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1 forming synapses with the impinging axons of Schaffer collateral.
2 tential-evoked [Ca(2+)](i) in the boutons of Schaffer collaterals.
3 mostly representing excitatory terminals of Schaffer collaterals.
4 approximately 80% of the synaptic input from Schaffer collaterals.
5 sociated with the axons and terminals of the Schaffer collaterals.
6 re also evident after tetanic stimulation of Schaffer collaterals.
7 rea CA1 following tetanic stimulation of the Schaffer collaterals.
8 tion spike by orthodromic stimulation of the Schaffer collaterals.
9 ippocampus in response to stimulation of the Schaffer collaterals.
10 in response to electrical stimulation of the Schaffer collaterals.
12 utamate released by repetitive activation of Schaffer collaterals activates group I metabotropic glut
13 theta cycle interval by proximally targeted Schaffer collateral activity, temporoammonic EPSPs propa
15 in hippocampal slices by stimulation of the Schaffer collaterals, an excitatory fibre tract that pro
16 on activity-dependent synaptic plasticity at Schaffer collateral and perforant path synapses in the h
17 ctionally important interactions between the Schaffer collateral and perforant pathways have been hyp
19 rons depends on the coincident activation of Schaffer collateral and temporoammonic inputs at the dis
21 amatergic or GABA-ergic transmission between Schaffer collaterals and CA1 neurons in rat hippocampal
22 cilitated glutamatergic transmission between Schaffer collaterals and CA1 neurons indicated that in a
23 on markedly impairs synaptic potentiation of Schaffer collaterals and commissural inputs to the CA1 a
25 paired-pulse stimulation was applied to the Schaffer collaterals and population spikes were monitore
26 CA or sham-operated rats by stimulating the Schaffer collaterals and recording in the CA1 pyramidal
27 implanted with stimulating electrodes in the Schaffer collaterals and with recording electrodes in th
28 LTP) evoked by high-frequency stimulation of Schaffer collaterals, and that CN2097 attenuates this LT
29 nerated mainly by the entorhinal input, CA3 (Schaffer) collaterals, and voltage-dependent Ca(2+) curr
30 of the normal CA3 outflow tract through the Schaffer collaterals are well known, their aberrant reor
31 (basket cells) or dendritically projecting (Schaffer collateral-associated cells) interneurons and p
34 terneuron, the so-called 'basket cells' and 'Schaffer collateral-associated' cells, which innervate s
35 ium to block synaptic transmission, allowing Schaffer-collateral axon fiber volleys to be recorded fr
38 e reported conflicting results as to whether Schaffer collateral axons have target-cell specific shor
39 ombine optogenetic stimulation of identified Schaffer collateral axons with two-photon imaging of pos
40 eduction of O-GlcNAc levels had no effect on Schaffer collateral CA1 basal hippocampal synaptic trans
41 forms of long-term potentiation (LTP) at the Schaffer collateral CA1 synapse require stimulation of b
43 sion and long-term potentiation (LTP) in the Schaffer Collateral-CA1 and the mossy fiber-CA3 pathways
44 n the strength of excitatory transmission at Schaffer collateral-CA1 cell synapses of the hippocampus
45 Eliprodil markedly improved the recovery of Schaffer collateral-CA1 excitatory postsynaptic potentia
46 y visualize presynaptic vesicular release at Schaffer collateral-CA1 excitatory synapses in hippocamp
47 as enhanced paired-pulse facilitation in the Schaffer Collateral-CA1 glutamatergic synapses of the cb
50 he efficacy of neurotransmission between the Schaffer collateral-CA1 pathway in the rat transverse hi
53 Through electrophysiological analysis of the Schaffer collateral-CA1 synapse in dorsal hippocampus, w
55 iation (LTP) of synaptic transmission at the Schaffer collateral-CA1 synapse in the hippocampus is su
57 e to block agonist-mediated responses at the Schaffer collateral-CA1 synapse, a location at which neu
61 ly disrupted, revealing hyperexcitability at Schaffer collateral-CA1 synapses and depression of mossy
62 tance of CC2D1A in the maintenance of LTP at Schaffer collateral-CA1 synapses and the formation of hi
63 erm depression (LTD) of synaptic strength at Schaffer collateral-CA1 synapses by simultaneously eleva
64 II mGlu receptors to synaptic plasticity at Schaffer collateral-CA1 synapses in acute slices of adul
65 ssion and synaptic plasticity at hippocampal Schaffer collateral-CA1 synapses in adult and juvenile m
66 red the function of SNAP-25a and SNAP-25b at Schaffer collateral-CA1 synapses in hippocampus using 4-
