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1 been documented at ultrastructurally defined neuronal gap junctions.
2 the basis of FRIL identification of Cx36 in neuronal gap junctions and IF imaging of Cx36 throughout
3 recent studies suggesting various roles for neuronal gap junctions and in particular their role in g
6 n mice with deletion of the primary gene for neuronal gap junctions (connexin36), suggesting that non
7 f Cx36 throughout rat brain and spinal cord, neuronal gap junctions containing Cx36 appear to occur i
9 oup II mGluRs increases background levels of neuronal gap junction coupling and expression of connexi
10 port here that the developmental increase in neuronal gap junction coupling and expression of connexi
11 neuronal death is discussed, which includes neuronal gap junction coupling as a critical part of the
12 view our recent studies on the regulation of neuronal gap junction coupling by glutamate during devel
13 mechanisms for the developmental increase in neuronal gap junction coupling directly control the deat
16 We report here that the ischemic increase in neuronal gap junction coupling is regulated by glutamate
17 t causal link among group II mGluR function, neuronal gap junction coupling, and neuronal death has a
19 r double-labeling for Cx36 and Cx43 by FRIL, neuronal gap junctions in inferior olive, spinal cord, a
21 Collectively, these findings suggest that neuronal gap junctions in the vHIP-mPFC pathway are impo
23 t retinal ganglion cells in mice lacking the neuronal gap junction protein connexin 36 (Cx36) have ne
24 f long-term running on the expression of the neuronal gap junction protein connexin-36 among inhibito
26 oupling and expression of connexin 36 (Cx36; neuronal gap junction protein) are regulated by an inter
27 upling and expression of connexin 36 (Cx36) (neuronal gap junction protein), and inactivation of grou
28 ectrical synapses) and the expression of the neuronal gap junction protein, connexin 36 (Cx36), trans
31 ble-labeled replicas from 10 CNS regions, no neuronal gap junctions were labeled for either Cx32 or C
32 ectrophysiology, we discovered that blocking neuronal gap junctions within the dorsal hippocampus imp
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