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1 ry conductances (i.e. approximately balanced synaptic currents).
2  Ca(2+) permeability and the waveform of the synaptic current.
3  temperature on the decay time constant of a synaptic current.
4 ers under motor neuron endings, and generate synaptic current.
5 c input was followed by a decrease in evoked synaptic current.
6 d a corresponding increase in AMPAR-mediated synaptic current.
7 e the size and the kinetics of the resulting synaptic current.
8 ncy of spontaneous excitatory and inhibitory synaptic currents.
9 re unlikely because Zn(2+) did not block the synaptic currents.
10 l recordings and reductions in NMDA-mediated synaptic currents.
11 in a dramatic acceleration of NMDAR-mediated synaptic currents.
12 5 mM as measured using spontaneous GABAergic synaptic currents.
13  frequency and size of spontaneous miniature synaptic currents.
14 PA glutamate receptor levels, and excitatory synaptic currents.
15 ndent effect on ethanol action in evoked and synaptic currents.
16  defects in activity-dependent regulation of synaptic currents.
17 oducing increased peak-to-peak modulation of synaptic currents.
18 euronal excitability and an increase in NMDA synaptic currents.
19 2 selectively reduced AMPA receptor-mediated synaptic currents.
20 ase without any change in the size of evoked synaptic currents.
21 appreciated, producing saturation effects on synaptic currents.
22  not preclude sensory-induced enhancement of synaptic currents.
23  decreases the strength of evoked excitatory synaptic currents.
24  had reduced inhibitory, but not excitatory, synaptic currents.
25 , leaving only "feedforward" thalamocortical synaptic currents.
26 mulation led to a 67% increase in inhibitory synaptic currents.
27 hroidine had no effect on VTA- or PPN-evoked synaptic currents.
28  AMPA-mediated over NMDA-mediated excitatory synaptic currents.
29 clamp, but had no effects on fast inhibitory synaptic currents.
30 apted despite essentially no gain control in synaptic currents.
31 pleting terminals of GABA slowed glycinergic synaptic currents.
32 at lowers input resistance increases unitary synaptic currents.
33 2+) transients amplify inspiratory-modulated synaptic currents.
34 of the A-type channel subunit Kv4.2 enhances synaptic currents.
35 y regulates spine growth and potentiation of synaptic currents.
36 kely accounting for the changes in miniature synaptic currents.
37 dent long-term depression of NMDA-R-mediated synaptic currents.
38 creases in the frequency of spontaneous mini-synaptic currents.
39 ithout blockade of inhibitory and excitatory synaptic currents.
40 mately 6x) and longer duration of inhibitory synaptic currents.
41 R spines and reduced rectification of MF-PYR synaptic currents.
42 litude and frequency of miniature inhibitory synaptic currents.
43 l model, and its regulation by intrinsic and synaptic currents.
44  in BCs was correlated with rapidly decaying synaptic currents.
45 rdings can be used to forecast modulation of synaptic currents.
46 ntrum through an increase in inhibitory post-synaptic currents.
47 ted a long-lasting increase in GABA-mediated synaptic currents.
48 o IMI responses, we found CCAP modulation of synaptic currents.
49 resent at synapses they contribute little to synaptic currents.
50 etermine both the shape and the amplitude of synaptic currents.
51 o able to prolong artificial excitatory post synaptic currents.
52  are correlated with a decrease in GABAergic synaptic currents.
53                               Integration of synaptic currents across an extensive dendritic tree is
54  receptor pool, as we observe no recovery of synaptic current after MK-801 synaptic blockade and wash
55 prefrontal cortex, miniature excitatory post synaptic current amplitude was slightly reduced, miniatu
56 brain slices revealed only partial rescue of synaptic current amplitude.
57 P-AP coupling because of the decrease in the synaptic current amplitude.
58 ply reduced synaptic release probability and synaptic current amplitude.
59 creasing and increasing miniature excitatory synaptic currents amplitude/frequency, respectively.
60 TP was characterized by measuring inhibitory synaptic current amplitudes in response to repetitive st
61  for a link between Abeta-induced effects on synaptic currents and AD-relevant neuronal network oscil
62 is condition, they receive fewer spontaneous synaptic currents and are more prone to die during the c
63 nd prolonged parallel fiber mGluR1-dependent synaptic currents and calcium signaling.
