Elevated intracellular calcium in transformed lymphoblasts in bipolar I disorder

Emamghoreishi, Masoumeh; Schlicter, L.; Li, P.; Parikh, Samir M.; Sen, Jonathan; Kamble, Arvind B.; Warsh, Jerry J.

doi:10.1016/0006-3223(96)84234-x

Cited by 42 publications

(66 citation statements)

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“…administration of thapsigargin, a compound which selectively inhibits Ca 2C uptake into the endoplasmic reticulum by inhibiting the sarco-endoplasmic reticulum ATPases (SERCAs) and thus increasing the intracellular Ca 2C concentration (Treiman et al, 1998), increased the mouse immobility time evidencing the induction of a depressant-like effect. These observations suggest that a supraspinal increase in intracellular calcium contents is involved in the modulation of mood leading to a depressant-like effect in laboratory animals further complementing and extending studies performed on peripheral blood cells from depressed subjects indicating that patients with affective disorders have an enhanced intracellular Ca 2C response (Emamghoreishi et al, 1997;Yamawaki et al, 1998;Manji and Lenox, 2000). Furthermore, these data indicate that an antidepressant-like effect can be obtained by blocking the release of Ca 2C from endoplasmic reticulum.…”

Section: Discussionsupporting

confidence: 70%

“…Furthermore, enhanced neutrophil response to chemotactic peptide and enhanced platelet thrombin response are also observed in some studies (Dubovsky et al, 1991;Kusumi et al, 1992;Bohus et al, 1996). Some investigations also suggested that baseline intracellular calcium levels are elevated in platelets or lymphoblasts of patients with bipolar affective disorders (Emamghoreishi et al, 1997). Other reports showed that dihydropyridine channel blockers displayed antidepressant-like activity in mice (Cohen et al, 1997;Biala, 1998) as well as some effectiveness in the treatment of patients with affective disorders (Dubovsky, 1993;Wisner et al, 2002).…”

Section: Introductionmentioning

confidence: 88%

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Blockade of intracellular calcium release induces an antidepressant-like effect in the mouse forced swimming test

2006

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The role of intracellular calcium in the modulation of a depressant-like condition was investigated in the mouse forced swimming test. I.c.v. administration of TMB-8 (0.23e46.3 nmol per mouse), a blocker of Ca 2C release from intracellular stores, decreased the mouse immobility time. I.c.v. injection of thapsigargin (0.003e3 nmol per mouse), compound which selectively inhibits Ca 2C uptake into the endoplasmic reticulum, produced, 60 min after administration, a depressant-like condition. Xestospongin C (1e100 pmol per mouse i.c.v.), an InsP 3 -receptor antagonist, decreased the mouse immobility time. By contrast, D-myo-inositol (5.4e540 pmol per mouse i.c.v.), compound which produces InsP 3 , resulted in a depressant-like effect. Similarly, ryanodine (0.1e600 pmol per mouse i.c.v.), an RyR antagonist, decreased the immobility time values whereas the administration of 4-chloro-m-cresol (0.1e100 pmol per mouse i.c.v.), an RyR agonist, showed an opposite effect. The antidepressant-like effects observed with TMB-8, xestospongin C and ryanodine were comparable to that produced by the antidepressant drugs amitriptyline and clomipramine. The treatments employed did not produce any behavioural impairment of mice as revealed by the rota-rod and hole board tests indicating that the antidepressant-and depressant-like effects were not due to a compromised locomotor activity and spontaneous motility of the treated animals. These results indicate that a central variation in intracellular calcium contents is involved in the modulation of a depressive-like condition in the mouse forced swimming test. In particular, the blockade of both InsP 3 Rs and RyRs appears to play an important role in the induction of an antidepressant-like effect, whereas the stimulation of these receptors is involved in a depressant-like response of mice.

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Section: Discussionsupporting

confidence: 70%

Section: Introductionmentioning

confidence: 88%

Blockade of intracellular calcium release induces an antidepressant-like effect in the mouse forced swimming test

2006

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“…6,9,20,37 Patients had a DSM-IV diagnosis of BD-I as established by the Structured Clinical Interview for DSM-IV (SCID), were physically healthy and had no recent (43 months) drug or alcohol abuse. 6 Healthy subjects had no past or current psychiatric illness as determined by SCID-I (nonpatient version) and were physically healthy as determined by systems review and physical examination. All subjects provided informed written consent.…”

Section: Subject B-lymphoblast Cell Linesmentioning

confidence: 99%

“…6 BLCLs were initially expanded in suspension culture in a 95% air/5% CO 2 humidified incubator at 371C for 13-16 passages (2-3 days/passage), then assayed for [Ca 2 þ ] B , 6,7 and either frozen and stored in the vapor phase of liquid nitrogen for later regeneration and use, or, in some cases, expanded further for study.…”

