GABAC receptor-mediated inhibition is altered but not eliminated in the superior colliculus of GABAC rho1 knockout mice.
GABAC receptor-mediated inhibition is altered but not eliminated in the superior colliculus of GABAC rho1 knockout mice.
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在 GABAC rho1 敲除小鼠的上丘中，GABAC 受体介导的抑制作用发生改变，但并未消除。
DOI：
10.1152/jn.91001.2008
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发表时间：
2009
影响因子：
2.5
通讯作者：
Schmidt,Matthias
中科院分区：
文献类型：
--
作者：
Schlicker,Katja;McCall,MaureenA;Schmidt,Matthias
GABACreceptors (GABACRs) are widely expressed in the mammalian subcortical visual system, particularly in the retina and superior colliculus (SC). GABACRs are composed of specific ρ1–3 subunits the expression of which varies among visual structures. Thus ρ1 subunits are most abundant in retina, and their loss eliminates GABACR expression and function. In the SC, ρ2 subunit expression may be equal to or stronger than ρ1 subunit expression; however, results across studies vary considerably. To more directly assess the expression of GABACR subunits, we characterized inhibition in the SC of wild-type (WT) and GABACρ1 Null mice that lack expression of GABACρ1 subunits. We used whole cell patch-clamp recordings and evaluated GABACR-mediated modulation of electrically evoked post synaptic currents using either agonists or antagonists in WT mice. In GABACρ1 Null stratum griseum superficiale (SGS) cells, inhibitory postsynaptic currents were shorter in duration and their excitatory postsynaptic currents (EPSCs) were longer, indicating that a slow GABACR-mediated inhibitory component was reduced in each case. In contrast to retina, GABACR-mediated currents in the SC were altered but not eliminated in GABACρ1 Null mice. In the majority of SC cells in GABACρ1 Null mice, GABACR activation could still be induced to alter EPSC peak amplitudes in putative interneurons and in many projection neurons. These results, compared with previously published data, indicate a fundamental difference between retina and SC in the control of GABACR expression and subunit composition.
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影响因子：
2.5
作者：
M. Pasternack;Mathias Boller;Belinda Pau;M. Schmidt
通讯作者：
M. Schmidt
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作者：
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DOI：
10.1113/jphysiol.2006.119560
发表时间：
2006
期刊：
The Journal of Physiology
影响因子：
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作者：
M. Palmer
通讯作者：
M. Palmer
影响因子：
2.5
作者：
Dong, CJ;Werblin, FS
通讯作者：
Werblin, FS
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影响因子：
3.8
作者：
Katja Schlicker;Mathias Boller;M. Schmidt
通讯作者：
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