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1 Schaffer collateral axons form excitatory synapses that
2 Schaffer collateral synapses on CA2 neurons are distinct
3 Schaffer collateral-CA1 tetanic long-term potentiation d
4 Schaffer-collateral long-term potentiation (LTP) was imp
5 y ramifying in the pyramidal cell layer; (2) Schaffer collateral/commissural pathway-associated inter
6 whenever tested (n = 5; 1 basket cell and 4 Schaffer-associated interneurons), were abolished by the
7 we measure this replenishment rate at active Schaffer collateral terminals by determining the maximum
8 ed transcripts in rat hippocampus 3 hr after Schaffer-CA1 LTP induction in vivo, we identified a neur
10 ium to block synaptic transmission, allowing Schaffer-collateral axon fiber volleys to be recorded fr
11 path-dentate gyrus granule cell, CA3-CA3 and Schaffer collateral-CA1 synapses without effects at moss
12 of anterior piriform (olfactory) cortex, and Schaffer-commissural synapses were studied in slices of
13 d activation of entorhinal cortical (EC) and Schaffer collateral (SC) inputs to hippocampal CA1 pyram
16 e dendrites were unlabeled, mossy fibers and Schaffer collaterals in the hippocampal formation, baske
18 n excitatory inputs, the perforant path, and Schaffer collaterals during theta and non-theta behavior
19 at the CA3 recurrent collateral synapses and Schaffer collateral-CA1 synapses, but not at the mossy f
20 terneuron, the so-called 'basket cells' and 'Schaffer collateral-associated' cells, which innervate s
23 (AMPA)-type glutamate receptors (AMPARs) at Schaffer collateral to CA1 synapses in postischemic hipp
24 nylglycine (DHPG) was markedly attenuated at Schaffer collateral-CA1 synapses of mice lacking caveoli
31 ly disrupted, revealing hyperexcitability at Schaffer collateral-CA1 synapses and depression of mossy
32 nd chemically induced NMDAR-dependent LTD at Schaffer collateral synapses but did not affect potentia
34 GluR-dependent long-term depression (LTD) at Schaffer collateral to CA1 pyramidal synapses of the hip
35 erm depression of synaptic strength (LTD) at Schaffer collateral-CA1, commissural/associational-CA3 a
36 lectively required for those forms of LTP at Schaffer collateral synapses that recruit a presynaptic
38 show normal synaptic transmission and LTP at Schaffer collateral-CA1 synapses, and have no deficits i
39 idylinositol 3-kinase (PI3-kinase) in LTP at Schaffer collateral/commissural fiber-CA1 synapses in ra
40 aCaMKII is essential for induction of LTP at Schaffer commissural-CA1 synapses in vivo, but is not re
41 equent threshold for the induction of LTP at Schaffer-commissural synapses through a reduction in the
42 mpal slices, long-term potentiation (LTP) at Schaffer collateral fiber synapses onto CA1 pyramidal ce
44 we show that long-term potentiation (LTP) at Schaffer collateral-CA1 synapses is greatly enhanced in
45 late-phase long-term potentiation (L-LTP) at Schaffer collateral/commissural fiber-CA1 synapses in ra
46 of synaptic transmission was not observed at Schaffer collateral-CA1 synapses, while the submaximal t
47 rences in short- and long-term plasticity at Schaffer collateral (SC) synapses in the dorsal and vent
48 on activity-dependent synaptic plasticity at Schaffer collateral and perforant path synapses in the h
49 ates the induction of synaptic plasticity at Schaffer collateral synapses and hippocampal-dependent l
50 arget cell-specific short-term plasticity at Schaffer collateral synapses in which the activation of
51 II mGlu receptors to synaptic plasticity at Schaffer collateral-CA1 synapses in acute slices of adul
53 f excitatory postsynaptic field potential at Schaffer collateral/commissural fiber-CA1 synapses showe
55 anced induction of long term potentiation at Schaffer-collateral synapses in area CA1 of the hippocam
56 y visualize presynaptic vesicular release at Schaffer collateral-CA1 excitatory synapses in hippocamp
57 ing up the majority of glutamate released at Schaffer collateral-commissural synapses in the hippocam
58 r a potential aspartate-mediated response at Schaffer collateral synapses in organotypic hippocampal
59 the rapidly recycling vesicle pool (RRP) at Schaffer collateral terminals in field CA1 of rat hippoc
60 ansmission and spine density specifically at Schaffer collateral synapses in the stratum radiatum (SR
62 m potentiation (LTP) of synaptic strength at Schaffer collateral synapses has largely been attributed
63 erm depression (LTD) of synaptic strength at Schaffer collateral-CA1 synapses by simultaneously eleva
66 eurons, deficits in synaptic transmission at Schaffer collateral synapses, and blunted plasticity and
67 n the strength of excitatory transmission at Schaffer collateral-CA1 cell synapses of the hippocampus
70 ave been shown to potentiate transmission at Schaffer collateral-commissural synapses on CA1 pyramida
73 ase across a range of Pr at synapses between Schaffer collaterals (SCs) and CA1 pyramidal cells in ac
74 amatergic or GABA-ergic transmission between Schaffer collaterals and CA1 neurons in rat hippocampal
75 cilitated glutamatergic transmission between Schaffer collaterals and CA1 neurons indicated that in a
76 c currents, evoked in CA1 principal cells by Schaffer collateral stimulation, were detected in hippoc
77 amate receptor (mGluR) stimulation either by Schaffer collateral input to CA1 neurones in brain slice
78 duced the amplitude of responses elicited by Schaffer collateral stimulation, without influencing mem
79 inhibits the population spike (PS) evoked by Schaffer collateral stimulation in hippocampal slices.