Section: Establishment Of B Lymphoblast Cell Linesmentioning

confidence: 99%

“…1,2 Among the abnormalities noted, disruption of intracellular calcium (Ca 2 þ ) homeostasis is a pivotal transition stage in the progression to cell death, whether by apoptosis or necrosis. 3,4 Reports of elevated basal and agonist-stimulated intracellular Ca 2 þ concentrations ([Ca 2 þ ] B and [Ca 2 þ ] S , respectively) in mononuclear leukocytes, platelets and transformed B lymphoblast cell lines (BLCLs) from bipolar I disorder I (BD-I) patients [5][6][7] therefore suggest that alterations of intracellular Ca 2 þ homeostasis play an important role in the pathophysiological changes that are thought to compromise cellular resilience and adaptive response to cellular stress in BD. The mechanism(s) involved in the altered Ca 2 þ homeostasis are still uncertain, but recent observations implicate possible disturbances in one or more of the molecular modules regulating intracellular Ca 2 þ such as mitochondrial Ca 2 þ flux, endoplasmic reticulum (ER) Ca 2 þ storage and release, and store-operated and receptor-operated Ca 2 þ entry (SOCE and ROCE).…”

Section: Introductionmentioning

confidence: 99%

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Chronic lithium treatment of B lymphoblasts from bipolar disorder patients reduces transient receptor potential channel 3 levels

et al. 2004

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Chronic lithium treatment of B-lymphoblast cell lines (BLCLs) from bipolar-I disorder (BD-I) patients and healthy subjects ex vivo attenuates agonist-and thapsigargin-stimulated intracellular calcium (Ca 2 þ ) responses. As these findings suggest that chronic lithium treatment modifies receptor (ROCE) and/or store-operated Ca 2 þ entry (SOCE) mechanisms, we determined whether chronic lithium treatment of BLCLs modified the expression of two members of the transient receptor potential channels (TRPC1 & 3), which participate in ROCE/SOCE. Chronic lithium treatment significantly reduced BLCL TRPC3 immunoreactivity (repeated-measures ANOVA, P ¼ 0.00005), with interaction effects of diagnosis (P ¼ 0.037) and sex (P ¼ 0.040). The lithium-induced decrease was greatest in BLCLs from female BD-I patients compared with those from healthy females (À27%) and with vehicle-treated BLCLs from female BD-I patients (À33%). However, lithium treatment did not affect TRPC1 and 3 mRNA levels, and TRPC1 immunoreactivity. Downregulation of TRPC3 may be an important mechanism by which lithium ameliorates pathophysiological Ca 2 þ disturbances as observed in BD.

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Characterization of αs-immunoreactive ADP-ribosylated proteins in postmortem human brain

Andreopoulos

Siu

et al. 1999

J. Neurosci. Res.

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ADP-ribosylation of the stimulatory G protein alpha subunit, alpha(s), has been demonstrated in a number of different mammalian tissues. However, little is known about the occurrence and role of this process in modifying alpha(s) levels/function in human brain. In the present study, endogenous and cholera toxin (CTX)-catalyzed [32P]ADP-ribosylated products were characterized in postmortem human temporal cortex by (1) immunoprecipitation with alpha(s) antisera (RM/1), (2) comparisons of immunoblots and autoradiograms of the [32P]ADP-ribosylated products, and (3) limited protease digestion. Of the three major endogenous [32P]ADP-ribosylated products (48, 45, and 39 kDa) in postmortem brain, the 48-kDa and 45-kDa bands were clearly identified as alpha(s-L) (long isoform) and alpha(s-S) (short isoform), respectively. RM/1 immunoprecipitated the 39-kDa [32P]ADP-ribosylated protein, and overlays of immunoblots and autoradiograms showed that this product corresponded to an alpha(s)-like-immunoreactive protein. Furthermore, limited protease digestion of the 39-kDa endogenous [32P]ADP-ribosylated band generated peptide fragments similar to both endogenous and CTX-catalyzed [32P]ADP-ribosylated alpha(s-S). Two major CTX-catalyzed [32P]ADP-ribosylated products were also identified as alpha(s-L) (52 kDa) and alpha(s-S) (45 kDa). These findings clearly demonstrate that alpha(s) is a substrate for endogenous and CTX-catalyzed [32P]ADP-ribosylation in postmortem human brain. Furthermore, a lower molecular weight alpha(s)-like immunoreactive protein is also expressed in human brain and is a substrate for endogenous but not CTX-catalyzed [32P]ADP-ribosylation.

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Elevated intracellular calcium in transformed lymphoblasts in bipolar I disorder

Cited by 42 publications

References 0 publications

Blockade of intracellular calcium release induces an antidepressant-like effect in the mouse forced swimming test

Blockade of intracellular calcium release induces an antidepressant-like effect in the mouse forced swimming test

Chronic lithium treatment of B lymphoblasts from bipolar disorder patients reduces transient receptor potential channel 3 levels

Characterization of αs-immunoreactive ADP-ribosylated proteins in postmortem human brain

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