Selective modulation of fibroblast growth factor-2 expression in the rat brain by the atypical antipsychotic clozapine

Riva, Marco A.; Molteni, Raffaella; Tascedda, Fabio; Massironi, Alessio; Racagni, Giorgio

doi:10.1016/s0028-3908(99)00031-3

Cited by 43 publications

(29 citation statements)

References 40 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…52 Furthermore, QUE and other atypical APDs have been shown to regulate/ modulate the expression of FGF-2 in the brain. 53,54 Together, these data suggest that QUE may target neural stem cells via regulating the expression of EGF and FGF-2 in the brain.…”

Section: Discussionmentioning

confidence: 83%

Quetiapine facilitates oligodendrocyte development and prevents mice from myelin breakdown and behavioral changes

et al. 2007

View full text Add to dashboard Cite

Recent neuroimaging and postmortem studies have reported abnormalities in white matter of schizophrenic brains, suggesting the involvement of oligodendrocytes in the etiopathology of schizophrenia. This view is being supported by gene microarray studies showing the downregulation of genes related to oligodendrocyte function and myelination in schizophrenic brain compared to control subjects. However, there is currently little information available on the response of oligodendrocytes to antipsychotic drugs (APDs), which could be invaluable for corroborating the oligodendrocyte hypothesis. In this study we found: (1) quetiapine (QUE, an atypical APD) treatment in conjunction with addition of growth factors increased the proliferation of neural progenitors isolated from the cerebral cortex of embryonic rats; (2) QUE directed the differentiation of neural progenitors to oligodendrocyte lineage through extracellular signal-related kinases; (3) addition of QUE increased the synthesis of myelin basic protein and facilitated myelination in rat embryonic cortical aggregate cultures; (4) chronic administration of QUE to C57BL/6 mice prevented cortical demyelination and concomitant spatial working memory impairment induced by cuprizone, a neurotoxin. These findings suggest a new neural mechanism of antipsychotic action of QUE, and help to establish a role for oligodendrocytes in the etiopathology and treatment of schizophrenia.

show abstract

Section: Discussionmentioning

confidence: 83%

Quetiapine facilitates oligodendrocyte development and prevents mice from myelin breakdown and behavioral changes

et al. 2007

View full text Add to dashboard Cite

show abstract

“…Olanzapine increased mRNA for FGF3 and decreased FGF receptor 2 in the frontal cortex of exposed rats, presumably facilitating signal transduction, cell communication, and neuronal growth (Tables 1, 3). FGFs appear to be targets of several psychotropic medications including clozapine (Riva et al, 1999), E-5842 (Ovalle et al, 2001), and olanzapine. Riva et al (1999) showed increases in levels of FGF2 mRNA and protein in rat striatum following administration of clozapine.…”

Section: Chronic Olanzapine Treatment Sh Fatemi Et Almentioning

confidence: 99%

“…FGFs appear to be targets of several psychotropic medications including clozapine (Riva et al, 1999), E-5842 (Ovalle et al, 2001), and olanzapine. Riva et al (1999) showed increases in levels of FGF2 mRNA and protein in rat striatum following administration of clozapine. Ovalle et al (2001) showed that E-5842, a preferential sigma-1 receptor agonist and ligand and a putative atypical antipsychotic, causes upregulation of FGF2 mRNA in the prefrontal cortex (PFC) and striatum and downregulation of FGF2 mRNA in the hypothalamus of rat brains following 21-day chronic exposure.…”

Section: Chronic Olanzapine Treatment Sh Fatemi Et Almentioning

confidence: 99%

“…Ovalle et al (2001) showed that E-5842, a preferential sigma-1 receptor agonist and ligand and a putative atypical antipsychotic, causes upregulation of FGF2 mRNA in the prefrontal cortex (PFC) and striatum and downregulation of FGF2 mRNA in the hypothalamus of rat brains following 21-day chronic exposure. Thus, it appears that FGF2 could play a role as a neuroprotective agent, which is upregulated by olanzapine, clozapine, and sigma-1 receptor ligand E-5842 (Ovalle et al, 2001;Riva et al, 1999). Olanzapine is also capable of upregulating levels of nerve growth factor and downregulating levels of BDNF in various areas of the rat brain (Angelucci et al, 2005) attesting to varied effects of olanzapine on different trophic factors in the brain.…”

Section: Chronic Olanzapine Treatment Sh Fatemi Et Almentioning

confidence: 99%

See 1 more Smart Citation

Chronic Olanzapine Treatment Causes Differential Expression of Genes in Frontal Cortex of Rats as Revealed by DNA Microarray Technique

