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1 c distribution of epsin1 and HIP1 in rat CA1 hippocampal synapse.
2 ted from the presynaptic side of the CA3-CA1 hippocampal synapse.
3 needs to be speeded up to supply vesicles at hippocampal synapses.
4 ary subunits, the principal AMPAR complex at hippocampal synapses.
5 ong-term depression (LTD) of transmission at hippocampal synapses.
6  into all-or-none potentiation of individual hippocampal synapses.
7 of long-term potentiation (LTP) at different hippocampal synapses.
8 lity and reuse during synaptic depression at hippocampal synapses.
9 es changes in the number and/or structure of 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 during NMDA-receptor-dependent LTP at mature hippocampal synapses.
19 naptic, processes; this contrasts with other hippocampal synapses.
20 n tomography to capture SV exocytosis in rat hippocampal synapses.
21 ease sites enriched near the center in mouse hippocampal synapses.
22 otein composition and plasticity in isolated hippocampal synapses.
23 ple distinct release sites within individual hippocampal synapses.
24 ptor properties at cortical, amygdaloid, and hippocampal synapses.
25 n important regulator of SV replenishment at hippocampal synapses.
26 ow endocytosis and bulk endocytosis at small hippocampal synapses.
27 late dynamics of SV pool partitioning at rat hippocampal synapses.
28 and normal encoding of information in native hippocampal synapses.
29 ily releasable pool (RRP) stimulation in rat hippocampal synapses.
30 hinning of the postsynaptic density (PSD) at hippocampal synapses.
31 y directly reflects the turnover dynamics of hippocampal synapses.
32 ize matches that of AMPARs and NMDARs in the hippocampal synapses.
33 impairs the efficacy of neurotransmission at hippocampal synapses.
34 tion between presynaptic features of typical hippocampal synapses.
35 eficit in paired pulse facilitation (PPF) at hippocampal synapses.
36 ion of brain networks and in their impact on hippocampal synapses.
37 beta) blocks long-term potentiation (LTP) of hippocampal synapses.
38 essions and correlates strongly with loss of hippocampal synapses.
39 ippocampus and examined them individually in hippocampal synapses.
40 expression and alter NMDAR properties at rat hippocampal synapses.
41 s used to analyze cryo-electron tomograms of hippocampal synapses.
42 or subtypes contribute to EPSCs at wild-type hippocampal synapses.
43 tic model of synaptic dynamics in excitatory hippocampal synapses.
44 egulation of synaptic function in excitatory hippocampal synapses.
45 ocytosis and long-term potentiation (LTP) at hippocampal synapses.
46 r collagen is necessary for the formation of hippocampal synapses.
47 ective OPHN1 signaling impairs SV cycling at hippocampal synapses.
48 t exclusive, mechanism of retrieval in small hippocampal synapses.
49 but not monomers, induce progressive loss of hippocampal synapses.
50  against the occurrence of 'kiss-and-run' in hippocampal synapses.
51 ribution of AP180 and CALM in the developing hippocampal synapses.
52 is a major mechanism of vesicle recycling at hippocampal synapses.
53 dopamine produce input-specific LTP in mouse hippocampal synapses 10 min after they were primed with
54 hermore, the long-term potentiation (LTP) of hippocampal synapses, a widely studied model of memory,
55                                           At hippocampal synapses, activation of group I metabotropic
56 to follow the fate of individual vesicles at hippocampal synapses after exocytosis.
57 of alphaCaMKII and increases GluA1 levels in hippocampal synapses after retrieval of contextual fear
58 urexin alternative splicing, we show that in hippocampal synapses, alternative splicing of presynapti
59 m the existence of multiple reserve pools at hippocampal synapses and a parallel organization that pr
60  tracking of individual synaptic vesicles in hippocampal synapses and advanced motion analysis tools
61 turation in these mice, leading to a loss of hippocampal synapses and dendritic branches by P42.
62  and functionally investigated Arf6-silenced hippocampal synapses and found an activity dependent acc
63 nsient retraction of astrocyte leaflets from hippocampal synapses and increased activation of NMDA re
64 ent regulator of neurotransmitter release at hippocampal synapses and maintains synapses in an optima
65 ibution of VGCCs in the active zone of small hippocampal synapses and revealed that spontaneous VGCCs
66 un is the dominant mode of vesicle fusion at hippocampal synapses and that the prevalence of kiss-and
67 ransmission in a use-dependent manner at rat hippocampal synapses and therefore can be used to interr
68 not induce a net gain in the total number of hippocampal synapses and, hence, a net synaptogenesis.
