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1 ted from the presynaptic side of the CA3-CA1 hippocampal synapse.
2 c distribution of epsin1 and HIP1 in rat CA1 hippocampal synapse.
3 ow endocytosis and bulk endocytosis at small hippocampal synapses.
4 ong-term depression (LTD) of transmission at hippocampal synapses.
5  into all-or-none potentiation of individual hippocampal synapses.
6 of long-term potentiation (LTP) at different hippocampal synapses.
7 lity and reuse during synaptic depression at hippocampal synapses.
8 es changes in the number and/or structure of hippocampal synapses.
9 late dynamics of SV pool partitioning at rat hippocampal synapses.
10  learning include the remodeling of existing hippocampal synapses.
11 otentiation (LTP) at Schaffer collateral-CA1 hippocampal synapses.
12 n astrocytes when glutamate is released from hippocampal synapses.
13 ormly sample the glutamate released from all hippocampal synapses.
14 bout the position of astrocytic processes at hippocampal synapses.
15 hysiological and biochemical deficits in the hippocampal synapses.
16  to the docked vesicle number in the smaller hippocampal synapses.
17 n applied to experimental data recorded from hippocampal synapses.
18 and normal encoding of information in native hippocampal synapses.
19 ily releasable pool (RRP) stimulation in rat hippocampal synapses.
20 hinning of the postsynaptic density (PSD) at hippocampal synapses.
21 y directly reflects the turnover dynamics of hippocampal synapses.
22 ize matches that of AMPARs and NMDARs in the hippocampal synapses.
23 impairs the efficacy of neurotransmission at hippocampal synapses.
24 during NMDA-receptor-dependent LTP at mature hippocampal synapses.
25 tion between presynaptic features of typical hippocampal synapses.
26 eficit in paired pulse facilitation (PPF) at hippocampal synapses.
27 ion of brain networks and in their impact on hippocampal synapses.
28 beta) blocks long-term potentiation (LTP) of hippocampal synapses.
29 essions and correlates strongly with loss of hippocampal synapses.
30 ippocampus and examined them individually in hippocampal synapses.
31 expression and alter NMDAR properties at rat hippocampal synapses.
32 or subtypes contribute to EPSCs at wild-type hippocampal synapses.
33 ple distinct release sites within individual hippocampal synapses.
34 tic model of synaptic dynamics in excitatory hippocampal synapses.
35 egulation of synaptic function in excitatory hippocampal synapses.
36 ocytosis and long-term potentiation (LTP) at hippocampal synapses.
37 ptor properties at cortical, amygdaloid, and hippocampal synapses.
38 r collagen is necessary for the formation of hippocampal synapses.
39 ective OPHN1 signaling impairs SV cycling at hippocampal synapses.
40 t exclusive, mechanism of retrieval in small hippocampal synapses.
41 but not monomers, induce progressive loss of hippocampal synapses.
42  against the occurrence of 'kiss-and-run' in hippocampal synapses.
43 n important regulator of SV replenishment at hippocampal synapses.
44 ribution of AP180 and CALM in the developing hippocampal synapses.
45 is a major mechanism of vesicle recycling at hippocampal synapses.
46 needs to be speeded up to supply vesicles at hippocampal synapses.
47 hermore, the long-term potentiation (LTP) of hippocampal synapses, a widely studied model of memory,
48                                           At hippocampal synapses, activation of group I metabotropic
49 to follow the fate of individual vesicles at hippocampal synapses after exocytosis.
50 of alphaCaMKII and increases GluA1 levels in hippocampal synapses after retrieval of contextual fear
51  tracking of individual synaptic vesicles in hippocampal synapses and advanced motion analysis tools
52 turation in these mice, leading to a loss of hippocampal synapses and dendritic branches by P42.
53  and functionally investigated Arf6-silenced hippocampal synapses and found an activity dependent acc
54 ent regulator of neurotransmitter release at hippocampal synapses and maintains synapses in an optima
55 ibution of VGCCs in the active zone of small hippocampal synapses and revealed that spontaneous VGCCs
56 un is the dominant mode of vesicle fusion at hippocampal synapses and that the prevalence of kiss-and
57 not induce a net gain in the total number of hippocampal synapses and, hence, a net synaptogenesis.