Fatemi

Reutiman

Folsom

et al. 2006

Neuropsychopharmacol

View full text Add to dashboard Cite

Recent emerging biochemical data indicate that several important neuroregulatory genes and proteins may be involved in the etiology of schizophrenia and bipolar disorder. Additionally, the same genes appear to be targets of several psychotropic medications that are used to treat these disorders. Recent DNA microarray studies show that genes involved in synaptic neurotransmission, signal transduction, and glutamate/GABA regulation may be differentially regulated in brains of subjects with schizophrenia. We hypothesized that chronic administration of olanzapine to rats would alter expression of various genes that may be involved in the etiology of schizophrenia and mood disorders. Rats were administered olanzapine (N ¼ 20, 2 mg/kg/day) or sterile saline intraperitoneally (N ¼ 20) daily for 21 days. Control and olanzapine-treated frontal cortices were analyzed using cDNA microarray technology. The results showed significant downregulation of 31 genes and upregulation of 38 genes by greater than two-fold in the drug-treated brains vs controls. Our results provide evidence for altered regulation of genes involved with signal transduction and cell communication, metabolism and energy pathways, transport, immune response, nucleic acid metabolism, and neuronal growth factors. Real-time quantitative RT-PCR analysis verified the direction and magnitude of change in six genes of interest: calbindin 3, homer 1, regulator of G-protein signaling (RGS) 2, pyruvate kinase, Reelin and insulin 2. Western blotting showed significant upregulation in protein products for Reelin 410 and Reelin 180 kDa and downregulation for NMDA3B and RGS2. Our results show for the first time that olanzapine causes changes in levels of several important genes that may be involved in the etiology and treatment of schizophrenia and other psychiatric disorders.

show abstract

“…Many studies have reported that either acute or chronic administration of typical or atypical antipsychotic drugs can differentially regulate a variety of genes expression in rat brain, such as c-fos, zif268 (Nguyen et al, 1992;Rogue and Vincendon 1992;Semba et al, 1996), Homer (de Bartolomeis et al, 2002;Polese et al, 2002), nuclear receptor genes (Beaudry et al, 2000;Langlois et al, 2001), neurotensin (Merchant et al, 1992(Merchant et al, , 1994), brain-derived neurotrophic factor (BDNF) (Chlan-Fourney et al, 2002), fibroblast growth factor 2 (Riva et al, 1999), glutamate receptor subunit genes (Riva et al, 1997;Toyoda et al, 1997), regulator of G-protein signalling 2 (Robinet et al, 2001), and so on. The studies of the altered gene expression pattern contribute substantially to our understanding of the mechanism of antipsychotic drug action.…”

Section: Introductionmentioning

confidence: 99%

Microarray Analysis of Differentially Expressed Genes in Rat Frontal Cortex Under Chronic Risperidone Treatment

Chen

2004

Neuropsychopharmacol

View full text Add to dashboard Cite

Long-term administration of antipsychotic drugs can induce differential expression of a variety of genes in the brain, which may underscore the molecular mechanism of the clinical efficacy and/or side effects of antipsychotic drugs. We used cDNA microarray analysis to screen differentially expressed genes in rat frontal cortex under 4 weeks' treatment of risperidone (1 mg/kg). Using real-time quantitative PCR, we were able to verify eight genes, whose expression were significantly upregulated in rat frontal cortex under chronic risperidone treatment when compared with control animals. These genes include receptor for activated protein kinase C, amida, cathepsin D, calpain 2, calcium-independent receptor for a-latrotoxin, monoamine oxidase B, polyubiquitin, and kinesin light chain. In view of the physiological function of these genes, the results of our study suggest that chronic risperidone treatment may affect the neurotransmission, synaptic plasticity, and proteolysis of brain cells. This study also demonstrates that cDNA mciroarray analysis is useful for uncovering genes that are regulated by chronic antipsychotic drugs treatment, which may help bring new insight into the molecular mechanism of antipsychotic drugs.

show abstract

Selective modulation of fibroblast growth factor-2 expression in the rat brain by the atypical antipsychotic clozapine

Cited by 43 publications

References 40 publications

Quetiapine facilitates oligodendrocyte development and prevents mice from myelin breakdown and behavioral changes

Quetiapine facilitates oligodendrocyte development and prevents mice from myelin breakdown and behavioral changes

Chronic Olanzapine Treatment Causes Differential Expression of Genes in Frontal Cortex of Rats as Revealed by DNA Microarray Technique

Microarray Analysis of Differentially Expressed Genes in Rat Frontal Cortex Under Chronic Risperidone Treatment

Contact Info

Product

Resources

About