69 TD) but not long-term potentiation of rodent hippocampal synapses, and during LTD but not long-term f
70  Abeta, prevents and/or reverses the loss of hippocampal synapses, and prevents the memory impairment
71 pontaneous glutamate release at rat cultured hippocampal synapses, and that R-type channels have a fa
72 acking individual VDCCs revealed that within hippocampal synapses, approximately 60% of VDCCs are mob
73                               During stress, hippocampal synapses are bathed in a mixture of stress-r
74 pagation and glutamate release at excitatory hippocampal synapses are directly modulated by Kv1 chann
75                 Thus, glutamate receptors at hippocampal synapses are not generally saturated by quan
76             To determine the extent to which hippocampal synapses are typical of those found in other
77  (LTP) and depression (LTD) at glutamatergic hippocampal synapses are well characterized examples of
78                                 Despite most hippocampal synapses being contacted by an astrocyte, th
79 ate active zones and enhance P at inhibitory hippocampal synapses, but ELKS functions at excitatory s
80 ies have implicated this mechanism in PTP at hippocampal synapses, but the results are controversial.
81 in, we found that CP-AMPARs are recruited to hippocampal synapses by anchored PKA during LTD inductio
82 e of vesicle pool organization at developing hippocampal synapses by monitoring vesicle recycling and
83 Ca(V)2s; however, here we find that at mouse hippocampal synapses, Ca(V)2 clustering and vesicle prim
84                              The strength of hippocampal synapses can be persistently increased by si
85 ponents, the properties of STP in excitatory hippocampal synapses change dramatically with temperatur
86                                              Hippocampal synapse changes were observed in Ex-M-cko mi
87 ptic efficacy, pathological levels of CRH at hippocampal synapses contribute to neuronal death.
88 ly releasable pool of synaptic vesicles at a hippocampal synapse, corresponding to about two dozen qu
89   In response to moderate 10 Hz stimulation, hippocampal synapses depressed less compared with neocor
90 e, complement activation and opsonization of hippocampal synapses directed ongoing microglia-dependen
91                                              Hippocampal synapses display a range of release probabil
92 ght derive from their differential impact on hippocampal synapses, distinguishing dorsal and ventral
93 ere, we demonstrate that at excitatory mouse hippocampal synapses, Doc2alpha is the major Ca(2+) sens
94 to observe changes in astroglial coverage of hippocampal synapses during consolidation of fear memory
95 amined whether this redistribution occurs at hippocampal synapses during LTP.
96 to test whether LTP-related changes occur in hippocampal synapses during unsupervised learning.
97                      Here we show that mouse hippocampal synapses employ this principle to trigger Ca
98            Long-term potentiation at CA3-CA1 hippocampal synapses exhibits an early phase and a late
99                                 We show that hippocampal synapses expressing VGCCs either with exon 4
100                                 Induction of hippocampal synapse formation by androgen is not mediate
101 e distribution of nectin-1 and afadin during hippocampal synapse formation using cultured primary hip
102 components to synaptic sites is critical for hippocampal synapse formation.
103 in the readily releasable pool at excitatory hippocampal synapses has recently been identified as a m
104 variability of mean SV size among excitatory hippocampal synapses -- if actively regulated -- is a po
105 ther P/Q- or N-type channel function at this hippocampal synapse, implicating rescue of presynaptic C
106 ecule necessary to form one specific type of hippocampal synapse in vivo Here, we developed an in vit
107 ong-term potentiation at the mossy fiber-CA3 hippocampal synapse in vivo in anesthetized rats.
108  report that BMAL1 rhythmically localizes to hippocampal synapses in a manner dependent on its phosph
109              Long-term potentiation (LTP) of hippocampal synapses in adult rats was reversed as rats
110                                         When hippocampal synapses in culture are pharmacologically si
111 the readily releasable pool at glutamatergic hippocampal synapses in culture through a protein kinase
112                       Here, we permeabilized hippocampal synapses in culture, manipulated their inter
113                                           At hippocampal synapses in culture, two modes of synaptic v
114 es, neurotransmitter release still occurs at hippocampal synapses in culture.
115 sis of vesicles docked to the active zone of hippocampal synapses in culture.
116  Xenopus neuromuscular junctions and for rat hippocampal synapses in culture; the exocytosis of exoge
117 activity, but shifts long-term plasticity of hippocampal synapses in favor of LTD.
118 rked presynaptic abnormalities at excitatory hippocampal synapses in Fmr1 knock-out (KO) mice leading
119 nctional synaptic plasticity, is impaired at hippocampal synapses in the Fmr1-knock-out (KO) mouse mo
120 lieved to maintain long term potentiation at hippocampal synapses in vitro.
121 and postsynaptic compartments in a subset of hippocampal synapses in vivo, and this coordination is c
122              Here, we report that at CA3-CA1 hippocampal synapses, individual potentiation and depres
123                                           At hippocampal synapses, induction of long term potentiatio
124 ts suggest that long-lasting potentiation at hippocampal synapses involves the rapid formation of clu
125 endent plasticity at mossy fiber-interneuron hippocampal synapses is impaired.