70 we show that long-term potentiation (LTP) at Schaffer collateral-CA1 synapses is greatly enhanced in
71 nylglycine (DHPG) was markedly attenuated at Schaffer collateral-CA1 synapses of mice lacking caveoli
73 path-dentate gyrus granule cell, CA3-CA3 and Schaffer collateral-CA1 synapses without effects at moss
74 iated excitation at TA-CA1 synapses, but not Schaffer collateral-CA1 synapses, after CUS, with a corr
75 show normal synaptic transmission and LTP at Schaffer collateral-CA1 synapses, and have no deficits i
76 z/1 s) in control slices elicited LTP at the Schaffer collateral-CA1 synapses, but neither LTP nor LT
77 at the CA3 recurrent collateral synapses and Schaffer collateral-CA1 synapses, but not at the mossy f
78 ion and the isolated NMDAR potentials at the Schaffer collateral-CA1 synapses, but without affecting
80 of synaptic transmission was not observed at Schaffer collateral-CA1 synapses, while the submaximal t
93 erm depression of synaptic strength (LTD) at Schaffer collateral-CA1, commissural/associational-CA3 a
95 synaptic plasticity was investigated at the Schaffer-collateral-CA1 pyramidal cell synapse of mouse
99 was tested with use of one such pathway, the Schaffer collateral-commissural projection to CA1 pyrami
101 ing up the majority of glutamate released at Schaffer collateral-commissural synapses in the hippocam
102 ave been shown to potentiate transmission at Schaffer collateral-commissural synapses on CA1 pyramida
104 est that the proline-induced potentiation of Schaffer collateral-commissural synaptic transmission pr
105 either concentration of proline potentiated Schaffer collateral-commissural synaptic transmission.
106 LTP in mossy fiber (MF)-CA3 pathway and the Schaffer collateral/commissural (SC)-CA1 pathway differ
107 have measured evoked glutamate release from Schaffer collateral/commissural fiber terminals in CA1 b
108 late-phase long-term potentiation (L-LTP) at Schaffer collateral/commissural fiber-CA1 synapses in ra
109 idylinositol 3-kinase (PI3-kinase) in LTP at Schaffer collateral/commissural fiber-CA1 synapses in ra
110 f excitatory postsynaptic field potential at Schaffer collateral/commissural fiber-CA1 synapses showe
113 ices in which the cell bodies of presynaptic Schaffer collateral/commissural fibres are removed.
115 y ramifying in the pyramidal cell layer; (2) Schaffer collateral/commissural pathway-associated inter
116 tion of various stimulation protocols to the Schaffer collateral/commissural projections in freely mo
117 release properties of zinc-positive CA3-CA1 Schaffer collateral/commissural synapses in the stratum
118 the amygdala and examining stress effects on Schaffer collateral/commissural-CA1 LTP and spatial memo
120 bserved that stress reduced the magnitude of Schaffer collateral/commissural-Cornu Ammonis field 1 lo
121 Hz) was delivered to one of two independent Schaffer-collateral/commissural projections, while the s
122 CRS reduced long-term potentiation (LTP) of Schaffer collateral/commisural-CA1 pathway, phospho-alph
123 egulating synaptic plasticity at hippocampal Schaffer collateral-cornu ammonis 1 (SC-CA1) synapses ha
124 otentiation of long-term potentiation at the Schaffer collateral/cornu ammonis 1 synapse in the dorsa
125 in two separate afferent pathways among the Schaffer collaterals during intracellular recording of C
126 n excitatory inputs, the perforant path, and Schaffer collaterals during theta and non-theta behavior
128 egion of the hippocampus, stimulation of the Schaffer collaterals elicits an alkaline pH(e) transient
129 g of back-propagating action potentials with Schaffer collateral EPSPs was accompanied by an overall
130 ected animals after 5 months showed that the Schaffer collateral-evoked EPSP was attenuated, the effe
131 tial strength and the short-term dynamics of Schaffer collateral excitatory synapses are regulated by
132 stigate in detail the short-term dynamics of Schaffer collateral excitatory synapses onto CA1 stratum
134 slices, we find that short trains (2-3 s) of Schaffer collateral fiber stimulation delivered at 5 Hz
135 gh CA3 pyramidal cells give rise to both the Schaffer collateral fiber synapses in CA1 and the assoc-
136 Glutamate spillover is observed between Schaffer collateral fiber synapses onto CA1 pyramidal ce
137 mpal slices, long-term potentiation (LTP) at Schaffer collateral fiber synapses onto CA1 pyramidal ce
139 We found that orthodromic stimulation of the Schaffer collaterals for 10 min reduces the amplitude of
141 tate gyrus as well as decremental LTP at the Schaffer collateral-->CA1 pyramidal cell synapse.
