Differential regulation of chromogranin A, chromogranin B and secretogranin II in rat brain by phencyclidine treatment

Marksteiner, Josef; Weiß, U.; Weis, Carla; Laslop, Andrea; Fischer‐Colbrie, Reiner; Humpel, C.; Feldon, Joram; Fleischhacker, W. Wolfgang

doi:10.1016/s0306-4522(01)00081-1

Cited by 16 publications

(8 citation statements)

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“…Scg2 is a plausible candidate for influencing PPI. Phencyclidine (PCP) modulates Scg2 expression in rats [62], [63]. Genes responding to PCP are good candidates for schizophrenia since PCP produces effects similar to schizophrenia in humans.…”

Section: Resultsmentioning

confidence: 99%

In Silico Whole Genome Association Scan for Murine Prepulse Inhibition

et al. 2009

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BackgroundThe complex trait of prepulse inhibition (PPI) is a sensory gating measure related to schizophrenia and can be measured in mice. Large-scale public repositories of inbred mouse strain genotypes and phenotypes such as PPI can be used to detect Quantitative Trait Loci (QTLs) in silico. However, the method has been criticized for issues including insufficient number of strains, not controlling for false discoveries, the complex haplotype structure of inbred mice, and failing to account for genotypic and phenotypic subgroups.Methodology/Principal FindingsWe have implemented a method that addresses these issues by incorporating phylogenetic analyses, multilevel regression with mixed effects, and false discovery rate (FDR) control. A genome-wide scan for PPI was conducted using over 17,000 single nucleotide polymorphisms (SNPs) in 37 strains phenotyped. Eighty-nine SNPs were significant at a false discovery rate (FDR) of 5%. After accounting for long-range linkage disequilibrium, we found 3 independent QTLs located on murine chromosomes 1 and 13. One of the PPI positives corresponds to a region of human chromosome 6p which includes DTNBP1, a gene implicated in schizophrenia. Another region includes the gene Tsn which alters PPI when knocked out. These genes also appear to have correlated expression with PPI.Conclusions/SignificanceThese results support the usefulness of using an improved in silico mapping method to identify QTLs for complex traits such as PPI which can be then be used for to help identify loci influencing schizophrenia in humans.

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Section: Resultsmentioning

confidence: 99%

In Silico Whole Genome Association Scan for Murine Prepulse Inhibition

et al. 2009

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“…In contrast to immediate-early gene expression, ProSN mRNA levels may better reflect specific changes in neuronal secretory activity associated with transmitter release and detect also those coupled to a decreased activity. amphetamine rat striatum +50% [81] phencyclidine rat prefrontal cortex increase [82] lithium differentiated PC12 +60% [83] haloperidol, clozapine rat striatum, raphe +290% [66] clozapine rat prefrontal cortex increase [84] citalopram rat zona inserta +50% [66] kainate rat hippocampus increase [85] kainate rat, gerbil hippocampus increase [86] kainate rat hippocampus +600% [87] kainate rat hippocampus +600% [88] reserpine rat adrenal medulla +150% [89] reserpine rat hypothalamus, brain stem +250% [90] histamine bovine chromaffin cells +400% [91] nicotine, prostaglandin E bovine chromaffin cells +330% [33,69] PACAP bovine chromaffin cells +60% [69,92] amphoterin (RAGE receptor agonist) mouse neuroblastoma cells +350% [93] hormones/trophic factors: estrogen male rat pituitary +155% [94] estrogen female rat hypothalamus +350% [95] adrenalectomy rat hypothalamus +380% [96] lactation rat hypothalamus +240% [96] ovariectomy female rat pituitary +300% [95,97] NGF rat PC12 cells +460% [98] bFGF human neuroblastoma cells +420% [99] EGF GH4 pituitary tumor cells +600% [100] interleukin 1 bovine chromaffin cells +230% [101] TNF-α bovine chromaffin cells +300% [101] hypoxia:…”

Section: Gene Expressionmentioning

confidence: 99%

Secretoneurin: A New Player in Angiogenesis and Chemotaxis Linking Nerves, Blood Vessels and the Immune System

Fischer‐Colbrie

Kirchmair²,

Kähler³

et al. 2005

CPPS

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Secretoneurin (SN) represents a 33 amino acid neuropeptide, which is highly conserved between mammals, reptiles, birds, amphibians and fish. It is specifically expressed in endocrine, neuroendocrine and neuronal tissues. In brain, the pattern of SN expression is widespread and unique, partially overlapping with established neurotransmitters. ProSN, the precursor protein, also named secretogranin II, belongs to a class of proteins collectively called chromogranins. Changes in ProSN mRNA, which is significantly regulated by cell depolarisation, represent a useful marker for both rapid and long-lasting changes (positive and negative) of neuronal activity. Under pathophysiological conditions, especially following cellular hypoxia, SN expression can be induced in non-endocrine tissues like muscle cells, pneumocytes or tumor epithelial cells. Several biological effects were attributed to SN. SN releases dopamine from rat striatal slices in a dose dependent manner and influences neurite outgrowth in the developing cerebellum. It potently and specifically attracts monocytes, eosinophils and endothelial cells towards a concentration gradient and acts as an angiogenic cytokine comparable in potency to VEGF. Thus, SN contributes to neurogenic inflammation and might play a role in the (hypoxia-driven) induction of neo-vascularisation in ischemic diseases like peripheral or coronary artery disease, diabetic retinopathia, cerebral ischemia or in solid tumors. The signalling pathways of various biological effects have not been identified in detail, but most data point to a G-protein coupled receptor structure with respective associated intracellular events.

