Regulation of glutamic acid decarboxylase mRNA expression in rat brain after sertraline treatment

Giardino, Luciana; Zanni, Massimo; Bettelli, Carla; Savina, Maria A.; Calzà, Laura

doi:10.1016/0014-2999(96)00588-2

Cited by 9 publications

(5 citation statements)

References 19 publications

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“…Studies by Mitoma and Konishi (12) also demonstrate the ability of monoamines to elicit both short-and long-term enhancement of GABA-ergic inhibitory transmission through presynaptic mechanisms. However, the mechanism of increased presynaptic GABA-ergic transmission remains unclear since long-term administration of sertraline was found to produce either no change or a decrease in expression of glutamic acid decarboxylase in rats (13).…”

Section: Discussionmentioning

confidence: 99%

Increased Occipital Cortex GABA Concentrations in Depressed Patients After Therapy With Selective Serotonin Reuptake Inhibitors

Sanacora¹,

Mason²,

Rothman³

et al. 2002

AJP

434

254

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Section: Discussionmentioning

confidence: 99%

Increased Occipital Cortex GABA Concentrations in Depressed Patients After Therapy With Selective Serotonin Reuptake Inhibitors

Sanacora¹,

Mason²,

Rothman³

et al. 2002

AJP

434

254

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“…Furthermore, studies have indicated that the c-aminobutyric acid (GABA) transmission system is also involved in the neurobiology of anxiety. Giardino et al (29) have investigated the effect of chronic treatment with sertraline on the GABA system in rats, using the expression of glutamic acid decarboxylase (the limiting enzyme in GABA synthesis) mRNA as a marker. Decreases in glutamic acid decarboxylase mRNA expression were found in the prefrontal cortex, the accumbens nucleus, the olfactory tubercle and the reticular nucleus of the thalamus, following 28 days of chronic treatment with sertraline.…”

Section: Discussionmentioning

confidence: 99%

Sequential improvement of anxiety, depression and anhedonia with sertraline treatment in patients with major depression

Boyer

Tassin

Falissart

et al. 2008

Journal of Clinical Pharmacy and Therapeutics

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Objective: To establish the therapeutic effect pro®le of sertraline in major depression. It was hypothesized that the antidepressant effect of sertraline showed three phases: Phase 1 where improvements in anxiety are most pronounced; Phase 2 where the greatest improvements are in depressive symptoms; and Phase 3 where the symptoms of anhedonia show the most improvement. To test this hypothesis, an 8-week, openlabel study was conducted. Methods: Patients with a major depressive episode (DSM-IV) and a score ³24 on the 17-item HAM-D were enrolled and treated with sertraline 50±150 mg/day. The three symptomatic clusters, anxiety, depression and hedonia, were de®ned a priori using the Inventory of Depressive Symptomatology-Clinician rated (IDS-C). Periods of interest were: Days 0±7 for anxiety, Days 7±21 for depression and Days 21±56 for anhedonia. Raters were blinded as to the constitution of the clusters and periods. Results: 140 patients were recruited. Improvement in the anxiety cluster of the IDS-C was greatest during Days 0±7, whereas over Days 7±21 most improvement was observed in the depression cluster and the greatest improvement in the hedonic cluster occurred during Days 21±56. Conclusions: These preliminary results are consistent with the hypothesis that the therapeutic effects of sertraline occur in a sequential manner. The symptoms of anxiety improved ®rst, followed by depression and then anhedonia.

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“…228,[234][235][236] Also, it has been reported that acute and chronic administration of phenelzine, a monoamine oxidase inhibitor, in rats may increase GABA brain levels by inhibiting GABA-T or GAD, 224,[237][238][239][240] or by increasing the GABA transporter GAT-1, 241 and that imipramine may enhance GABA release in thalamus in rats. 242 Sertraline 243 and reboxetine 244 have also been shown to reduce GAD expression in rat brain (ie prefrontal cortex, nucleus accumbens, thalamus, and limbic structures). Hyperforin, a major component of hypericum extract, which has been reported to be effective as antidepressant, 245 may inhibit GABA synaptosomal uptake in rat forebrain, elevating GABA levels.…”

Section: 218mentioning

confidence: 99%

GABAergic dysfunction in mood disorders

et al. 2003

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Regulation of glutamic acid decarboxylase mRNA expression in rat brain after sertraline treatment

Cited by 9 publications

References 19 publications

Increased Occipital Cortex GABA Concentrations in Depressed Patients After Therapy With Selective Serotonin Reuptake Inhibitors

Increased Occipital Cortex GABA Concentrations in Depressed Patients After Therapy With Selective Serotonin Reuptake Inhibitors

Sequential improvement of anxiety, depression and anhedonia with sertraline treatment in patients with major depression

GABAergic dysfunction in mood disorders

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