64 tely increase NMDA receptor (NMDAR)-mediated synaptic currents and decrease AMPA receptor (AMPAR)/NMD
65 , however, had normal spontaneous excitatory synaptic currents and dendritic arbors.
66 s in glutamate transport, glutamate-mediated synaptic currents and dendritic spine morphology.
67 h, before the behavioral phenotype develops, synaptic currents and glutamate release were increased.
68  with a shift toward inward rectification of synaptic currents and increased expression of GluR1, but
69        These results suggest that changes in synaptic currents and intrinsic properties of PCs produc
70           Moreover, spontaneous KAR-mediated synaptic currents and metabotropic KAR signaling were ab
71      Here we describe a method for recording synaptic currents and potentials from identified neurons
72 ipulation is compensated for at the level of synaptic currents and receptive fields (RFs) in the soma
73 enuates GABA(A) receptor-mediated inhibitory synaptic currents and reduces sensitivity to exogenously
74                              Moreover, AMPAR synaptic currents and surface expression and their regul
75 differential effects in elevating excitatory synaptic currents and surface GluA2 levels compared with
76  CREB activity increases both NMDAR-mediated synaptic currents and surface level of NMDARs, while inh
77 es consists of varying contributions of fast synaptic currents and sustained inhibition.
78 of the altered muscle membrane properties on synaptic currents and thus provides hitherto the most de
79 ties of neurons are also altered: inhibitory synaptic currents and vesicular gamma-aminobutyric acid
80 R-16/alpha7 AChRs, a consequent reduction in synaptic current, and predictable behavioral defects.
81 ent potentiation of NMDAR Ca(2+) permeation, synaptic currents, and Ca(2+) rises in dendritic spines.
82     These findings reveal a central role for synaptic currents, and especially inhibition, in the rel
83 olved both AMPA receptor-mediated changes in synaptic currents, and faster decay rates of NMDA recept
84 413L displays deficits in NMDAR trafficking, synaptic currents, and spine density, raising the possib
85 uration, level of background noise, ratio of synaptic currents, and strengths of short-term depressio
86                The magnitude and kinetics of synaptic currents, and the relative contribution of glut
87 computational models, approximately balanced synaptic currents are also more energy efficient than ot
88                              Inhibitory post-synaptic currents are eliminated in double mutants lacki
89  that significantly more frequent and larger synaptic currents are likely due to more numerous, large
90                          Instead, excitatory synaptic currents are potentiated by combinations of inh
91 s disease, GABA(A)R transport and inhibitory synaptic currents are reduced.
92          The effective block by quinidine on synaptic currents as well as nonliganded openings points
93 ificant reduction of NMDAR-mediated ionic or synaptic current, as well as the surface expression of N
94                                         Fast synaptic current at most excitatory synapses in the brai
95 ncy of both miniature (mini) and spontaneous synaptic currents at excitatory and inhibitory synapses.
96 es on newborn GCs in adult mice, we examined synaptic currents at the developmental stage when NMDA r
97                     They receive oscillatory synaptic currents at the stimulus frequency, and they ba
98               Evoked and miniature GABAergic synaptic currents between NTS and identified gastric-pro
99 itude of spontaneous excitatory postsynaptic synaptic currents between preterm and term MNTB neurons.
100 cytes significantly accelerated the onset of synaptic currents but did not alter action potential gen
101 sed propagation of GABA(A) receptor-mediated synaptic currents, but did not change significantly dire
102 reduction of PPN-evoked, and not VTA-evoked, synaptic currents by the alpha7-nAChR antagonist methyll
103 termined by scaling the effect of excitatory synaptic currents by the input resistance.
104 aptic NMDARs induces a lasting change in the synaptic current, by changing the subunit composition of
105                              Thus, if native synaptic currents can be mediated by alpha3 glycine rece
106                           Electric fields of synaptic currents can influence diffusion of charged neu
107 s exhibited prolonged NMDA receptor-mediated synaptic currents, caused by a deficit in glutamate upta
108                     However when spontaneous synaptic currents ceased with MeHg, Fluo-4 fluorescence
109 ides remained constant, the first changes in synaptic currents, compared to wild-type mice could be d
110 rticular, the slow decay of kainate receptor synaptic currents contrasts with the rapid deactivation
111                            To understand how synaptic currents contribute to rhythmic activity and sp
112                             Yet how balanced synaptic currents contribute to the coding efficiency an
113 nd the presence or absence of EtOH-sensitive synaptic currents correlated with cell surface peptide l
