treatment in partial responders or non-responders to selegiline.

Keywords

clorgylinein vivo microdialysisnoradrenalineselegilineserotonin
Type
Research Article
Information
Acta Neuropsychiatrica , Volume 24 , Issue 6 , December 2012 , pp. 369 - 373
Copyright
Copyright © Cambridge University Press 2012

Access options

Get access to the full version of this content by using one of the access options below. (Log in options will check for institutional or personal access. Content may require purchase if you do not have access.)

References

1.Lam, RW, Kennedy, SH, Grigoriadis, S et al. , Canadian Network for Mood and Anxiety Treatments (CANMAT). Clinical guidelines for the management of major depressive disorder in adults: III. Pharmacotherapy. J Affect Disord 2009;117:S26–S43.CrossRefGoogle ScholarPubMed
2.Tundo, A, Cavalieri, P, Navari, S, Marchetti, F.Treating bipolar depression – antidepressants and alternatives: a critical review of the literature. Acta Neuropsychiatr 2011;23:94–105.CrossRefGoogle ScholarPubMed
3.Murck, A.Atypical depression spectrum disorder – neurobiology and treatment. Acta Neuropsychiatr 2003;15:227–241.CrossRefGoogle ScholarPubMed
4.Lipper, S, Murphy, DL, Slater, S, Buchsbaum, MS.Comparative behavioral effects of clorgyline and pargyline in man: a preliminary evaluation. Psychopharmacology (Berl) 1979;62:123–128.CrossRefGoogle ScholarPubMed
5.Mann, JJ, Aarons, SF, Wilner, PJ et al. A controlled study of the antidepressant efficacy and side effects of (-)-deprenyl. A selective monoamine oxidase inhibitor. Arch Gen Psychiatry 1989;46:45–50.CrossRefGoogle ScholarPubMed
6.Lotufo-Neto, F, Trivedi, M, Thase, ME.Meta-analysis of the reversible inhibitors of monoamine oxidase type A moclobemide and brofaromine for the treatment of depression. Neuropsychopharmacology 1999;20:226–247.CrossRefGoogle ScholarPubMed
7.Stahl, SM, Felker, A.Monoamine oxidase inhibitors: a modern guide to an unrequited class of antidepressants. CNS Spectr 2008;13:855–870.CrossRefGoogle Scholar
8.Frampton, JE, Plosker, GL.Selegiline transdermal system: in the treatment of major depressive disorder. Drugs 2007;67:257–265.CrossRefGoogle ScholarPubMed
9.Celada, P, Artigas, F.Monoamine oxidase inhibitors increase preferentially extracellular 5-hydroxytryptamine in the midbrain raphe nuclei. A brain microdialysis study in the awake rat. Naunyn Schmiedebergs Arch Pharmacol 1993;347:583–590.CrossRefGoogle ScholarPubMed
10.Celada, P, Artigas, F.Plasma 5-hydroxyindoleacetic acid as an indicator of monoamine oxidase-A inhibition in rat brain and peripheral tissues. J Neurochem 1993;61:2191–2198.CrossRefGoogle ScholarPubMed
11.Da Prada, M, Kettler, R, Keller, HH, Burkard, WP, Muggi-Maniglio, D, Haefely, WE.Neurochemical profile of moclobemide, a short-acting and reversible inhibitor of monoamine oxidase type A. J Pharmacol Exp Ther 1998;248:400–414.Google Scholar
12.Henriot, S, Kuhn, C, Kettler, R, Da Prada, M.Lazabemide (Ro 19-6327), a reversible and highly sensitive MAO-B inhibitor: preclinical and clinical findings. J Neural Transm Suppl 1994;41:321–325.Google ScholarPubMed
13.Paterson, IA, Juorio, AV, Berry, MD, Zhu, MY.Inhibition of monoamine oxidase-B by (-)-deprenyl potentiates neuronal responses to dopamine agonists but does not inhibit dopamine catabolism in the rat striatum. J Pharmacol Exp Ther 1991;258:1019–1026.Google Scholar
14.Kitaichi, Y, Inoue, T, Nakagawa, S, Boku, S, Izumi, T, Koyama, T.Combined treatment with MAO-A inhibitor and MAO-B inhibitor increases extracellular noradrenaline levels more than MAO-A inhibitor alone through increases in β-phenylethylamine. Eur J Pharmacol 2010;637:77–82.CrossRefGoogle ScholarPubMed
15.Paxinos, G, Watson, C.The rat brain in stereotaxic coordinates, 3rd edn. San Diego: Academic Press, 1997.Google Scholar
16.Chen, K, Holschneider, DP, Wu, W, Rebrin, I, Shih, JC.A spontaneous point mutation produces monoamine oxidase A/B knock-out mice with greatly elevated monoamines and anxiety-like behavior. J Biol Chem 2004;279:39645–39652.CrossRefGoogle ScholarPubMed
17.Curet, O, Damoiseau-Ovens, G, Sauvage, C et al. Preclinical profile of befloxatone, a new reversible MAO-A inhibitor. J Affect Disord 1998;51:287–303.CrossRefGoogle ScholarPubMed
18.Kitaichi, Y, Inoue, T, Nakagawa, S, Izumi, T, Koyama, T.Effect of co-administration of subchronic lithium pretreatment and acute MAO inhibitors on extracellular monoamine levels and the expression of contextual conditioned fear in rats. Eur J Pharmacol 2006;532:236–245.CrossRefGoogle ScholarPubMed
19.Tyacke, RJ, Robinson, ES, Lalies, MD, Hume, SP, Hudson, AL, Nutt, DJ.Estimation of endogenous noradrenaline release in rat brain in vivo using [3H]RX 821002. Synapse 2005;55:126–132.CrossRefGoogle ScholarPubMed
20.Magyar, K, Pálfi, M, Tábi, T, Kalász, H, Szende, B, Szöko, E.Pharmacological aspects of (-)-deprenyl. Curr Med Chem 2004;11:2017–2031.CrossRefGoogle ScholarPubMed