142 erm potentiation (LTP) can be induced in the Schaffer collateral-->CA1 synapse of hippocampus by stim
144 long-term potentiation (LTP) at hippocampal Schaffer collateral-->CA1 synapses in an activity- and t
145 SCs) evoked by electrical stimulation of the Schaffer collaterals in CA1 hippocampal pyramidal cells.
146 e dendrites were unlabeled, mossy fibers and Schaffer collaterals in the hippocampal formation, baske
147 induction of inflammation revealed enhanced Schaffer collateral-induced excitatory field potentials
148 gh and low levels of nAChR activation in the Schaffer collaterals inhibit and facilitate, respectivel
149 dendrites that receive a uniform density of Schaffer collateral input (approximately 100-250 microme
150 amate receptor (mGluR) stimulation either by Schaffer collateral input to CA1 neurones in brain slice
151 receptors modulate synaptic function at the Schaffer collateral input to CA1 pyramidal cells, thereb
153 tion (LTP) induced by theta-burst pairing of Schaffer collateral inputs and postsynaptic firing is as
154 udies revealed that the amplitude of unitary Schaffer collateral inputs increases with distance from
155 induction of long-term potentiation (LTP) of Schaffer collateral inputs to hippocampal CA1 pyramidal
159 nged in epileptic animals, and input via the Schaffer collaterals is actually decreased despite reduc
163 TP elicited by either tetanic stimulation of Schaffer collaterals or a pairing protocol, and persiste
165 P16-CREB, enhanced in vivo LTP evoked in the Schaffer collateral pathway and caused significant chang
166 Here we show that tetanic stimulation of the Schaffer collateral pathway causes an increase in the co
169 paired cAMP-dependent LTP in the hippocampal Schaffer collateral pathway induced by either forskolin
170 TORC1-mediated late-LTP in SOM-INs regulated Schaffer collateral pathway LTP in pyramidal neurons.
171 We suggest that tetanic stimulation of the Schaffer collateral pathway may induce new synthesis of
172 ction of long-term potentiation (LTP) in the Schaffer collateral pathway of CA1 pyramidal neurons and
173 roscopy revealed that LTP stimulation of the Schaffer collateral pathway promoted MAP2 labeling in sp
176 Using a computer model of the hippocampal Schaffer collateral pathway that incorporates evidence f
177 rine) on input-output (I-O) relations in the Schaffer collateral pathway to CA1 (SC-CA1) and mossy fi
178 opment, basic synaptic transmission from the Schaffer collateral pathway to CA1 pyramidal neurons rem
179 were determined in acute brain sections; the Schaffer collateral pathway was stimulated and the field
180 y-phase LTP to late-phase LTP (L-LTP) in the Schaffer collateral pathway, likely as a result of incre
181 ircuit-specific and were not observed in the Schaffer collateral pathway-associated inhibitory synaps
182 circuit-specific and are not observed in the Schaffer collateral pathway-associated inhibitory synaps
194 ium Green AM to measure Ca(2+) transients in Schaffer collateral presynaptic terminals simultaneously
195 We provide the first evidence of novel CA3 Schaffer collateral projection to the entorhinal cortex.
199 torhinal perforant path (PP) and hippocampal Schaffer collateral (SC) inputs to CA1 pyramidal cells s
200 d activation of entorhinal cortical (EC) and Schaffer collateral (SC) inputs to hippocampal CA1 pyram
202 ly established long-term potentiation in the Schaffer collateral (SC) pathway through complex signali
203 rences in short- and long-term plasticity at Schaffer collateral (SC) synapses in the dorsal and vent
204 mission and plasticity at dorsal and ventral Schaffer collateral (SC) synapses in the mouse hippocamp
208 oach, induced different types of hippocampal Schaffer collateral (SC) to CA1 synaptic plasticity, dep
209 nd persistent potentiation of AMPAR-mediated Schaffer collateral (SC)-CA1 fEPSPs in slices derived fr
210 ly mGlu7 is expressed presynaptically at the Schaffer collateral (SC)-CA1 synapse in the hippocampus
213 ding NMDAR-mediated responses at hippocampal Schaffer collaterals (SC)-CA1 and medial perforant path-
217 ase across a range of Pr at synapses between Schaffer collaterals (SCs) and CA1 pyramidal cells in ac
218 t path (PP) of the entorhinal cortex and the Schaffer collaterals (SCs) from individual CA3 pyramidal
220 inhibits the population spike (PS) evoked by Schaffer collateral stimulation in hippocampal slices.