114 ABA(A) receptor subunit mRNAs, and GABAergic synaptic current decay in the medial preoptic area (mPOA
115 GCs, because GCs require a larger excitatory synaptic current density to reach spike threshold.
116 le abolishing GABAA receptor-mediated phasic synaptic currents, did not reveal a tonic GABAA receptor
117 t clusters, spontaneous and evoked GABAergic synaptic currents disappeared in thalamocortical cells w
118                                              Synaptic currents display a large degree of heterogeneit
119 exhibiting electrically excitable membranes, synaptic currents, dopamine release, and substantial red
120                                Recordings of synaptic currents during gamma activity revealed that NM
121                              Analysis of the synaptic currents during SWRs uncovered that the dominan
122 -4-isoxazolepropionic acid receptor-mediated synaptic current (eEPSC) amplitude in both lamina I and
123    Interestingly, the NMDA/AMPA ratio of the synaptic current elicited in mPFC neurons by afferent fi
124                                            A synaptic current entering a spine with a high R(neck) wi
125 mportant synaptic behaviors, excitatory post-synaptic current (EPSC), has been updated as a stretched
126 microM) reversibly inhibited excitatory post synaptic currents (EPSCs) recorded from subiculum neuron
127    Using these models, we show that balanced synaptic currents evoke fewer spikes per second than exc
128 ound to account for <3% of the PC inhibitory synaptic currents evoked by electrical stimulation.
129 y, both forms of plasticity uniformly scaled synaptic currents evoked by pulse trains, and these chan
130         In marked contrast, the amplitude of synaptic currents evoked in the postsynaptic muscle cell
131 siological experiments, larger NMDA-mediated synaptic currents, evoked in CA1 principal cells by Scha
132 effects on spontaneously occurring miniature synaptic currents, except that there is a decrease in re
133 g-lasting increases in sharp wave-associated synaptic currents, exhibits enhanced excitatory synaptic
134                         Cholinergic efferent synaptic currents first appeared in a subset of IHCs at
135 ion ([Ca(2+)](i)) and changes in spontaneous synaptic current frequency caused by the neurotoxicant m
136  amacrine cells and by recording RB-mediated synaptic currents from AII amacrine cells in mouse retin
137                           Inferring putative synaptic currents from field potentials advances our abi
138                    By recording light-evoked synaptic currents from GCs, we determined that the Na ch
139 lish sharply delimited spatial domains where synaptic currents from one or another input appear to be
140 e a faster time constant of decay and evoked synaptic currents have a smaller NMDA/AMPA ratio than th
141  for the postsynaptic clustering of GABAARs, synaptic currents have been detected in neurons obtained
142 ulate brain function by generating tonic and synaptic currents; however, it remains unknown whether H
143 plitude, but not the duration, of excitatory synaptic currents improves memory performance.
144 eduction of NMDA receptor-mediated ionic and synaptic current in cortical pyramidal neurons.
145 scape probability mirrors the time course of synaptic current in the command neuron.
146        Furthermore, the amplitude of unitary synaptic currents in a PN is matched to the size of its
147                                              Synaptic currents in afferent fibers occurred with high
148 potentials, as well as action potentials and synaptic currents in anatomically identified CA1 and CA3
149               Ankle rotation produced larger synaptic currents in ankle extensors than knee or hip ro
150 on of spontaneous, but not evoked, GABAergic synaptic currents in BLA principal neurons; the effect w
151 ificant reduction in amplitude of inhibitory synaptic currents in both cultured neurons and hippocamp
152                               Although basal synaptic currents in CA1 and CA2 are quite similar, syna
153 ed the frequency and amplitude of inhibitory synaptic currents in CA1 pyramidal cells.
154  recording was used to analyze glutamatergic synaptic currents in CN neurons.
155 re informative spikes approximately balanced synaptic currents in cortical neurons can promote both c
156 st spiking activity followed by recording of synaptic currents in distinct types of anatomically iden
157                                Recordings of synaptic currents in dorsal horn neurons and population
158 ergic interneurons triggers large inhibitory synaptic currents in dorsal striatal projection neurons,
159                                  We measured synaptic currents in E18.5 hypoglossal MNs from brain sl
160 3 pyramidal cells and measuring light-evoked synaptic currents in ex vivo S1 slices.
