Fluoxetine tenth anniversary update: the progress continues

Stokes, Peter E.; Holtz, Aliza

doi:10.1016/s0149-2918(97)80066-5

Cited by 120 publications

(82 citation statements)

References 300 publications

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“…In our experiment, treatment with fluoxetine, a serotonin (5-HT) selective reuptake inhibitor (SSRI) with well-known clinical efficacy (Stokes and Holtz, 1997) prevented the chronic stressinduced effect. The serotonergic innervation of the hippocampus originates from the dorsal and median raphe nuclei, but only 21% of serotonin-containing varicosities make synaptic contacts, mostly with dendrites and somata of GABAergic interneurons, and it has been suggested that those varicosities without synaptic contact release 5-HT at nonsynaptic sites for long distance diffusion (Vizi and Kiss, 1998).…”

Section: Antidepressant Treatment Can Counteract the Effect Of Stressmentioning

confidence: 81%

Chronic Stress Decreases the Number of Parvalbumin-Immunoreactive Interneurons in the Hippocampus: Prevention by Treatment with a Substance P Receptor (NK1) Antagonist

Czéh

Simon

Hart

et al. 2004

Neuropsychopharmacol

126

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Previous studies have demonstrated that stress may affect the hippocampal GABAergic system. Here, we examined whether long-term psychosocial stress influenced the number of parvalbumin-containing GABAergic cells, known to provide the most powerful inhibitory input to the perisomatic region of principal cells. Adult male tree shrews were submitted to 5 weeks of stress, after which immunocytochemical and quantitative stereological techniques were used to estimate the total number of hippocampal parvalbuminimmunoreactive (PV-IR) neurons. Stress significantly decreased the number of PV-IR cells in the dentate gyrus (DG) (À33%), CA2 (À28%), and CA3 (À29%), whereas the CA1 was not affected. Additionally, we examined whether antidepressant treatment offered protection from this stress-induced effect. We administered fluoxetine (15 mg/kg per day) and SLV-323 (20 mg/kg per day), a novel neurokinin 1 receptor (NK 1 R) antagonist, because the NK 1 R has been proposed as a possible target for novel antidepressant therapies. Animals were subjected to a 7-day period of psychosocial stress before the onset of daily oral administration of the drugs, with stress continued throughout the 28-day treatment period. NK 1 R antagonist administration completely prevented the stress-induced reduction of the number of PV-IR interneurons, whereas fluoxetine attenuated this decrement in the DG, without affecting the CA2 and CA3. The effect of stress on interneuron numbers may reflect real cell loss; alternatively, parvalbumin concentration is diminished in the neurons, which might indicate a compensatory attempt. In either case, antidepressant treatment offered protection from the effect of stress and appears to modulate the hippocampal GABAergic system. Furthermore, the NK 1 R antagonist SLV-323 showed neurobiological efficacy similar to that of fluoxetine.

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Section: Antidepressant Treatment Can Counteract the Effect Of Stressmentioning

confidence: 81%

Chronic Stress Decreases the Number of Parvalbumin-Immunoreactive Interneurons in the Hippocampus: Prevention by Treatment with a Substance P Receptor (NK1) Antagonist

Czéh

Simon

Hart

et al. 2004

Neuropsychopharmacol

126

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“…We focused on astroglia because of the growing number of data indicating that the role of astrocytes in function of the central nervous system so far has been considerably underestimated (Fields and Stevens-Graham, 2002). Additionally, we examined whether treatment with the antidepressant fluoxetine, a selective serotonin reuptake inhibitor (SSRI) with well-known clinical efficacy (Stokes and Holtz, 1997), offers protection from possible stressinduced morphological alterations. This approach was based on recent clinical and preclinical findings, which suggest that depressive disorders may be associated with an impairment of structural plasticity and cellular resilience, and that antidepressant medications may correct this dysfunction (Manji and Duman, 2001;Manji et al, 2000Manji et al, , 2003.…”

Section: Introductionmentioning

confidence: 99%

Astroglial Plasticity in the Hippocampus is Affected by Chronic Psychosocial Stress and Concomitant Fluoxetine Treatment

