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1 re limited by their ability to only modulate synaptic receptors.
2 nock-out mice as templates for diheteromeric synaptic receptors.
3 mediated by dynamic regulation of excitatory synaptic receptors.
4 or by altering the functional properties of synaptic receptors.
5 synapse and not a decrease in the amount of synaptic receptors.
6 expression do not change the total number of synaptic receptors.
7 is to establish the activation mechanism of synaptic receptors.
8 he activity mediated by synaptic release and synaptic receptors.
9 chanism for controlling Ca2+ permeability of synaptic receptors.
10 tics may reflect a functional fingerprint of synaptic receptors.
11 SHR is due to the altered expression of post-synaptic receptors.
13 this study, we identified the principal post-synaptic receptors activated in cardiac vagal neurons up
15 cological modulators targeting pre- and post-synaptic receptors (AMPA, NMDA, GABA-A, mGluR2/3 recepto
17 efines the molecular diversity of a critical synaptic receptor and provides evidence that neurexin di
18 , YEKL, significantly increase the number of synaptic receptors and allow the synaptic localization o
19 ntracellular receptors is related to that of synaptic receptors and suggest that a mechanism exists i
21 compatible with physiology, the occupancy of synaptic receptors and the depletion of Ca(2+) in the cl
22 nflux of Ca2+ ions into such spines--through synaptic receptors and voltage-sensitive Ca2+ channels (
25 eature of the brain, yet routine turnover of synaptic receptors appears to be intrinsically paradoxic
27 rons in slices of rat visual cortex in which synaptic receptors are blocked pharmacologically, while
30 ogical, and pharmacological conditions where synaptic receptors are transiently exposed to GABA agoni
34 und that extrasynaptic receptors outnumbered synaptic receptors by 3:1; thus whole-cell currents were
35 lated addition and continuous replacement of synaptic receptors can stabilize long-term changes in sy
36 nding of neurotransmitter triggers gating of synaptic receptor channels, but our understanding of the
38 topes do not result in a loss of surface and synaptic receptor clusters, suggesting specific effects
39 mmon vesicles onto spatially segregated post-synaptic receptors clusters, but a pre-synaptic segregat
40 ween intracellular protein mediators and the synaptic receptor complex composed of cellular prion pro
42 elevant light stimuli can induce a change in synaptic receptor composition of ON RGCs, providing a me
44 We suggest that rather early in development synaptic receptors comprising NR1/NR2B subunits could be
45 erties and single-channel conductance of the synaptic receptors, consistent with an upregulation of t
47 rast, GluR2/GluR3 receptors replace existing synaptic receptors continuously; this occurs only at syn
48 en the glutamate source is synaptic and when synaptic receptor contributions are rigorously defined.
52 mechanisms, such as vesicle depletion, post-synaptic receptor desensitization, and autoreceptor inhi
53 g pathways that promote rapid importation of synaptic receptors do not involve insertion from intrace
54 s in the alpha-bungarotoxin-labeled ACh post-synaptic receptor elements of the trunk skeletal muscles
55 a family of neuronal proteins implicated in synaptic receptor endocytosis and recycling, as well as
57 ole in organizing signaling complexes around synaptic receptors for efficient signal transduction.
58 ing through an unexpected pathway, activates synaptic receptors for one of the brain's primary trophi
59 While the regulatory mechanisms governing synaptic receptors have begun to be defined, little is k
64 A provides a gateway for cellular control of synaptic receptor internalization through second messeng
66 bunit of GABA(A)Rs, preferentially enhancing synaptic receptors largely composed of alpha(1-3, 5), be
67 GABA(A)R residency time at EZs, steady-state synaptic receptor levels, and pathological loss of GABA(
72 endent variation in the mean and variance of synaptic receptor numbers for a variety of initial condi
75 AII and A17 amacrines, diabetes changes the synaptic receptors on A17, but not AII amacrine cells.
76 n slice preparation we studied appearance of synaptic receptors on second order rNST neurons and inve
77 independent approaches suggest strongly that synaptic receptors participate prominently in hypoxic ex
78 ng stimulus can induce a long-term change in synaptic receptor phenotype and may alter the activity o
79 DARs is stable and does not shuttle into the synaptic receptor pool, as we observe no recovery of syn
80 ing AMPA receptors between extrasynaptic and synaptic receptor pools is critically involved in establ
81 In contrast, after selective inhibition, the synaptic receptor population rapidly recovers by the imp
82 eting of a distinct NMDA receptor subtype to synaptic receptor populations in cerebellar granule neur
83 erve pool by exocytosis or from nearby extra-synaptic receptors pre-existing on the neuronal surface.
84 e interplay between binding and unbinding of synaptic receptor proteins at synapses plays an importan
87 ver, after ganglion cell axons were crushed, synaptic receptors showed greater lateral mobility and t
90 These findings demonstrate that BAI1 is a synaptic receptor that can activate both the Rho and ERK
91 BDNF receptor TrkB and beta1-integrins, two synaptic receptors that engage actin regulatory RhoA sig
96 outside the context of normal circuits, and synaptic receptor turnover has not been measured at indi
99 seizure activity may result in expression of synaptic receptors with altered properties driven by an
100 fenprodil block of EPSCs was attributable to synaptic receptors with lower ifenprodil sensitivity rat
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