161                   In contrast, glutamatergic synaptic currents in FS interneurons have a large, stron
162 e examined whether BRAG1 and BRAG2 influence synaptic currents in hippocampal CA1 pyramidal neurons u
163   Here we examined excitatory and inhibitory synaptic currents in human tissue samples obtained from
164 of D1/D5 receptors increased auditory-evoked synaptic currents in infragranular layers, prolonging lo
165 d N-methyl-D-aspartic acid receptor-mediated synaptic currents in lamina I neurons.
166 ature IPSCs, and reduced electrically evoked synaptic currents in MCH cells.
167                       We show that the first synaptic currents in newborn GCs are generated by activa
168 MDAR) antagonists, we demonstrate that NMDAR synaptic currents in NRG2 KOs are augmented at hippocamp
169 regulation of AMPA receptor (AMPAR)-mediated synaptic currents in pyramidal neurons of prefrontal cor
170 uency and amplitude of spontaneous miniature synaptic currents in rat hippocampal neurons in culture.
171                  A2 cells receive excitatory synaptic currents in response to both directions of move
172 ture and amplitude of evoked excitatory post-synaptic currents in second-order neurons as well as inc
173 us pain, inward currents in DRG neurons, and synaptic currents in spinal cord neurons are all reduced
174                  AMPARs mediate the briefest synaptic currents in the brain by virtue of their rapid
175 injections of identical simulated excitatory synaptic currents in the dendrites.
176 ge inputs, we used dynamic clamp to simulate synaptic currents in the dendrites.
177 tion, with decreased amplitude of excitatory synaptic currents in the developing hippocampus and redu
178 educed the amplitude of evoked glutamatergic synaptic currents in the NAcore in an mGluR2/3-dependent
179  synapses in spinal cord slices by recording synaptic currents in the presence of a low-affinity comp
180 naptic currents, indicating a major role for synaptic currents in the relationship between cortical L
181  currents relative to AMPA receptor-mediated synaptic currents in the remaining transfected neurons w
182 hermore, this current amplifies and prolongs synaptic currents in the subthreshold range.
183                                              Synaptic currents in these embryos had a smaller amplitu
184     We investigated in rat cerebellar slices synaptic currents in Unipolar Brush Cells (UBCs), which
185 whereas 100 mum Thio-THIP did not affect the synaptic currents in ventrobasal thalamus neurons or str
186 hannel properties of mutant receptors to the synaptic currents in vivo.
187           We recorded uEPSCs (evoked unitary synaptic currents) in response to pairs of action potent
188 res exhibited potentiation of AMPAR-mediated synaptic currents, including an increase in the amplitud
189 redicted membrane potential as accurately as synaptic currents, indicating a major role for synaptic
190 en mGluRs were activated by trains of evoked synaptic currents instead of direct application of agoni
191  in monosynaptic spontaneous inhibitory post-synaptic currents (IPSCs) in MSNs.
192 ent integration of excitatory and inhibitory synaptic currents is an important process for shaping th
193 he decay time course of GABAergic inhibitory synaptic currents is considerably faster when recorded w
194 t unitary amplitude of spontaneous miniature synaptic currents is decreased dramatically in FUS-ALS f
195                              The increase in synaptic currents is dependent upon an increase in newly
196 ileptic DGCs, the neurosteroid modulation of synaptic currents is diminished and alpha4 subunit-conta
197 with depression, direct proof for changes in synaptic currents is lacking in large brain areas such a
198 the integration of excitatory and inhibitory synaptic currents is lacking.
199  A balance between excitatory and inhibitory synaptic currents is thought to be important for several
200 d to treat the human disorder, restored fast synaptic current kinetics and the ability to swim.
201 , associated with higher-frequency miniature synaptic currents, larger long-term potentiation, and de
202 otostimulation with whole-cell recordings of synaptic currents makes it possible to map circuits betw
203 fluence of these subunits on GABAAR-mediated synaptic currents may help in identifying the roles and
204 e impact of nanomolar zinc concentrations on synaptic currents mediated by 2A-type NMDA receptors.
205 uency stimulation of afferent fibers elicits synaptic currents mediated by alpha7 nAChRs.
206 curs via the PKA pathway and does not affect synaptic currents mediated by AMPA or NMDA receptors.
207 tion also increased the amplitude of quantal synaptic currents mediated by AMPA- and NMDA-type glutam
208 ectrical synapses, and evoke slow inhibitory synaptic currents mediated by GABA(A) and GABA(B) recept
209        Here we characterized the dynamics of synaptic currents mediated by GABA(A) and glutamate rece
210 ferentially blocks extrasynaptic rather than synaptic currents mediated by NMDARs in the same neuron.
