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1 nvestigated due to postmortem degradation of synaptic receptors.
2 SHR is due to the altered expression of post-synaptic receptors.
3 lease glutamate continually to activate post-synaptic receptors.
4 positioned to orchestrate the endocytosis of synaptic receptors.
5 nock-out mice as templates for diheteromeric synaptic receptors.
6 mediated by dynamic regulation of excitatory synaptic receptors.
7  or by altering the functional properties of synaptic receptors.
8  synapse and not a decrease in the amount of synaptic receptors.
9 expression do not change the total number of synaptic receptors.
10  is to establish the activation mechanism of synaptic receptors.
11 he activity mediated by synaptic release and synaptic receptors.
12 chanism for controlling Ca2+ permeability of synaptic receptors.
13 re limited by their ability to only modulate synaptic receptors.
14 tics may reflect a functional fingerprint of synaptic receptors.
15                                              Synaptic receptor accumulation is regulated by the trans
16 this study, we identified the principal post-synaptic receptors activated in cardiac vagal neurons up
17 ay permit rapid Ca(2+) influx in response to synaptic receptor activation.
18 -simultaneous recording of microtransplanted synaptic receptors after simulated morgue conditions all
19 from an unconnected afferent pathway co-opts synaptic receptors, allowing activation of postsynaptic
20 cological modulators targeting pre- and post-synaptic receptors (AMPA, NMDA, GABA-A, mGluR2/3 recepto
21 hort-lived to long-lasting binding between a synaptic receptor and its transducer.
22 efines the molecular diversity of a critical synaptic receptor and provides evidence that neurexin di
23 , YEKL, significantly increase the number of synaptic receptors and allow the synaptic localization o
24 ntracellular receptors is related to that of synaptic receptors and suggest that a mechanism exists i
25   These changes led to near-complete loss of synaptic receptors and synaptic depression.
26 compatible with physiology, the occupancy of synaptic receptors and the depletion of Ca(2+) in the cl
27 nflux of Ca2+ ions into such spines--through synaptic receptors and voltage-sensitive Ca2+ channels (
28               We used reversible infusion of synaptic receptor antagonists to show that blocking inhi
29 resence of a large panel of onconeuronal and synaptic receptor antibodies.
30 eature of the brain, yet routine turnover of synaptic receptors appears to be intrinsically paradoxic
31                                              Synaptic receptors are allosteric proteins that switch o
32 rons in slices of rat visual cortex in which synaptic receptors are blocked pharmacologically, while
33 e whenever the ligand-binding sites of their synaptic receptors are buried in the lipid bilayer.
34                                        Other synaptic receptors are completely unaffected by the AAbs
35 ogical, and pharmacological conditions where synaptic receptors are transiently exposed to GABA agoni
36             Induction requires activation of synaptic receptors as well as voltage-gated Ca channels.
37                             In contrast, few synaptic receptors associate with SAP97, suggesting that
38 ng and internalization allows for modulating synaptic receptor availability.
39 emantine based on differential extrasynaptic/synaptic receptor blockade.
40 und that extrasynaptic receptors outnumbered synaptic receptors by 3:1; thus whole-cell currents were
41 lated addition and continuous replacement of synaptic receptors can stabilize long-term changes in sy
42 nding of neurotransmitter triggers gating of synaptic receptor channels, but our understanding of the
43        The extent to which agonists activate synaptic receptor-channels depends on both the intrinsic
44 topes do not result in a loss of surface and synaptic receptor clusters, suggesting specific effects
45 mmon vesicles onto spatially segregated post-synaptic receptors clusters, but a pre-synaptic segregat
46 ween intracellular protein mediators and the synaptic receptor complex composed of cellular prion pro
47         Finally, we provide evidence linking synaptic receptor composition and cycling, showing that
48 elevant light stimuli can induce a change in synaptic receptor composition of ON RGCs, providing a me
49 icity of synapses require dynamic changes in synaptic receptor composition.
50  We suggest that rather early in development synaptic receptors comprising NR1/NR2B subunits could be
51 erties and single-channel conductance of the synaptic receptors, consistent with an upregulation of t
52 ete synaptic domains and cause a decrease of synaptic receptor content.
53 rast, GluR2/GluR3 receptors replace existing synaptic receptors continuously; this occurs only at syn
54 en the glutamate source is synaptic and when synaptic receptor contributions are rigorously defined.
55                                    Normally, synaptic receptor densities were maintained by rapid exc
56 hich can be counterbalanced by the increased synaptic receptor density.
57 ma membrane receptor pools in the control of synaptic receptor density.
58 ighly dynamic and are involved in regulating synaptic receptor density.