81 release properties of zinc-positive CA3-CA1 Schaffer collateral/commissural synapses in the stratum
84 esponding to the gamma-paced CA3 output (CA1 Schaffer potentials) and CA3 somatic inhibition within a
87 We provide the first evidence of novel CA3 Schaffer collateral projection to the entorhinal cortex.
88 cture of a single presynaptic input, the CA3 Schaffer pathway, and its contribution to the spontaneou
89 nerated mainly by the entorhinal input, CA3 (Schaffer) collaterals, and voltage-dependent Ca(2+) curr
90 amidal cells and interneurons, the so-called Schaffer-driven spikes, revealing the presynaptic origin
93 ds preceding the seizure without bursts (cut Schaffer collateral tract) and in comparison with bursts
94 in CA3 pyramidal neurons and its efferents - Schaffer collateral, which causes the depolarization, ac
96 induction of inflammation revealed enhanced Schaffer collateral-induced excitatory field potentials
98 denosine receptors at neighboring excitatory Schaffer collateral terminals, which could counteract ef
100 To counteract this amplitude filtering, Schaffer collateral synapses onto CA1 pyramidal cells co
101 h axons ramifying in the SO and SR; all five Schaffer-associated cells whose axons ramified extensive
102 amidal neurones revealed that high frequency Schaffer collateral stimulation resulted in a prolonged
104 have measured evoked glutamate release from Schaffer collateral/commissural fiber terminals in CA1 b
107 torhinal perforant path (PP) and hippocampal Schaffer collateral (SC) inputs to CA1 pyramidal cells s
111 and neurotransmitter release at hippocampal Schaffer collateral synapses in both tottering (tg, alph
112 long-term potentiation (LTP) at hippocampal Schaffer collateral-->CA1 synapses in an activity- and t
114 ssion and synaptic plasticity at hippocampal Schaffer collateral-CA1 synapses in adult and juvenile m
119 egulating synaptic plasticity at hippocampal Schaffer collateral-cornu ammonis 1 (SC-CA1) synapses ha
120 ding NMDAR-mediated responses at hippocampal Schaffer collaterals (SC)-CA1 and medial perforant path-
121 contrast, we show that at mature hippocampal Schaffer collateral synapses the magnitudes of Ca2+ tran
122 oach, induced different types of hippocampal Schaffer collateral (SC) to CA1 synaptic plasticity, dep
123 paired cAMP-dependent LTP in the hippocampal Schaffer collateral pathway induced by either forskolin
124 Using a computer model of the hippocampal Schaffer collateral pathway that incorporates evidence f
126 n the functional dynamics of the hippocampal Schaffer collateral synapse by using data-driven nonpara
131 ked in CA1 minislices by sub-threshold 35 Hz Schaffer collateral stimulation that activated fast-spik
132 ombine optogenetic stimulation of identified Schaffer collateral axons with two-photon imaging of pos
136 ium Green AM to measure Ca(2+) transients in Schaffer collateral presynaptic terminals simultaneously
139 In contrast, AMPAR-mediated input at local Schaffer-collateral synapses on neurogliaform cells rema
140 ippocampus of symptomatic Mecp2(308/Y) mice, Schaffer-collateral synapses exhibited enhanced basal sy
141 n, whereas the release of NPY that modulates Schaffer collateral synapses requires integration of bot
143 iated excitation at TA-CA1 synapses, but not Schaffer collateral-CA1 synapses, after CUS, with a corr
146 rons depends on the coincident activation of Schaffer collateral and temporoammonic inputs at the dis
147 utamate released by repetitive activation of Schaffer collaterals activates group I metabotropic glut
148 t can be facilitated by modest activation of Schaffer-collateral synapses in the upper apical dendrit
149 odependent mechanism involving activation of Schaffer-specific NMDA receptors and presynaptic inhibit
153 dendrites that receive a uniform density of Schaffer collateral input (approximately 100-250 microme
154 tial strength and the short-term dynamics of Schaffer collateral excitatory synapses are regulated by
155 stigate in detail the short-term dynamics of Schaffer collateral excitatory synapses onto CA1 stratum
156 of estradiol on the functional integrity of Schaffer collateral to CA1 (Sch-CA1) pyramidal cell syna
157 B, we measured long-term depression (LTD) of Schaffer-collateral synapses in the hippocampus of c-Rel
158 c deletion of TRPA1 channels affected LTP of Schaffer collateral to CA1 pyramidal neuron synapses.