58 TD) but not long-term potentiation of rodent hippocampal synapses, and during LTD but not long-term f
59  Abeta, prevents and/or reverses the loss of hippocampal synapses, and prevents the memory impairment
60 pontaneous glutamate release at rat cultured hippocampal synapses, and that R-type channels have a fa
61 acking individual VDCCs revealed that within hippocampal synapses, approximately 60% of VDCCs are mob
62                               During stress, hippocampal synapses are bathed in a mixture of stress-r
63 pagation and glutamate release at excitatory hippocampal synapses are directly modulated by Kv1 chann
64                 Thus, glutamate receptors at hippocampal synapses are not generally saturated by quan
65             To determine the extent to which hippocampal synapses are typical of those found in other
66  (LTP) and depression (LTD) at glutamatergic hippocampal synapses are well characterized examples of
67 ate active zones and enhance P at inhibitory hippocampal synapses, but ELKS functions at excitatory s
68 ies have implicated this mechanism in PTP at hippocampal synapses, but the results are controversial.
69 in, we found that CP-AMPARs are recruited to hippocampal synapses by anchored PKA during LTD inductio
70 e of vesicle pool organization at developing hippocampal synapses by monitoring vesicle recycling and
71                              The strength of hippocampal synapses can be persistently increased by si
72 ponents, the properties of STP in excitatory hippocampal synapses change dramatically with temperatur
73 ptic efficacy, pathological levels of CRH at hippocampal synapses contribute to neuronal death.
74 ly releasable pool of synaptic vesicles at a hippocampal synapse, corresponding to about two dozen qu
75   In response to moderate 10 Hz stimulation, hippocampal synapses depressed less compared with neocor
76                                              Hippocampal synapses display a range of release probabil
77 ght derive from their differential impact on hippocampal synapses, distinguishing dorsal and ventral
78 amined whether this redistribution occurs at hippocampal synapses during LTP.
79 to test whether LTP-related changes occur in hippocampal synapses during unsupervised learning.
80            Long-term potentiation at CA3-CA1 hippocampal synapses exhibits an early phase and a late
81                                 Induction of hippocampal synapse formation by androgen is not mediate
82 e distribution of nectin-1 and afadin during hippocampal synapse formation using cultured primary hip
83 components to synaptic sites is critical for hippocampal synapse formation.
84 in the readily releasable pool at excitatory hippocampal synapses has recently been identified as a m
85 variability of mean SV size among excitatory hippocampal synapses -- if actively regulated -- is a po
86 ther P/Q- or N-type channel function at this hippocampal synapse, implicating rescue of presynaptic C
87 ong-term potentiation at the mossy fiber-CA3 hippocampal synapse in vivo in anesthetized rats.
88              Long-term potentiation (LTP) of hippocampal synapses in adult rats was reversed as rats
89                                         When hippocampal synapses in culture are pharmacologically si
90 the readily releasable pool at glutamatergic hippocampal synapses in culture through a protein kinase
91                       Here, we permeabilized hippocampal synapses in culture, manipulated their inter
92                                           At hippocampal synapses in culture, two modes of synaptic v
93 es, neurotransmitter release still occurs at hippocampal synapses in culture.
94 sis of vesicles docked to the active zone of hippocampal synapses in culture.
95  Xenopus neuromuscular junctions and for rat hippocampal synapses in culture; the exocytosis of exoge
96 activity, but shifts long-term plasticity of hippocampal synapses in favor of LTD.
97 rked presynaptic abnormalities at excitatory hippocampal synapses in Fmr1 knock-out (KO) mice leading
98 nctional synaptic plasticity, is impaired at hippocampal synapses in the Fmr1-knock-out (KO) mouse mo
99 lieved to maintain long term potentiation at hippocampal synapses in vitro.
100 and postsynaptic compartments in a subset of hippocampal synapses in vivo, and this coordination is c
101              Here, we report that at CA3-CA1 hippocampal synapses, individual potentiation and depres
102                                           At hippocampal synapses, induction of long term potentiatio
103 ts suggest that long-lasting potentiation at hippocampal synapses involves the rapid formation of clu
104 endent plasticity at mossy fiber-interneuron hippocampal synapses is impaired.
