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  Genetic manipulation of key determinants of ion flow in glutamate receptor channels in the mouse

Seeburg, P. H., Single, F. N., Kuner, T., Higuchi, M., & Sprengel, R. (2001). Genetic manipulation of key determinants of ion flow in glutamate receptor channels in the mouse. Brain Research, 907(1), 233-243. doi:10.1016/S0006-8993(01)02445-3.

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Genre: Journal Article
Alternative Title : Genetic manipulation of key determinants of ion flow in glutamate receptor channels in the mouse

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BrainRes_907_2001_233.pdf (Any fulltext), 3MB
 
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Seeburg, Peter H.1, Author           
Single, Frank Nicolai1, Author           
Kuner, Thomas1, 2, 3, 4, 5, Author           
Higuchi, Miyoko1, Author           
Sprengel, Rolf1, Author           
Affiliations:
1Department of Molecular Neurobiology, Max Planck Institute for Medical Research, Max Planck Society, ou_1497704              
2Interdisciplinary WIN-Research Group on Olfactory Dynamics, Max Planck Institute for Medical Research, Max Planck Society, ou_1497717              
3Synaptic Transmission MNTB, Max Planck Institute for Medical Research, Max Planck Society, ou_1497745              
4Synaptic Transmission, Max Planck Institute for Medical Research, Max Planck Society, ou_1497744              
5Department of Cell Physiology, Max Planck Institute for Medical Research, Max Planck Society, ou_1497701              

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Free keywords: Neurotransmitters, modulators, transporters and receptors, Excitatory amino acid receptors: ligand-gated ion channels; AMPA and NMDA receptors; Gene targeting in the mouse; Insertional gene silencing; RNA editing; Adenosine deaminases acting on RNA (ADARs)
 Abstract: Glutamate receptor channels are built around an ancient pore loop structure which defines the inner channel environment and which is connected to structures for channel gating. This pore loop, which corresponds to the M2 region of the receptor subunits, enters the lipid bilayer from the intracellular side in an α-helical configuration, then kinks to form a random coil and exits the lipid bilayer at the intracellular side. The narrow constriction of the channel is formed by amino acid residues that occupy a position shortly after the end of the α-helical part of M2. These residues determine ion selectivity and conductance properties of the glutamate-gated channel. The critical residues are asparagines for NMDA receptor subunits and glutamine or arginine for AMPA and kainate receptor subunits. Presence of arginine in the critical channel position of AMPA and kainate receptors is controlled by site-selective RNA editing. To study the importance of these critical channel residues in the mouse, we introduced codon changes in the endogenous genes for NMDA and AMPA receptor subunits. Our results show that changes in the critical channel position are not tolerated, but lead to early death. Therefore, the impact on adult synaptic function and plasticity by glutamate receptor channels with changed ion selectivity and conductance needs to be addressed by conditional expression of the mutant receptors.

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Language(s): eng - English
 Dates: 2001-04-062001-06-052001-07-13
 Publication Status: Published in print
 Pages: 11
 Publishing info: -
 Table of Contents: -
 Rev. Type: Peer
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Title: Brain Research
  Other : Brain Res.
Source Genre: Journal
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Publ. Info: Amsterdam : Elsevier
Pages: - Volume / Issue: 907 (1) Sequence Number: - Start / End Page: 233 - 243 Identifier: ISSN: 0006-8993
CoNE: https://pure.mpg.de/cone/journals/resource/954926250616