159 induction of long-term potentiation (LTP) of Schaffer collateral inputs to hippocampal CA1 pyramidal
160 CRS reduced long-term potentiation (LTP) of Schaffer collateral/commisural-CA1 pathway, phospho-alph
161 bserved that stress reduced the magnitude of Schaffer collateral/commissural-Cornu Ammonis field 1 lo
162 tion (LTP) induced by theta-burst pairing of Schaffer collateral inputs and postsynaptic firing is as
163 est that the proline-induced potentiation of Schaffer collateral-commissural synaptic transmission pr
164 on markedly impairs synaptic potentiation of Schaffer collaterals and commissural inputs to the CA1 a
166 in the fundamental presynaptic properties of Schaffer collateral synapses that could account for dist
167 Prolonged 1 Hz stimulation (900 pulses) of Schaffer collaterals, which normally depresses CA3/CA1 s
168 Eliprodil markedly improved the recovery of Schaffer collateral-CA1 excitatory postsynaptic potentia
169 slices, we find that short trains (2-3 s) of Schaffer collateral fiber stimulation delivered at 5 Hz
170 production of distance-dependent scaling of Schaffer collateral synapses is an elevated postsynaptic
174 TP elicited by either tetanic stimulation of Schaffer collaterals or a pairing protocol, and persiste
175 LTP) evoked by high-frequency stimulation of Schaffer collaterals, and that CN2097 attenuates this LT
181 eduction of O-GlcNAc levels had no effect on Schaffer collateral CA1 basal hippocampal synaptic trans
182 the amygdala and examining stress effects on Schaffer collateral/commissural-CA1 LTP and spatial memo
184 WT mice, but not in Prnp(0/0) mice, pairing Schaffer collateral stimulation with depolarization of C
185 either concentration of proline potentiated Schaffer collateral-commissural synaptic transmission.
187 ices in which the cell bodies of presynaptic Schaffer collateral/commissural fibres are removed.
188 (basket cells) or dendritically projecting (Schaffer collateral-associated cells) interneurons and p
189 s long-term potentiation at the CA1 proximal Schaffer collateral synapses when the two inputs are pai
195 theta cycle interval by proximally targeted Schaffer collateral activity, temporoammonic EPSPs propa
197 eurons containing somatostatin, we show that Schaffer collateral synapses onto the EGFP-expressing so
199 in two separate afferent pathways among the Schaffer collaterals during intracellular recording of C
201 LTP in mossy fiber (MF)-CA3 pathway and the Schaffer collateral/commissural (SC)-CA1 pathway differ
202 t path (PP) of the entorhinal cortex and the Schaffer collaterals (SCs) from individual CA3 pyramidal
203 ly mGlu7 is expressed presynaptically at the Schaffer collateral (SC)-CA1 synapse in the hippocampus
204 forms of long-term potentiation (LTP) at the Schaffer collateral CA1 synapse require stimulation of b
205 receptors modulate synaptic function at the Schaffer collateral input to CA1 pyramidal cells, thereb
208 ng-term synaptic potentiation (L-LTP) at the Schaffer collateral synapse of the hippocampus is an exp
209 activity induces synaptic plasticity at the Schaffer collateral synapse onto CA1 pyramidal neurones.
210 tential diversity of nAChR influences at the Schaffer collateral synapse onto CA1 pyramidal neurons.