105              Long-term potentiation (LTP) at hippocampal synapses is thought to involve the insertion
106                                           At hippocampal synapses, large, multiquantal IPSCs were inh
107                                           At hippocampal synapses, long-term potentiation and long-te
108 either 12 or 16 months of age fully reverses hippocampal synapse loss and completely rescues preexist
109                                  Remarkably, hippocampal synapse loss and impaired synaptic function
110  complexity of hippocampal dendritic arbors, hippocampal synapse loss, impaired hippocampus-dependent
111  tested the prediction that the lifetimes of hippocampal synapses match the longevity of hippocampal
112 mate released at approximately two-thirds of hippocampal synapses might diffuse to other synapses, un
113 esence of astrocytic processes at particular hippocampal synapses might signal which ones are releasi
114 gical studies at several synapses, including hippocampal synapses, neuromuscular junctions and retina
115 ent endocytosis at the conventional cultured hippocampal synapse of rats and mice.
116                      Staurosporine, which at hippocampal synapses partially inhibits unloading of FM1
117 rage, there has been no direct evidence that hippocampal synapses persist for time intervals commensu
118                            Here we show that hippocampal synapses potentiate robustly in response to
119                                     Although hippocampal synapses provide as a good model system for
120 PA/NMDA ratio is decreased at MHCI-deficient hippocampal synapses, reflecting an increase in NMDAR-me
121 n during long-term potentiation (LTP) at CA1 hippocampal synapses remain elusive.
122 tch in NR2 subunit composition at developing hippocampal synapses requires CK2 activity.
123      Moreover, 7,8-DHF inhibited the loss of hippocampal synapses, restored synapse number and synapt
124 ntly have increased levels of gamma-actin at hippocampal synapses, resulting in higher spine densitie
125          Electron microscopic examination of hippocampal synapses revealed a striking selective defic
126 lusion that mossy fiber LTP and LTP at other hippocampal synapses share a common induction mechanism
127              Ultrastructural analysis of CA1 hippocampal synapses showed a significantly lower number
128     In electron micrographs of permeabilized hippocampal synapses stimulated with 1 microm Ca2+, we c
129                                In excitatory hippocampal synapses, STP serves as a high-pass filter o
130                                         Thus hippocampal synapses take advantage of efficient mechani
131 bpopulation of "immature" high-Pr, GluN2B(+) hippocampal synapses that are maintained throughout late
132 me 12-lipoxygenase (12-LO) in LTP at CA3-CA1 hippocampal synapses that is dependent on the pattern of
133 nts reveal a novel type of plasticity at CA1 hippocampal synapses that is expressed by the activation
134           The presence of Syt2 in inhibitory hippocampal synapses, the altered distribution of Gad67
135 mechanism for release heterogeneity at small hippocampal synapses, the inter-synaptic variation of th
136 suggest that the decreased responsiveness of hippocampal synapses to estrogen in aged animals may res
137 his effect was due to an enhanced ability of hippocampal synapses to respond to tetanic stimulation,
138                                           At hippocampal synapses, two modes of synaptic vesicle exoc
139 ately 27 nm localization precision at single hippocampal synapses under physiological conditions.
140 rgistic actions of corticosterone and CRH at hippocampal synapses underlie memory impairments after c
141    This has been explained by tagging of the hippocampal synapses used in extinction, followed by cap
142               Therefore, during stimulation, hippocampal synapses used more vesicles from the reserve
143 . re-examine the mechanism of endocytosis at hippocampal synapses using a new optical reporter, sypHy
144 aptors are required for vesicle retrieval at hippocampal synapses using a targeted RNAi screen couple
145  vesicle pool sizes across a large number of hippocampal synapses using FM 1-43 and confocal fluoresc
146 endocytic processing of synaptic vesicles at hippocampal synapses, using synaptobrevin/vesicle-associ
147                These results suggest that in hippocampal synapses, vesicle mobilization and replenish
148  at a conventional synapse, the rat cultured hippocampal synapse, we found that SNAP25 is involved in
149  XIX is required for the normal formation of hippocampal synapses, we examined synaptic morphology an
150 -stained vesicles and electron microscopy of hippocampal synapses, we find evidence that the populati
151 he origin of spontaneously fused vesicles in hippocampal synapses, we tagged vesicles with fluorescen
152  local distribution of endocytic proteins at hippocampal synapses, which could in turn affect express
153  principles of functional vesicles at native hippocampal synapses with nanoscale resolution using flu
154 easing hormone (CRH) permeate memory-forming hippocampal synapses, yet it is unknown whether (and how

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