126              Long-term potentiation (LTP) at hippocampal synapses is thought to involve the insertion
127                                           At hippocampal synapses, large, multiquantal IPSCs were inh
128                                           At hippocampal synapses, long-term potentiation and long-te
129 either 12 or 16 months of age fully reverses hippocampal synapse loss and completely rescues preexist
130                                  Remarkably, hippocampal synapse loss and impaired synaptic function
131  complexity of hippocampal dendritic arbors, hippocampal synapse loss, impaired hippocampus-dependent
132 iform cortex, and amygdala, thus attenuating hippocampal synapse loss, neuronal death, neuroinflammat
133  tested the prediction that the lifetimes of hippocampal synapses match the longevity of hippocampal
134 mate released at approximately two-thirds of hippocampal synapses might diffuse to other synapses, un
135 esence of astrocytic processes at particular hippocampal synapses might signal which ones are releasi
136 gical studies at several synapses, including hippocampal synapses, neuromuscular junctions and retina
137 ent endocytosis at the conventional cultured hippocampal synapse of rats and mice.
138                      Staurosporine, which at hippocampal synapses partially inhibits unloading of FM1
139 rage, there has been no direct evidence that hippocampal synapses persist for time intervals commensu
140                            Here we show that hippocampal synapses potentiate robustly in response to
141                                     Although hippocampal synapses provide as a good model system for
142 PA/NMDA ratio is decreased at MHCI-deficient hippocampal synapses, reflecting an increase in NMDAR-me
143 n during long-term potentiation (LTP) at CA1 hippocampal synapses remain elusive.
144  modulation of Ca(V) 2.2 channels at plastic hippocampal synapses remains to be elucidated.
145 tch in NR2 subunit composition at developing hippocampal synapses requires CK2 activity.
146      Moreover, 7,8-DHF inhibited the loss of hippocampal synapses, restored synapse number and synapt
147 e, complement activation and opsonization of hippocampal synapses resulted in synaptic phagocytosis a
148 ntly have increased levels of gamma-actin at hippocampal synapses, resulting in higher spine densitie
149          Electron microscopic examination of hippocampal synapses revealed a striking selective defic
150 on detection of individual release events in hippocampal synapses revealed unprecedented heterogeneit
151 lusion that mossy fiber LTP and LTP at other hippocampal synapses share a common induction mechanism
152              Ultrastructural analysis of CA1 hippocampal synapses showed a significantly lower number
153     In electron micrographs of permeabilized hippocampal synapses stimulated with 1 microm Ca2+, we c
154                                In excitatory hippocampal synapses, STP serves as a high-pass filter o
155                                         Thus hippocampal synapses take advantage of efficient mechani
156 perform distinct nonoverlapping functions at hippocampal synapses that are independently regulated by
157 bpopulation of "immature" high-Pr, GluN2B(+) hippocampal synapses that are maintained throughout late
158 me 12-lipoxygenase (12-LO) in LTP at CA3-CA1 hippocampal synapses that is dependent on the pattern of
159 nts reveal a novel type of plasticity at CA1 hippocampal synapses that is expressed by the activation
160                              Here we show in hippocampal synapses, that binding of presynaptic neurex
161           The presence of Syt2 in inhibitory hippocampal synapses, the altered distribution of Gad67
162 mechanism for release heterogeneity at small hippocampal synapses, the inter-synaptic variation of th
163 suggest that the decreased responsiveness of hippocampal synapses to estrogen in aged animals may res
164 his effect was due to an enhanced ability of hippocampal synapses to respond to tetanic stimulation,
165                                           At hippocampal synapses, two modes of synaptic vesicle exoc
166 ately 27 nm localization precision at single hippocampal synapses under physiological conditions.
167 rgistic actions of corticosterone and CRH at hippocampal synapses underlie memory impairments after c
168    This has been explained by tagging of the hippocampal synapses used in extinction, followed by cap
169               Therefore, during stimulation, hippocampal synapses used more vesicles from the reserve
170 . re-examine the mechanism of endocytosis at hippocampal synapses using a new optical reporter, sypHy
171 aptors are required for vesicle retrieval at hippocampal synapses using a targeted RNAi screen couple
172  vesicle pool sizes across a large number of hippocampal synapses using FM 1-43 and confocal fluoresc
173 endocytic processing of synaptic vesicles at hippocampal synapses, using synaptobrevin/vesicle-associ
174                These results suggest that in hippocampal synapses, vesicle mobilization and replenish
175 nd enhanced short-term facilitation in mouse hippocampal synapses via inhibition of synaptic vesicle
176  at a conventional synapse, the rat cultured hippocampal synapse, we found that SNAP25 is involved in
177  XIX is required for the normal formation of hippocampal synapses, we examined synaptic morphology an
178 -stained vesicles and electron microscopy of hippocampal synapses, we find evidence that the populati
179 ynaptic vesicle exocytosis at cultured mouse hippocampal synapses, we induced single action potential
180  imaging of individual release events in rat hippocampal synapses, we observed two spatially distinct
181 onous and asynchronous release in excitatory hippocampal synapses, we obtained high-resolution profil
182 he origin of spontaneously fused vesicles in hippocampal synapses, we tagged vesicles with fluorescen
183 analysis was done in mice whose cortical and hippocampal synapses were previously measured, revealing
184  local distribution of endocytic proteins at hippocampal synapses, which could in turn affect express
185  principles of functional vesicles at native hippocampal synapses with nanoscale resolution using flu
186 easing hormone (CRH) permeate memory-forming hippocampal synapses, yet it is unknown whether (and how

 
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