215 iation (LTP) of synaptic transmission at the Schaffer collateral-CA1 synapse in the hippocampus is su
217 e to block agonist-mediated responses at the Schaffer collateral-CA1 synapse, a location at which neu
220 z/1 s) in control slices elicited LTP at the Schaffer collateral-CA1 synapses, but neither LTP nor LT
223 otentiation of long-term potentiation at the Schaffer collateral/cornu ammonis 1 synapse in the dorsa
224 synaptic plasticity was investigated at the Schaffer-collateral-CA1 pyramidal cell synapse of mouse
225 ctionally important interactions between the Schaffer collateral and perforant pathways have been hyp
226 he efficacy of neurotransmission between the Schaffer collateral-CA1 pathway in the rat transverse hi
228 gh CA3 pyramidal cells give rise to both the Schaffer collateral fiber synapses in CA1 and the assoc-
229 opment, basic synaptic transmission from the Schaffer collateral pathway to CA1 pyramidal neurons rem
230 P16-CREB, enhanced in vivo LTP evoked in the Schaffer collateral pathway and caused significant chang
233 rine) on input-output (I-O) relations in the Schaffer collateral pathway to CA1 (SC-CA1) and mossy fi
234 y-phase LTP to late-phase LTP (L-LTP) in the Schaffer collateral pathway, likely as a result of incre
235 ircuit-specific and were not observed in the Schaffer collateral pathway-associated inhibitory synaps
236 circuit-specific and are not observed in the Schaffer collateral pathway-associated inhibitory synaps
241 d that deletion of Cdc42 impaired LTP in the Schaffer collateral synapses and postsynaptic structural
242 be related to impairment of the E-LTP in the Schaffer collateral synapses but not of that of the perf
244 erm potentiation (LTP) can be induced in the Schaffer collateral-->CA1 synapse of hippocampus by stim
245 sion and long-term potentiation (LTP) in the Schaffer Collateral-CA1 and the mossy fiber-CA3 pathways
246 as enhanced paired-pulse facilitation in the Schaffer Collateral-CA1 glutamatergic synapses of the cb
247 implanted with stimulating electrodes in the Schaffer collaterals and with recording electrodes in th
248 gh and low levels of nAChR activation in the Schaffer collaterals inhibit and facilitate, respectivel
250 at hippocampal long-term potentiation in the Schaffer collaterals was identical in homozygous, hetero
251 very different time-varying responses in the Schaffer-commissural projections than in the lateral per
254 Here we show that tetanic stimulation of the Schaffer collateral pathway causes an increase in the co
255 We suggest that tetanic stimulation of the Schaffer collateral pathway may induce new synthesis of
262 h that under intact pharmacology, LTP of the Schaffer collateral to CA1 pyramidal neuron synapses wil
263 Through electrophysiological analysis of the Schaffer collateral-CA1 synapse in dorsal hippocampus, w
265 egion of the hippocampus, stimulation of the Schaffer collaterals elicits an alkaline pH(e) transient
266 We found that orthodromic stimulation of the Schaffer collaterals for 10 min reduces the amplitude of
268 SCs) evoked by electrical stimulation of the Schaffer collaterals in CA1 hippocampal pyramidal cells.
269 ease during low-frequency stimulation of the Schaffer collaterals were altered in scrapie-infected mi
270 in hippocampal slices by stimulation of the Schaffer collaterals, an excitatory fibre tract that pro
277 was tested with use of one such pathway, the Schaffer collateral-commissural projection to CA1 pyrami
278 were determined in acute brain sections; the Schaffer collateral pathway was stimulated and the field
280 CA or sham-operated rats by stimulating the Schaffer collaterals and recording in the CA1 pyramidal
283 ected animals after 5 months showed that the Schaffer collateral-evoked EPSP was attenuated, the effe
284 of the normal CA3 outflow tract through the Schaffer collaterals are well known, their aberrant reor
285 tion of various stimulation protocols to the Schaffer collateral/commissural projections in freely mo
286 paired-pulse stimulation was applied to the Schaffer collaterals and population spikes were monitore
288 nged in epileptic animals, and input via the Schaffer collaterals is actually decreased despite reduc
293 atio onto CA1 pyramidal cells in response to Schaffer collateral stimulation in slices from young adu
295 udies revealed that the amplitude of unitary Schaffer collateral inputs increases with distance from
297 mission and plasticity at dorsal and ventral Schaffer collateral (SC) synapses in the mouse hippocamp
298 e reported conflicting results as to whether Schaffer collateral axons have target-cell specific shor
299 ine (10 microM) enhanced NMDAR currents with Schaffer collateral stimulation in WT mice but not HZ mi
300 g of back-propagating action potentials with Schaffer collateral EPSPs was accompanied by an overall
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