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1 ain and touch pathways through both pre- and postsynaptic inhibition.
2 suggesting an exclusive role for glycine in postsynaptic inhibition.
3 ely to be involved in presynaptic as well as postsynaptic inhibition.
4 c GABA receptors can mediate presynaptic and postsynaptic inhibition.
5 ligand-gated chloride channels that mediate postsynaptic inhibition.
6 e role of KCC2 in neuronal Cl- extrusion and postsynaptic inhibition.
7 citatory synaptic inputs and thereby produce postsynaptic inhibition.
8 ruder (NKCC1) antagonist, on presynaptic and postsynaptic inhibition.
9 synaptic inhibition of the H-reflex, but not postsynaptic inhibition.
10 synaptic inhibition of the H-reflex, but not postsynaptic inhibition.
11 metanide might be a viable option to improve postsynaptic inhibition after SCI, but it also decreases
12 of previously unknown proteins that regulate postsynaptic inhibition and might contribute to developm
13 via ghrelin-receptor-dependent increases in postsynaptic inhibition and promoted the initiation of e
14 level of KCC2 function sets the strength of postsynaptic inhibition and suggests that the downregula
15 spiratory rhythm following interference with postsynaptic inhibition and the subsequent discovery of
16 antagonism, discounting both presynaptic and postsynaptic inhibition as sources of cone opponency.
19 r show that a prolonged bumetanide increased postsynaptic inhibition by hyperpolarizing the reversal
21 d dendrites, where GIRK channels may mediate postsynaptic inhibition, GIRK1 proteins were also found
22 e- and postsynaptic inhibition, we show that postsynaptic inhibition has a predominant role, suggesti
24 ry synaptic input and strong presynaptic and postsynaptic inhibition in both ON and OFF pathways.
25 s), together with GABA(A) receptors, mediate postsynaptic inhibition in most spinal cord and hindbrai
26 ings emphasize the importance of glycinergic postsynaptic inhibition in motor neurons and challenge t
27 imals, there are conflicting results showing postsynaptic inhibition in motor neurons by corelease of
28 differentially mediate slow presynaptic and postsynaptic inhibition in PVIs and can contribute to th
31 centration at low levels, a prerequisite for postsynaptic inhibition mediated by GABA and glycine.
32 an active Cl- extrusion pathway important in postsynaptic inhibition mediated by ligand-gated anion c
33 ynaptic inhibition of auditory afferents and postsynaptic inhibition of an identified auditory intern
37 e of GABA, NPY, and SST, leading to pre- and postsynaptic inhibition of excitatory hippocampal circui
38 sion occurred even when LTP was inhibited by postsynaptic inhibition of exocytosis or PKA (protein ki
39 te release by glucocorticoids was blocked by postsynaptic inhibition of G-protein activity with intra
40 f glutamatergic transmission is abolished by postsynaptic inhibition of G-protein signaling with GDPb
41 n presynaptic inhibition of Ia afferents and postsynaptic inhibition of motoneurons, and the developm
43 e afferent neurons together with distributed postsynaptic inhibition of several downstream interneuro
44 dial medulla neurons in the mediation of the postsynaptic inhibition of spinal motoneurons necessary
45 hloride intruder, NKCC1) treatment increases postsynaptic inhibition of the H-reflex, and it hyperpol
46 ferent classes of neuron are responsible for postsynaptic inhibition of these interneurons, and the p
47 terneurons responsible for the nonreciprocal postsynaptic inhibition of trigeminal motoneurons that o
49 f KCC2 function would reduce the strength of postsynaptic inhibition, physiological evidence is still
51 The relative significance of presynaptic and postsynaptic inhibition to opioid analgesia is essential
52 upled receptor agonists involves coordinated postsynaptic inhibition via G protein-coupled inwardly r
53 oride regulation, which sets the strength of postsynaptic inhibition via GABA(A) receptors in cortica
54 elative contributions of GABA and glycine to postsynaptic inhibition, we performed in vivo intracellu
55 tive activation and inactivation of pre- and postsynaptic inhibition, we show that postsynaptic inhib
56 and (3) SST(+)-neuron-mediated pathways and postsynaptic inhibition within preBotC modulate breathin