Prenatal propofol exposure downregulates NMDA receptor expression and causes cognitive and emotional disorders in rats

2019 ◽  
Vol 843 ◽  
pp. 268-276 ◽  
Author(s):  
Daili Chen ◽  
Xiaofei Qi ◽  
Renkun Zhuang ◽  
Jun Cao ◽  
Yang Xu ◽  
...  
Keyword(s):  
Nmda Receptor ◽  
Emotional Disorders ◽  
Receptor Expression

Pilocapine alters NMDA receptor expression and function in hippocampal neurons: NADPH oxidase and ERK1/2 mechanisms

2011 ◽  
Vol 42 (3) ◽  
pp. 482-495 ◽  
Author(s):  
Roberto Di Maio ◽  
Pier G. Mastroberardino ◽  
Xiaoping Hu ◽  
Laura Montero ◽  
J. Timothy Greenamyre
Keyword(s):  
Nmda Receptor ◽  
Nadph Oxidase ◽  
Hippocampal Neurons ◽  
Receptor Expression ◽  
And Function

FC29-03 - Effects of chronic oral treatment with aripiprazole on expression of nmda receptor subunits and binding sites in rat brain

2011 ◽  
Vol 26 (S2) ◽  
pp. 1979-1979
Author(s):  
M. Zink ◽  
N. Segnitz ◽  
T. Ferbert ◽  
A. Schmitt ◽  
P. Gass ◽  
...  
Keyword(s):  
Nmda Receptor ◽  
Negative Symptoms ◽  
Oral Treatment ◽  
Antipsychotic Agents ◽  
Brain Regions ◽  
Relative Increase ◽  
Receptor Expression ◽  
Sprague Dawley ◽  
Adult Type ◽  
Mk 801

IntroductionThe glutamatergic theory of schizophrenia proposes a dysfunction of ionotropic N-Methyl-D-aspartate (NMDA)-receptors (NR). Several therapeutic strategies address NR function and effects of antipsychotic agents on NR expression have been described.ObjectivesThe partial dopaminergic and serotonergic agonist aripiprazole (APZ) was able to counteract behavioural effects of NR antagonists, but effects of APZ on NR expression have not been investigated.AimsTo evaluate effects of APZ on NR mRNA and protein expressionMethodsWe treated Sprague-Dawley rats for 4 weeks or 4 months with APZ in daily oral doses of 10 and 40 mg per kg body weight. Expression of the NR subunits NR1, NR2A, NR2B, NR2C and NR2D was assessed by semiquantitative radioactive in situ-hybridization, and in parallel receptor binding using 3H-MK-801 receptor autoradiography.ResultsIncreased expression levels of NR1 (4 weeks), NR2A (4 weeks), NR2C (4 weeks and 4 months) and NR2D (4 months) were observed in several hippocampal and cortical brain regions. The parallel reduced expression of NR2B mRNAs (4 months) resulted in a relative increase of the NR2A/NR2B ratio. Marked differences between specific brain regions, the doses and time points of assessment became obvious. On the receptor level, increased MK-801-binding was found after 4 weeks in the 40 mg-group and after 4 months in the 10 mg-group.ConclusionsThe effects of APZ converge in enhanced NMDA-receptor expression and a shift of subunit-composition towards adult-type receptors. Our results confirm regulatory connections between dopaminergic, serotonergic and glutamatergic neurotransmission with relevance for cognitive and negative symptoms of schizophrenia.

scholarly journals Effects of Repeated Ethanol Exposures on NMDA Receptor Expression and Locomotor Sensitization in Mice Expressing Ethanol Resistant NMDA Receptors

2017 ◽  
Vol 11 ◽  
Author(s):  
Carolina R. den Hartog ◽  
Meghin Gilstrap ◽  
Bethany Eaton ◽  
Daniel H. Lench ◽  
Patrick J. Mulholland ◽  
...  
Keyword(s):  
Nmda Receptor ◽  
Nmda Receptors ◽  
Receptor Expression ◽  
Locomotor Sensitization

NMDA receptor blocker ameliorates ischemia-reperfusion-induced renal dysfunction in rat kidneys

2008 ◽  
Vol 294 (6) ◽  
pp. F1433-F1440 ◽  
Author(s):  
Chih-Ching Yang ◽  
Chiang-Ting Chien ◽  
Ming-Hsiou Wu ◽  
Ming-Chieh Ma ◽  
Chau-Fong Chen
Keyword(s):  
Nmda Receptor ◽  
Renal Dysfunction ◽  
Metabotropic Glutamate Receptor ◽  
Ischemia Reperfusion ◽  
Nmda Antagonist ◽  
Receptor Expression ◽  
Functional Assay ◽  
Tubular Dysfunction ◽  
Group I ◽  
Rat Kidneys

