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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
4                        Bilateral infusion of neuronal gap junction blockers into the vHIP decreased a
5            Using pharmacological blockade of neuronal gap junctions combined with electrophysiologica
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
8 tion prevents, the developmental increase in neuronal gap junction coupling and Cx36 expression.
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
14                    Our results indicate that neuronal gap junction coupling is a critical component o
15  and neuronal injury, i.e., at the time when neuronal gap junction coupling is increased.
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
18                                              Neuronal gap junction (GJ) channels composed of connexin
19 r double-labeling for Cx36 and Cx43 by FRIL, neuronal gap junctions in inferior olive, spinal cord, a
20                   The physiological roles of neuronal gap junctions in the intact brain are not known
21    Collectively, these findings suggest that neuronal gap junctions in the vHIP-mPFC pathway are impo
22  junctions (connexin36), suggesting that non-neuronal gap junctions may be involved.
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
25                                    The major neuronal gap junction protein connexin36 (Cx36) exhibits
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
29 ons of knock-out (KO) mice for connexin36, a neuronal gap junction protein.
30                      Electrical synapses are neuronal gap junctions that mediate fast transmission in
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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