Effects of Acute Amphetamine Administration on AMPA-Mediated Synaptic Activity and Expression of AMPA Receptor Subunit 2 of Brain Neurons

2005 ◽  
Vol 25 (2) ◽  
pp. 171-182 ◽  
Author(s):  
Meng-Fen Yu ◽  
Chung-Liang Chien ◽  
Wang-Tso Lee ◽  
Hsiang-Shu Yin
Keyword(s):  
Ampa Receptor ◽  
Synaptic Activity ◽  
Receptor Subunit ◽  
Brain Neurons ◽  
Amphetamine Administration ◽  
Ampa Receptor Subunit

scholarly journals miR-501-3p mediates the activity-dependent regulation of the expression of AMPA receptor subunit GluA1

2015 ◽  
Vol 208 (7) ◽  
pp. 949-959 ◽  
Author(s):  
Zhonghua Hu ◽  
Jun Zhao ◽  
Tianyi Hu ◽  
Yan Luo ◽  
Jun Zhu ◽  
...  
Keyword(s):  
Ampa Receptor ◽  
Dendritic Spines ◽  
Untranslated Region ◽  
Synaptic Activity ◽  
Receptor Subunit ◽  
Local Regulation ◽  
Physiological Conditions ◽  
Ampa Receptor Subunit ◽  
Nmdar Subunit ◽  
Activity Dependent

The number of α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptors (AMPARs) in synapses determines synaptic strength. AMPAR expression can be regulated locally in dendrites by synaptic activity. The mechanisms of activity-dependent local regulation of AMPAR expression, however, remain unclear. Here, we tested whether microRNAs (miRNAs) are involved in N-methyl-d-aspartate (NMDA) receptor (NMDAR)–dependent AMPAR expression. We used the 3′ untranslated region of Gria1, which encodes the AMPA receptor subunit GluA1, to pull down miRNAs binding to it and analyzed these miRNAs using next-generation deep sequencing. Among the identified miRNAs, miR-501-3p is also a computationally predicted Gria1-targeting miRNA. We confirmed that miR-501-3p targets Gria1 and regulates its expression under physiological conditions. The expression of miR-501-3p and GluA1, moreover, is inversely correlated during postnatal brain development. miR-501-3p expression is up-regulated locally in dendrites through the NMDAR subunit GluN2A, and this regulation is required for NMDA-induced suppression of GluA1 expression and long-lasting remodeling of dendritic spines. These findings elucidate a miRNA-mediated mechanism for activity-dependent, local regulation of AMPAR expression in dendrites.

scholarly journals Dissociating Representations of Time and Number in Reinforcement-Rate Learning by Deletion of the GluA1 AMPA Receptor Subunit in Mice

2021 ◽  
Vol 32 (2) ◽  
pp. 204-217
Author(s):  
Joseph M. Austen ◽  
Corran Pickering ◽  
Rolf Sprengel ◽  
David J. Sanderson
Keyword(s):  
Associative Strength ◽  
Ampa Receptor ◽  
Reinforcement Rate ◽  
Statistical Properties ◽  
Temporal Information ◽  
Receptor Subunit ◽  
Male And Female ◽  
Female Mice ◽  
Ampa Receptor Subunit ◽  
Numeric Information

Theories of learning differ in whether they assume that learning reflects the strength of an association between memories or symbolic encoding of the statistical properties of events. We provide novel evidence for symbolic encoding of informational variables by demonstrating that sensitivity to time and number in learning is dissociable. Whereas responding in normal mice was dependent on reinforcement rate, responding in mice that lacked the GluA1 AMPA receptor subunit was insensitive to reinforcement rate and, instead, dependent on the number of times a cue had been paired with reinforcement. This suggests that GluA1 is necessary for weighting numeric information by temporal information in order to calculate reinforcement rate. Sample sizes per genotype varied between seven and 23 across six experiments and consisted of both male and female mice. The results provide evidence for explicit encoding of variables by animals rather than implicit encoding via variations in associative strength.

Q/R RNA editing of the AMPA receptor subunit 2 (GRIA2) transcript evolves no later than the appearance of cartilaginous fishes

FEBS Letters ◽  
2001 ◽  
Vol 509 (2) ◽  
pp. 277-281 ◽  
Author(s):  
Shieh-Shiuh Kung ◽  
Yu-Chia Chen ◽  
Wei-Hsiang Lin ◽  
Chun-Chen Chen ◽  
Wei-Yuan Chow
Keyword(s):  
Rna Editing ◽  
Ampa Receptor ◽  
Receptor Subunit ◽  
Ampa Receptor Subunit ◽  
Cartilaginous Fishes

scholarly journals Long-Lasting Alterations in Gene Expression of Postsynaptic Density 95 and Inotropic Glutamatergic Receptor Subunit in the Mesocorticolimbic System of Rat Offspring Born to Morphine-Addicted Mothers

2018 ◽  
Vol 2018 ◽  
pp. 1-9 ◽  
Author(s):  
Pei-Ling Wu ◽  
Yung-Ning Yang ◽  
Jau-Ling Suen ◽  
Yu-Chen S. H. Yang ◽  
Chun-Hwa Yang ◽  
...  
Keyword(s):  
Gene Expression ◽  
Nmda Receptor ◽  
Glutamate Receptor ◽  
Ampa Receptor ◽  
Prenatal Exposure ◽  
Molecular Mechanisms ◽  
Postsynaptic Density ◽  
Receptor Subunit ◽  
Rat Offspring ◽  
Ampa Receptor Subunit

Prenatal exposure to morphine causes altered glutamatergic neurotransmission, which plays an important pathophysiological role for neurobiological basis of opiate-mediated behaviors in such offspring. However, it is still not clear whether such alteration involves gene expression of ionotropic glutamate receptor subunits. In this study, we further studied whether prenatal morphine exposure resulted in long-term changes in the gene expression of α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) receptor, N-methyl-d-aspartate (NMDA) receptor, and postsynaptic density 95 in the mesocorticolimbic area (an essential integration circuitry for drug craving behavior), nucleus accumbens (NAc), ventral tegmental area (VTA), and prefrontal cortex (PFC), of rat offspring from morphine-addicted mothers. Experimental results showed that prenatal morphine exposure led to a persistent downregulation of gene expression in the AMPA and NMDA receptor subunit, with a differential manner of decreased magnitudes, at the age of postnatal days 14 (P14) and P30. However, in PFC, the gene expression of the AMPA receptor subunit was not synchronized in observed rat offspring subjected to prenatal morphine exposure. An upregulation of gene expression in the AMPA receptor subunit 3 (GluR3) was persistently observed at P14 and P30. Furthermore, the gene expressions of PSD-95 in NAc, VTA, and PFC were all decreased concurrently. Collectively, the results suggest that prenatal exposure to morphine may initiate molecular mechanisms leading to a long-lasting, differential alteration in gene expression of the inotropic glutamate receptor subunit and PSD-95 in the mesocorticolimbic circuitry in rat offspring. This study raises a possibility in which differential changes in gene expression with a long-lasting manner may play a role for the development of nearly permanent changes in opiate-mediated behaviors, at least in part for the neurobiological pathogenesis in offspring.

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