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“…For testing this time dependency, phencylidine was applied for 4, 8 and 28 h and for 5 days. The latest time point is most comparable to the in vivo experiments in which rats have been treated for 5 days with phencylidine (Marksteiner et al . 2001).…”

mentioning

confidence: 73%

“…A single dose of PCP led to a transient decrease in secretoneurin tissue levels in the rat prefrontal cortex after 4 h followed by an increase in secretoneurin tissue levels after 12 h. Repeated PCP treatment for 5 days resulted in an elevated expression of sg II (Marksteiner et al . 2001).…”

Section: Discussionmentioning

confidence: 99%

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Differential effects of phencyclidine application on secretogranin II expression in organotypic slices of rat prefrontal cortex

Hinterhoelzl

Salimi

Humpel

et al. 2003

Journal of Neurochemistry

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Phencyclidine (PCP) is a non-competitive NMDA glutamate receptor antagonist that induces psychotomimetic effects in humans and experimental animals. Chronic PCP exposure elicits signs of persistently altered frontal brain activity and related behaviors which are also seen in patients with schizophrenia. Secretogranin II (sg II) belongs to the chromogranin family of proteins that exist in large dense core vesicles in nervous tissue. In the brain, 90% of sg II is processed to the small peptide secretoneurin. We previously detected differential effects of single-dose and subchronic PCP administration on sg II expression in the rat prefrontal cortex (PFC). In the present study, we applied PCP to organotypic PFC slices. PCP application for 28 h induced decreased tissue and culture medium secretoneurin content. In contrast, incubation with the adenylate cyclase activator forskolin caused significantly increased secretoneurin levels after 8 h. PCP for 4 h followed by 24 h without PCP resulted in increased culture medium secretoneurin content but no change in tissue levels. sg II mRNA expression was decreased after 28 h PCP application in cortical neurons. Immunohistochemical and TUNEL staining profiles indicated that the alterations were not due to neurodegeneration. PCP for 5 days changed neither the secretoneurin tissue or culture medium levels, nor the sg II mRNA expression. These results demonstrate that PCP modulates sg II expression in PFC tissue in the absence of afferent inputs and that the nature of these changes is dependent upon the duration of exposure to and/or withdrawal from PCP. Keywords: gene expression, in vitro, neuropeptides, NMDA antagonist, prefrontal cortex, schizophrenia. J. Neurochem. (2003) 87, 13-21. Noncompetitive antagonists of the NMDA glutamate receptor, including the dissociative anesthetic phencyclidine (PCP), cause a psychotic reaction in humans comprising many of the positive and negative symptoms of schizophrenia (Tamminga 1998). Chronic PCP exposure elicits a schizophrenia-like pattern of impairment in social and cognitive performance that is thought to result from disturbed prefrontal cortical function (Andreasen et al. 1997;Bunney and Bunney 2000). NMDA glutamate receptor antagonism exerts effects on prefrontal cortical metabolism and neurotransmitter tone the quality and duration of which varies considerably depending on dosing regimen (for review, see Jentsch and Roth 1999). Specifically, chronic PCP exposure induces lasting cognitive impairment (Jentsch et al. 2000) as well as reduced frontal blood flow in humans (Hertzmann et al. 1990) and persistent deficits in prefrontal cortical dopamine utilization and prefrontal cortex (PFC)-dependent cognitive function in rats and monkeys (Balla et al. 2001).The chromogranins comprise a group of acidic secretory proteins which are stored with other neuropeptides in secretory large dense core vesicles (Winkler and Fischer-Colbrie 1992). Chromogranins are involved in the sorting, processing, Received April 23, 2003; accepted May...

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Differential regulation of chromogranin A, chromogranin B and secretogranin II in rat brain by phencyclidine treatment

Cited by 16 publications

References 48 publications

In Silico Whole Genome Association Scan for Murine Prepulse Inhibition

In Silico Whole Genome Association Scan for Murine Prepulse Inhibition

Secretoneurin: A New Player in Angiogenesis and Chemotaxis Linking Nerves, Blood Vessels and the Immune System

Differential effects of phencyclidine application on secretogranin II expression in organotypic slices of rat prefrontal cortex

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