N-methyl-d-aspartate (NMDA) receptor activated by glutamate/glycine is located in the kidneys. The NMDA receptor subunit NR1 is increased in damaged renal tissue. This study explored the role of NMDA receptors in ischemia-reperfusion-induced renal dysfunction in rats. With Western blot analysis and renal functional assay, NMDA receptor expression was evaluated, as well as its functional role in female Wistar rat kidneys after 45 min of unilateral ischemia followed by 24 h of reperfusion. The effects of intrarenal NMDA receptor agonist and antagonist on renal blood flow (RBF), glomerular filtration rate (GFR), urine volume (UV), sodium (UNaV), and potassium (UKV) excretion were determined. NMDA NR1 was present in the glomeruli, brush-border membrane, and outer medulla but not in the cortex and inner medulla. Homogenous distribution of non-NMDA GluR2/3, sparse kainate KA1, and undetectable group I of metabotropic glutamate receptor were noted in the control kidneys. Ischemia-reperfusion kidneys showed enhanced renal NR1, but not NR2C and GluR2/3 expression, and were associated with decreased GFR/RBF and natriuretic/diuretic responses. Intrarenal NMDA agonists significantly reduced GFR, UV, UNaV, and UKV but had no effect on blood pressure and RBF in sham control and ischemia-reperfusion kidneys. NMDA antagonist d-2-amino-5-phosphonopentanoic acid (D-AP-5) treatment completely abolished NMDA-induced renal dysfunction. D-AP-5 treatment significantly ameliorated ischemia-reperfusion-induced glomerular and tubular dysfunction by restoring decreased GFR, UV, and UNaV levels. Ischemia-reperfusion upregulates renal NMDA NR1 receptor expression, leading to reduced glomerular and tubular function in the kidneys. The NMDA antagonist can ameliorate ischemia-reperfusion-induced renal dysfunction.

scholarly journals Changes in Glutamate/NMDA Receptor Subunit 1 Expression in Rat Brain after Acute and Subacute Exposure to Methamphetamine

2009 ◽  
Vol 2009 ◽  
pp. 1-4 ◽  
Author(s):  
Walailuk Kerdsan ◽  
Samur Thanoi ◽  
Sutisa Nudmamud-Thanoi
Keyword(s):  
Nmda Receptor ◽  
Frontal Cortex ◽  
Behavioral Sensitization ◽  
Hippocampal Formation ◽  
Receptor Expression ◽  
Receptor Subunit ◽  
Sprague Dawley ◽  
Acute Group ◽  
And Control ◽  
Subacute Exposure

Methamphetamine (METH) is a psychostimulant drug of abuse that produces long-term behavioral changes including behavioral sensitization, tolerance, and dependence. METH has been reported to induce neurotoxic effects in several areas of the brain via the dopaminergic system. Changes of dopamine function can induce malfunction of the glutamatergic system. Therefore, the aim of the present study was to examine the effects of METH administration on the expression of glutamate N-methyl-D-aspartate receptor subunit 1 (NMDAR1) in frontal cortex, striatum, and hippocampal formation after acute and subacute exposure to METH by western blotting. Male Sprague-Dawley rats were injected intraperitoneally with a single dose of 8 mg/kg METH, 4 mg/kg/day METH for 14 days and saline in acute, subacute, and control groups, respectively. A significant increase in NMDAR1 immunoreactive protein was found in frontal cortex in the subacute group (P=.036) but not in the acute group (P=.580). Moreover, a significant increase in NMDAR1 was also observed in striatum in both acute (P=.025) and subacute groups (P=.023). However, no significant differences in NMDAR1 in hippocampal formation were observed in either acute or subacute group. The results suggest that an upregulation of NMDA receptor expression may be a consequence of glutamatergic dysfunction induced by METH.

scholarly journals Tau accumulation activates STAT1 triggering memory deficits via suppressing NMDA receptor expression

2018 ◽  
Author(s):  
Xiao-Guang Li ◽  
Xiao-Yue Hong ◽  
Ya-li Wang ◽  
Shu-Juan Zhang ◽  
Jun-Fei Zhang ◽  
...  
Keyword(s):  
Nmda Receptor ◽  
Nuclear Translocation ◽  
Memory Performance ◽  
Memory Deficits ◽  
Dominant Negative ◽  
Receptor Expression ◽  
Signal Transducer ◽  
Synaptic Functions ◽  
Direct Binding ◽  
The Brain

ABSTRACTIntracellular tau accumulation forming neurofibrillary tangles is hallmark pathology of Alzheimer's disease (AD), but how tau accumulation induces synapse impairment is elusive. By overexpressing human full-length wildtype tau (termed hTau) to mimic tau abnormality as seen in the brain of sporadic AD patients, we found that hTau accumulation activated JAK2 to phosphorylate STAT1 (Signal Transducer and Activator of Transcription 1) at Tyr701 leading to STAT1 dimerization, nuclear translocation and its activation. STAT1 activation suppressed expression of N-methyl-D-aspartate receptors (NMDARs) through direct binding to the specific GAS element of GluN1, GluN2A and GluN2B promoters, while knockdown STAT1 by AAV-Cre in STAT1flox/flox mice or expressing dominant negative Y701F-STAT1 efficiently rescued hTau-induced suppression of NMDARs expression with amelioration of synaptic functions and memory performance. These findings indicate that hTau accumulation impairs synaptic plasticity through JAK2/STAT1-induced suppression of NMDARs expression, revealing a novel mechanism for hTau-associated synapse and memory deficits.

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