Using the RNA arbitrarily-primed PCR and the competitive RT-PCR, we have isolated the neocortical transcripts that are upregulated and unchanged in the adult and infant rats, respectively, after a systemic injection of an N-methyl-d-aspartate (NMDA) receptor antagonist phencyclidine (PCP), and found them identical to the synapse-associated protein-97 (SAP97) gene mRNAs. The upregulation of the SAP97 transcripts in the adult neocortex after the acute PCP injection was mimicked by another NMDA antagonist, dizocilpine, but not by the indirect dopamine agonists, methamphetamine and cocaine, a selective D1 receptor antagonist SCH23390, a D2 receptor-preferring antagonist haloperidol and a GABAergic anesthetic pentobarbital. Moreover, the pretreatment with a typical antipsychotic haloperidol failed to antagonize the increased neocortical SAP97 gene expression by PCP. These findings suggest that SAP97 might be involved in the molecular basis of the development-dependent onset of the non-dopaminergic symptoms seen in schizophrenia and the schizophrenia-like psychosis induced by NMDA receptor blocking.
Download full-text PDF |
Source |
|---|---|
| http://dx.doi.org/10.1016/j.euroneuro.2009.08.007 | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
The Scribble-SGEF-Dlg1 complex regulates E-cadherin and ZO-1 stability, turnover and transcription in epithelial cells.
J Cell Sci
October 2024
Department of Biological Sciences, University of Toledo, Toledo, OH 43606, USA.
SGEF (also known as ARHGEF26), a RhoG specific GEF, can form a ternary complex with the Scribble polarity complex proteins Scribble and Dlg1, which regulates the formation and maintenance of adherens junctions and barrier function of epithelial cells. Notably, silencing SGEF results in a dramatic downregulation of both E-cadherin and ZO-1 (also known as TJP1) protein levels. However, the molecular mechanisms involved in the regulation of this pathway are not known.
View Article and Find Full Text PDFCKIP-1 mediates CK2 translocation to regulate Nav1.5 and Kir2.1 channel complexes in cardiomyocytes.
J Biochem Mol Toxicol
August 2024
Department of Cardiology, Shandong Medicine and Health Key Laboratory of Cardiac Electrophysiology and Arrhythmia, The First Affiliated Hospital of Shandong First Medical University & Shandong Provincial Qianfoshan Hospital, Jinan, People's Republic of China.
Sodium and potassium channels, especially Nav1.5 and Kir2.1, play key roles in the formation of action potentials in cardiomyocytes.
View Article and Find Full Text PDFDLG1 functions upstream of SDCCAG3 and IFT20 to control ciliary targeting of polycystin-2.
EMBO Rep
July 2024
Department of Biology, University of Copenhagen, Copenhagen, Denmark.
Polarized vesicular trafficking directs specific receptors and ion channels to cilia, but the underlying mechanisms are poorly understood. Here we describe a role for DLG1, a core component of the Scribble polarity complex, in regulating ciliary protein trafficking in kidney epithelial cells. Conditional knockout of Dlg1 in mouse kidney causes ciliary elongation and cystogenesis, and cell-based proximity labeling proteomics and fluorescence microscopy show alterations in the ciliary proteome upon loss of DLG1.
View Article and Find Full Text PDFPreliminary Study on Clinical Characteristics and Pathogenesis of Mutations Patients.
Pharmgenomics Pers Med
May 2024
Department of Neurology, Shanghai Children's Hospital, School of Medicine, Shanghai JiaoTong University, Shanghai, People's Republic of China.
Background: The IQ motif and Sec7 domain ArfGEF 2 (), an X-linked gene that encodes the BRAG1 protein, is a guanine nucleotide exchange factor for the ADP ribosylation factor (ARF) protein family in the small guanosine triphosphate (GTP) binding protein. Mutations in this gene result in disorders such as intellectual disability (ID) and epilepsy. In this study, we analyze the clinical features of two patients with -mutation-related disease and discuss their possible pathogenesis.
View Article and Find Full Text PDFSpinal nerve transection-induced upregulation of SAP97 via promoting membrane trafficking of GluA1-containing AMPA receptors in the dorsal horn contributes to the pathogenesis of neuropathic pain.
Neurobiol Dis
May 2024
Department of Physiology and Neurobiology, School of Basic Medical Sciences, Zhengzhou University, 100 Science Avenue, Zhengzhou 450001, China; Neuroscience Research Institute, Zhengzhou University, 100 Science Avenue, Zhengzhou 450001, China. Electronic address:
Article Synopsis
- - The study investigates the role of the protein SAP97 in neuropathic pain following spinal nerve injury in rats, finding that SAP97 helps transport GluA1-containing AMPARs in the spinal cord.
- - After spinal nerve transection (SNT), an increase in SAP97 was observed, which enhanced its interaction with GluA1 and boosted membrane trafficking of these receptors, contributing to neuropathic pain.
- - Targeting SAP97 through methods like microinjections of specific RNA or antagonists reduced pain symptoms, suggesting that manipulating SAP97 could be a new approach for treating chronic pain conditions.
Want AI Summaries of new PubMed Abstracts delivered to your In-box?
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!