scholarly journals Impairment of Catecholamine Systems during Induction of Long-Term Potentiation at Hippocampal CA1 Synapses in HPC-1/Syntaxin 1A Knock-out Mice

2012 ◽  
Vol 32 (1) ◽  
pp. 381-389 ◽  
Author(s):  
T. Mishima ◽  
T. Fujiwara ◽  
T. Kofuji ◽  
K. Akagawa
2018 ◽  
Author(s):  
Jonathan M. Wong ◽  
John A. Gray

AbstractNMDA receptors (NMDARs) mediate major forms of both long-term potentiation (LTP) and long-term depression (LTD) and understanding how a single receptor can initiate both phenomena remains a major question in neuroscience. A prominent hypothesis implicates the NMDAR subunit composition, specifically GluN2A and GluN2B, in dictating the rules of synaptic plasticity. However, studies testing this hypotheses have yielded inconsistent and often contradictory results, especially for LTD. These inconsistent results may be due to challenges in the interpretation of subunit-selective pharmacology and in dissecting out the contributions of differential channel properties versus the interacting proteins unique to GluN2A or GluN2B. In this study, we address the pharmacological and biochemical challenges by utilizing a single-neuron genetic approach to delete NMDAR subunits in both male and female conditional knock-out mice. In addition, emerging evidence that non-ionotropic signaling through the NMDAR is sufficient for NMDAR-dependent LTD allowed the rigorous assessment of unique subunit contributions to NMDAR-dependent LTD while eliminating the variable of differential charge transfer. Here we find that neither the GluN2A nor the GluN2B subunit is strictly necessary for either non-ionotropic or ionotropic LTD.


2002 ◽  
Vol 22 (7) ◽  
pp. 2753-2763 ◽  
Author(s):  
Yanghong Gu ◽  
Kellie L. McIlwain ◽  
Edwin J. Weeber ◽  
Takanori Yamagata ◽  
Bisong Xu ◽  
...  

2007 ◽  
Vol 27 (39) ◽  
pp. 10487-10496 ◽  
Author(s):  
J. L. W. Yau ◽  
K. M. McNair ◽  
J. Noble ◽  
D. Brownstein ◽  
C. Hibberd ◽  
...  

2002 ◽  
Vol 13 (10) ◽  
pp. 3696-3705 ◽  
Author(s):  
Chin-Hung Cheng ◽  
David Tai-Wai Yew ◽  
Hiu-Yee Kwan ◽  
Qing Zhou ◽  
Yu Huang ◽  
...  

CNG channels are cyclic nucleotide-gated Ca2+-permeable channels that are suggested to be involved in the activity-dependent alterations of synaptic strength that are thought to underlie information storage in the CNS. In this study, we isolated an endogenous RNA transcript antisense to CNGα1 mRNA. This transcript was capable of down-regulating the expression of sense CNGα1 in theXenopus oocyte expression system. RT-PCR, Northern blot, and in situ hybridization analyses showed that the transcript was coexpressed with CNGα1 mRNA in many regions of human brain, notably in those regions that were involved in long-term potentiation and long-term depression, such as hippocampal CA1 and CA3, dentate gyrus, and cerebellar Purkinje layer. Comparison of expression patterns between adult and fetal cerebral cortex revealed that there were concurrent developmental changes in the expression levels of anti-CNG1 and CNGα1. Treatment of human glioma cell T98 with thyroid hormone T3 caused a significant increase in anti-CNG1 expression and a parallel decrease in sense CNGα1 expression. These data suggest that the suppression of CNGα1 expression by anti-CNG1 may play an important role in neuronal functions, especially in synaptic plasticity and cortical development. Endogenous antisense RNA-mediated regulation may represent a new mechanism through which the activity of ion channels can be regulated in the human CNS.


Sign in / Sign up

Export Citation Format

Share Document