221 atio onto CA1 pyramidal cells in response to Schaffer collateral stimulation in slices from young adu
222 ine (10 microM) enhanced NMDAR currents with Schaffer collateral stimulation in WT mice but not HZ mi
223 amidal neurones revealed that high frequency Schaffer collateral stimulation resulted in a prolonged
224 ked in CA1 minislices by sub-threshold 35 Hz Schaffer collateral stimulation that activated fast-spik
225 WT mice, but not in Prnp(0/0) mice, pairing Schaffer collateral stimulation with depolarization of C
227 c currents, evoked in CA1 principal cells by Schaffer collateral stimulation, were detected in hippoc
228 duced the amplitude of responses elicited by Schaffer collateral stimulation, without influencing mem
231 n the functional dynamics of the hippocampal Schaffer collateral synapse by using data-driven nonpara
233 ng-term synaptic potentiation (L-LTP) at the Schaffer collateral synapse of the hippocampus is an exp
234 activity induces synaptic plasticity at the Schaffer collateral synapse onto CA1 pyramidal neurones.
235 tential diversity of nAChR influences at the Schaffer collateral synapse onto CA1 pyramidal neurons.
240 ates the induction of synaptic plasticity at Schaffer collateral synapses and hippocampal-dependent l
241 lecular composition between commonly studied Schaffer collateral synapses and perforant path-dentate
242 d that deletion of Cdc42 impaired LTP in the Schaffer collateral synapses and postsynaptic structural
243 nd chemically induced NMDAR-dependent LTD at Schaffer collateral synapses but did not affect potentia
244 be related to impairment of the E-LTP in the Schaffer collateral synapses but not of that of the perf
245 m potentiation (LTP) of synaptic strength at Schaffer collateral synapses has largely been attributed
246 and neurotransmitter release at hippocampal Schaffer collateral synapses in both tottering (tg, alph
247 r a potential aspartate-mediated response at Schaffer collateral synapses in organotypic hippocampal
249 ansmission and spine density specifically at Schaffer collateral synapses in the stratum radiatum (SR
250 arget cell-specific short-term plasticity at Schaffer collateral synapses in which the activation of
251 production of distance-dependent scaling of Schaffer collateral synapses is an elevated postsynaptic
253 To counteract this amplitude filtering, Schaffer collateral synapses onto CA1 pyramidal cells co
255 eurons containing somatostatin, we show that Schaffer collateral synapses onto the EGFP-expressing so
256 n, whereas the release of NPY that modulates Schaffer collateral synapses requires integration of bot
257 in the fundamental presynaptic properties of Schaffer collateral synapses that could account for dist
258 lectively required for those forms of LTP at Schaffer collateral synapses that recruit a presynaptic
259 contrast, we show that at mature hippocampal Schaffer collateral synapses the magnitudes of Ca2+ tran
260 s long-term potentiation at the CA1 proximal Schaffer collateral synapses when the two inputs are pai
261 eurons, deficits in synaptic transmission at Schaffer collateral synapses, and blunted plasticity and
272 ippocampus of symptomatic Mecp2(308/Y) mice, Schaffer-collateral synapses exhibited enhanced basal sy
273 anced induction of long term potentiation at Schaffer-collateral synapses in area CA1 of the hippocam
274 B, we measured long-term depression (LTD) of Schaffer-collateral synapses in the hippocampus of c-Rel
275 t can be facilitated by modest activation of Schaffer-collateral synapses in the upper apical dendrit
276 AMPA-receptor-mediated synaptic responses at Schaffer-collateral synapses monitored in juvenile mice,
277 In contrast, AMPAR-mediated input at local Schaffer-collateral synapses on neurogliaform cells rema
278 ively direct formation of perforant-path and Schaffer-collateral synapses, respectively, to hippocamp
282 we measure this replenishment rate at active Schaffer collateral terminals by determining the maximum
283 the rapidly recycling vesicle pool (RRP) at Schaffer collateral terminals in field CA1 of rat hippoc
284 denosine receptors at neighboring excitatory Schaffer collateral terminals, which could counteract ef
286 of estradiol on the functional integrity of Schaffer collateral to CA1 (Sch-CA1) pyramidal cell syna
288 h that under intact pharmacology, LTP of the Schaffer collateral to CA1 pyramidal neuron synapses wil
289 c deletion of TRPA1 channels affected LTP of Schaffer collateral to CA1 pyramidal neuron synapses.
290 GluR-dependent long-term depression (LTD) at Schaffer collateral to CA1 pyramidal synapses of the hip
291 (AMPA)-type glutamate receptors (AMPARs) at Schaffer collateral to CA1 synapses in postischemic hipp
294 ds preceding the seizure without bursts (cut Schaffer collateral tract) and in comparison with bursts
296 at hippocampal long-term potentiation in the Schaffer collaterals was identical in homozygous, hetero
297 ease during low-frequency stimulation of the Schaffer collaterals were altered in scrapie-infected mi
299 in CA3 pyramidal neurons and its efferents - Schaffer collateral, which causes the depolarization, ac
300 Prolonged 1 Hz stimulation (900 pulses) of Schaffer collaterals, which normally depresses CA3/CA1 s