Effects of long-term treatment with desipramine on microtubule proteins in rat cerebral cortex

Miyamoto, Seiya; Asakura, Mikio; Sasuga, Y.; Osada, Keizo; Bodaiji, N.; Imafuku, Jun; Aoba, A.

doi:10.1016/s0014-2999(97)01140-0

Cited by 25 publications

(17 citation statements)

References 48 publications

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“…Studies by Miyamoto et al (1997) revealed that chronic, but not acute treatment of rats with desipramine resulted in decreased microtubule assembly and nucleation in the cerebral cortex. Chronic desipramine treatment has also been reported to phosphorylate certain microtubule-associated proteins (Perez et al, 1989).…”

Section: Discussionmentioning

confidence: 99%

Chronic Antidepressant Treatment Prevents Accumulation of Gsα in Cholesterol-Rich, Cytoskeletal-Associated, Plasma Membrane Domains (Lipid Rafts)

Donati

Rasenick

2005

Neuropsychopharmacol

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Previous studies demonstrated that Gsa migrates from a Triton X-100 (TTX-100) insoluble membrane domain to a TTX-100 soluble membrane domain in response to chronic treatment with the antidepressants desipramine and fluoxetine. Antidepressant treatment also causes a Gsa redistribution in cells as seen by confocal microscopy. The current studies have focused on examining the possibility that the association between Gsa and the plasma membrane and/or cytoskeleton is altered in response to antidepressant treatment, and that this is relevant to both Gsa redistribution and the increased coupling between Gsa and adenylyl cyclase seen after chronic antidepressant treatment. Chronic treatment of C6 cells with two fuctionally and structurally distinct antidepressants, desipramine and fluoxetine, decreased the Gsa content of TTX-100 insoluble membrane domains by as much as 60%, while the inactive fluoxetine analog LY368514 had no effect. Disruption of these membrane domains with the cholesterol chelator methyl-b-cyclodextrin altered the localization of many proteins involved in the cAMP signaling cascade, but only Gsa localization was altered by antidepressant treatment. In addition, microtubule disruption with colchicine elicited the movement of Gsa out of detergent-resistant membrane domains in a manner identical to that seen with antidepressant treatment. The data presented here further substantiate the role of Gsa as a major player in antidepressant-induced modification of neuronal signaling and also raise the possibility that an interaction between Gsa and the cytoskeleton is involved in this process.

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Section: Discussionmentioning

confidence: 99%

Chronic Antidepressant Treatment Prevents Accumulation of Gsα in Cholesterol-Rich, Cytoskeletal-Associated, Plasma Membrane Domains (Lipid Rafts)

Donati

Rasenick

2005

Neuropsychopharmacol

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“…Chronic but not acute treatment with desipramine inhibited microtubule assembly in vivo and the degree of phosphorylation of serine residues of MAP2 was significantly increased after chronic administration of desipramine without changes in the total concentration of MAP2. 45 Given that MAP2 and Tau are major cytoskeletal proteins in neurons, which are involved in the pathogenesis of Alzheimer's and other neuropsychiatric diseases, 46,47 and that it is not uncommon that antidepressants are included in the treatment regimen of those conditions, a better understanding of the effects of antidepressant treatment on microtubule proteins would be relevant.…”

Section: Discussionmentioning

confidence: 99%

St John's wort and imipramine-induced gene expression profiles identify cellular functions relevant to antidepressant action and novel pharmacogenetic candidates for the phenotype of antidepressant treatment response

Wong¹,

O'Kirwan²,

Hannestad³

et al. 2004

Mol Psychiatry

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Both the prototypic tricyclic antidepressant imipramine (IMI) and the herbal product St John's wort (SJW) can be effective in the treatment of major depressive disorder. We studied hypothalamic gene expression in rats treated with SJW or IMI to test the hypothesis that chronic antidepressant treatment by various classes of drugs results in shared patterns of gene expression that may underlie their therapeutic effects. Individual hypothalami were hybridized to individual Affymetrix chips; we studied three arrays per group treatment. We constructed 95% confidence intervals for expression fold change for genes present in at least one treatment condition and we considered genes to be differentially expressed if they had a confidence interval excluding 1 (or À1) and had absolute difference in expression value of 10 or greater. SJW treatment differentially regulated 66 genes and expression sequence tags (ESTs) and IMI treatment differentially regulated 74 genes and ESTs. We found six common transcripts in response to both treatments. The likelihood of this occurring by chance is 1.14 Â 10 À23 . These transcripts are relevant to two molecular machines, namely the ribosomes and microtubules, and one cellular organelle, the mitochondria. Both treatments also affected different genes that are part of the same cell function processes, such as glycolytic pathways and synaptic function. We identified single-nucleotide polymorphisms in the human orthologs of genes regulated both treatments, as those genes may be novel candidates for pharmacogenetic studies. Our data support the hypothesis that chronic antidepressant treatment by drugs of various classes may result in a common, final pathway of changes in gene expression in a discrete brain region.

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“…Bearing in mind that lithium and antidepressant drugs have many dissimilar clinical effects and could affect components of cAMP signaling differently, [17][18][19][20][21][22][23][24][25][26][27][28][29]31,41 it will be interesting to test whether these compounds could cause the levels of PKA and Rap1 in patients with bipolar disorder to return to normal.…”

Section: Discussionmentioning

confidence: 99%

“…Furthermore, alterations in the levels of PKA have been reported 22 after lithium treatment. Changes in either the phosphorylation state or the levels of some cAMP-dependent phosphoproteins were also reported 20,[23][24][25][26][27][28][29] following treatment with these medications.…”

Section: Arch Genmentioning

confidence: 99%

Abnormalities of Cyclic Adenosine Monophosphate Signaling in Platelets From Untreated Patients With Bipolar Disorder

Pérez¹,

Tardito²,

Mori³

et al. 1999

Arch Gen Psychiatry

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Background: Abnormalities in the cyclic adenosine monophosphate (cAMP)-dependent phosphorylation system have been recently reported in patients with bipolar disorder. We evaluated the immunoreactivity of the regulatory and catalytic subunits of cAMP-dependent protein kinase (protein kinase A) and 1 of its substrates, Rap1, in platelets from untreated euthymic, manic, and depressed patients with bipolar disorder and healthy subjects.

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Effects of long-term treatment with desipramine on microtubule proteins in rat cerebral cortex

Cited by 25 publications

References 48 publications

Chronic Antidepressant Treatment Prevents Accumulation of Gsα in Cholesterol-Rich, Cytoskeletal-Associated, Plasma Membrane Domains (Lipid Rafts)

Chronic Antidepressant Treatment Prevents Accumulation of Gsα in Cholesterol-Rich, Cytoskeletal-Associated, Plasma Membrane Domains (Lipid Rafts)

St John's wort and imipramine-induced gene expression profiles identify cellular functions relevant to antidepressant action and novel pharmacogenetic candidates for the phenotype of antidepressant treatment response

Abnormalities of Cyclic Adenosine Monophosphate Signaling in Platelets From Untreated Patients With Bipolar Disorder

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