59  mechanisms, such as vesicle depletion, post-synaptic receptor desensitization, and autoreceptor inhi
60                           Different types of synaptic receptors distributed over dendrites are respon
61 g pathways that promote rapid importation of synaptic receptors do not involve insertion from intrace
62 s in the alpha-bungarotoxin-labeled ACh post-synaptic receptor elements of the trunk skeletal muscles
63  a family of neuronal proteins implicated in synaptic receptor endocytosis and recycling, as well as
64                  However, the development of synaptic receptor expression and colocalization has been
65        Our findings identify GABA(B)R1a as a synaptic receptor for sAPP and reveal a physiological ro
66 es, we show here that blockade of excitatory synaptic receptors for 2 to 3 d induces an up-regulation
67 ole in organizing signaling complexes around synaptic receptors for efficient signal transduction.
68 ing through an unexpected pathway, activates synaptic receptors for one of the brain's primary trophi
69    While the regulatory mechanisms governing synaptic receptors have begun to be defined, little is k
70 TS that activates NMDA and kainate/AMPA post-synaptic receptors in cardiac vagal neurons.
71       Our results also establish that TARPed synaptic receptors in granule cells require both gamma-2
72 mbient light can modulate the composition of synaptic receptors in ON ganglion cells.
73 an modify tonically and phasically activated synaptic receptors in opposite directions.
74                                 In contrast, synaptic receptors included both a highly ifenprodil-sen
75 A provides a gateway for cellular control of synaptic receptor internalization through second messeng
76 MDA receptors, indicating that the number of synaptic receptors is tightly regulated.
77 bunit of GABA(A)Rs, preferentially enhancing synaptic receptors largely composed of alpha(1-3, 5), be
78 GABA(A)R residency time at EZs, steady-state synaptic receptor levels, and pathological loss of GABA(
79                       Moreover, AP-activated synaptic receptor-mediated phasic currents were not affe
80  neuronal isoform content of the polymorphic synaptic receptors neurexin-1, -2, and -3.
81 is thought to depend on cues provided by pre-synaptic receptor neurons.
82 or these synaptic changes are alterations in synaptic receptor number and density.
83 endent variation in the mean and variance of synaptic receptor numbers for a variety of initial condi
84  its extrasynaptic anchor, thereby enriching synaptic receptor numbers.
85 to 250 Hz, leaving a substantial fraction of synaptic receptors occupied persistently by GABA.
86  AII and A17 amacrines, diabetes changes the synaptic receptors on A17, but not AII amacrine cells.
87 n slice preparation we studied appearance of synaptic receptors on second order rNST neurons and inve
88 independent approaches suggest strongly that synaptic receptors participate prominently in hypoxic ex
89 ng stimulus can induce a long-term change in synaptic receptor phenotype and may alter the activity o
90 DARs is stable and does not shuttle into the synaptic receptor pool, as we observe no recovery of syn
91 ing AMPA receptors between extrasynaptic and synaptic receptor pools is critically involved in establ
92 In contrast, after selective inhibition, the synaptic receptor population rapidly recovers by the imp
93 eting of a distinct NMDA receptor subtype to synaptic receptor populations in cerebellar granule neur
94 erve pool by exocytosis or from nearby extra-synaptic receptors pre-existing on the neuronal surface.
95 e interplay between binding and unbinding of synaptic receptor proteins at synapses plays an importan
96 cts synaptic translation, transcription, and synaptic receptor regulation.
97                                              Synaptic receptors respond to neurotransmitters by openi
98 ver, after ganglion cell axons were crushed, synaptic receptors showed greater lateral mobility and t
99 n this review, this renewed understanding of synaptic receptor signaling interactions and the clinica
100 y their shapes, subcellular composition, and synaptic receptor subtypes.
101                This is particularly true for synaptic receptors such as the alpha(2A)-adrenergic rece
102 urons, in which dendrite-specific changes in synaptic receptors support input-localized decoding.
103    These findings demonstrate that BAI1 is a synaptic receptor that can activate both the Rho and ERK
104  BDNF receptor TrkB and beta1-integrins, two synaptic receptors that engage actin regulatory RhoA sig
105 ches to exogenous GABA applications and fast synaptic receptors that generate rapid IPSCs.
106  social memory formation, through regulating synaptic receptor trafficking in pyramidal neurons by So
107 orting receptor SorCS1 as a key regulator of synaptic receptor trafficking.
108    PICK1 is a modular scaffold implicated in synaptic receptor trafficking.
109 p mechanism involving extrasynaptic and then synaptic receptor transport.
110 y synaptic structure proteins and excitatory synaptic receptors/transporters occurred primarily in OF
111 to excitatory synaptic structure, excitatory synaptic receptors/transporters, and GABA synapses.
112  outside the context of normal circuits, and synaptic receptor turnover has not been measured at indi
113 urces of synaptic excitation, as well as the synaptic receptors used for such excitation.
114                       The composition of the synaptic receptors was not uniform: clusters distributed
115 ey functional genes such as ion channels and synaptic receptors, we found matching known mouse intern
116                                     However, synaptic receptors were not altered by the patch excisio
117 ng of these antibodies causes dysfunction of synaptic receptors, which leads to neurological symptoms
118 seizure activity may result in expression of synaptic receptors with altered properties driven by an
119 fenprodil block of EPSCs was attributable to synaptic receptors with lower ifenprodil sensitivity rat

 
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