Czéh

Simon

Schmelting

et al. 2005

Neuropsychopharmacol

406

252

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Analysis of post-mortem tissue from patients with affective disorders has revealed a decreased number of glial cells in several brain areas. Here, we examined whether long-term psychosocial stress influences the number and morphology of hippocampal astrocytes in an animal model with high validity for research on the pathophysiology of major depression. Adult male tree shrews were submitted to 5 weeks of psychosocial stress, after which immunocytochemical and quantitative stereological techniques were used to estimate the total number and somal volume of glial fibrillary acidic protein-positive astrocytes in the hippocampal formation. Stress significantly decreased both the number (À25%) and somal volume (À25%) of astroglia, effects that correlated notably with the stress-induced hippocampal volume reduction. Additionally, we examined whether antidepressant treatment with fluoxetine, a selective serotonin reuptake inhibitor, offered protection from these stress-induced effects. Animals were subjected to 7 days of psychosocial stress before the onset of daily oral administration of fluoxetine (15 mg/kg per day), with stress continued throughout the 28-day treatment period. Fluoxetine treatment prevented the stress-induced numerical decrease of astrocytes, but had no counteracting effect on somal volume shrinkage. In nonstressed animals, fluoxetine treatment had no effect on the number of astrocytes, but stress exposure significantly reduced their somal volumes (À20%). These notable changes of astroglial structural plasticity in response to stress and antidepressant treatment support the notion that glial changes may contribute to the pathophysiology of affective disorders as well as to the cellular actions of antidepressants.

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“…The very slow elimination of fluoxetine and norfluoxetine differentiates it from other SSRIs (28). Compared with other antidepressants, it is safer in terms of overdose and causes fewer and less severe side effects, which has enhanced patient compliance (56). Fluoxetine has been proposed to have an anti-inflammatory effect.…”

mentioning

confidence: 99%

Fluoxetine inhibits NF-κB signaling in intestinal epithelial cells and ameliorates experimental colitis and colitis-associated colon cancer in mice

Koh

Kim

et al. 2011

American Journal of Physiology-Gastrointestinal and Liver Physi

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Although fluoxetine, a selective serotonin reuptake inhibitor, is known to demonstrate antiinflammatory activity, little information is available on the effect of fluoxetine regarding intestinal inflammation. This study investigates the role of fluoxetine in the attenuation of acute murine colitis by suppression of the NF-B pathway in intestinal epithelial cells (IEC). Fluoxetine significantly inhibited activated NF-B signals and the upregulated expression of interleukin-8 (IL-8) in COLO 205 colon epithelial cells stimulated with tumor necrosis factor-␣ (TNF-␣). Pretreatment with fluoxetine attenuated the increased IB kinase (IKK) and IB␣ phosphorylation induced by TNF-␣. In a murine model, administration of fluoxetine significantly reduced the severity of dextran sulfate sodium (DSS)-induced colitis, as assessed by the disease activity index, colon length, and histology. In addition, the DSS-induced phospho-IKK activation, myeloperoxidase activity, a parameter of neutrophil accumulation, and the secretion of macrophage-inflammatory protein-2, a mouse homolog of IL-8, were significantly decreased in fluoxetine-pretreated mice. Moreover, fluoxetine significantly attenuated the development of colon cancer in mice inoculated with azoxymethane and DSS. These results indicate that fluoxetine inhibits NF-B activation in IEC and that it ameliorates DSS-induced acute murine colitis and colitis-associated tumorigenesis, suggesting that fluoxetine is a potential therapeutic agent for the treatment of inflammatory bowel disease.

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Fluoxetine tenth anniversary update: the progress continues

Cited by 120 publications

References 300 publications

Chronic Stress Decreases the Number of Parvalbumin-Immunoreactive Interneurons in the Hippocampus: Prevention by Treatment with a Substance P Receptor (NK1) Antagonist

Chronic Stress Decreases the Number of Parvalbumin-Immunoreactive Interneurons in the Hippocampus: Prevention by Treatment with a Substance P Receptor (NK1) Antagonist

Astroglial Plasticity in the Hippocampus is Affected by Chronic Psychosocial Stress and Concomitant Fluoxetine Treatment

Fluoxetine inhibits NF-κB signaling in intestinal epithelial cells and ameliorates experimental colitis and colitis-associated colon cancer in mice

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