211 significantly inhibited evoked and miniature synaptic currents mediated by non-NMDA receptors through
212 of glutamate are voltage-independent, as are synaptic currents mediated by the electrically neutral n
213  DR neurons exhibit inhibitory 'phasic' post-synaptic currents mediated primarily by synaptic GABAA r
214  mice frequency of miniature excitatory post-synaptic currents (mEPSC) and inhibitory post-synaptic c
215 e exhibited normal miniature excitatory post-synaptic currents (mEPSC), suggesting that action-potent
216 e loss and smaller miniature excitatory post-synaptic currents (mEPSCs) in granule cells of the DG.
217  channels enhances miniature excitatory post-synaptic currents (mEPSCs) onto EC layer III pyramidal n
218 ynaptic currents (mEPSC) and inhibitory post-synaptic currents (mIPSC) are elevated at 2 weeks and, m
219 ked IPSCs (eIPSCs) and spontaneous miniature synaptic currents (mIPSCs) of visualized nRT cells in yo
220 (increased frequency of miniature excitatory synaptic currents, modestly enhanced long-term potentiat
221 he amplitude and duration of excitatory post synaptic currents near the action potential threshold.
222    We found that the amplitude of excitatory synaptic currents necessary to fire rodent pyramidal cel
223                 The properties of spines and synaptic currents of individual layer 3 pyramidal neuron
224 hough field potentials (FPs) may reflect the synaptic currents of neurons near the recording electrod
225 are accompanied by increased contribution to synaptic currents of the NMDA component.
226 es and the frequency of miniature excitatory synaptic currents onto CRH neurons were reduced in "care
227 passive integration of inspiratory-modulated synaptic currents or do active processes modulate these
228  There were no differences in the excitatory synaptic currents or the passive and active properties o
229 ariability in pyramidal cells as a result of synaptic current- or conductance-mediated membrane fluct
230 nism of GluN1a, reversibly blocks excitatory synaptic currents, prevents the induction of long-term p
231  using channelrhodopsin while recording post-synaptic currents (PSCs) in layer 1 interneurons.
232                                              Synaptic currents recorded from DGCs of epileptic animal
233                                Properties of synaptic currents recorded from epileptic DGCs appeared
234                                              Synaptic currents recorded from epileptic DGCs were less
235                              The analysis of synaptic currents recorded from KI mice showed that the
236                                   Excitatory synaptic currents recorded from PLTS interneurons are ch
237 the development of glycine-receptor-mediated synaptic currents recorded from the interneurons of the
238 of H2O2 on GABAA receptor-mediated tonic and synaptic currents recorded in cultured mouse hippocampal
239                          In addition, direct synaptic current recordings show out-of-phase excitation
240                                 By inferring synaptic currents related to spike generation in simulta
241  and significantly reduced GABA(A)R-mediated synaptic currents relative to AMPA receptor-mediated syn
242                                              Synaptic currents revealed a different pattern of activa
243 he amplitude of light-evoked thalamocortical synaptic currents selectively onto L4.
244  or kinetics, of spontaneous excitatory post-synaptic currents (sEPSC) in Dyt1 DeltaGAG heterozygous
245    We found no changes in the size of evoked synaptic currents, short-term plasticity, or apparent ca
246                       Analysis of inhibitory synaptic currents showed glycinergic transmission is the
247                      Simultaneous, transient synaptic current sinks appeared first in layers III and
248 lyses revealed an LTP-associated increase of synaptic current sinks in layer IV/lower layer II/III at
249 SC-CM increased the frequency of spontaneous synaptic currents (SSCs) within 3-15 min by an average o
250 bility increased in relation to a comparable synaptic current stimulus.
251 es drove IN activity despite small amplitude synaptic currents, suggesting an active role in IN infor
252 ate (NMDA) receptor-mediated excitatory post-synaptic currents, suggesting intact excitatory transmis
253  examining the dopamine D2 receptor-mediated synaptic current that resulted from somatodendritic rele
254 he well described primary rod pathway, evoke synaptic currents that are preferentially mediated by CP
255               Whole-cell recordings revealed synaptic currents that decayed along a multiexponential
256  of serotype 1, 5, and 8 led to light-evoked synaptic currents that depressed much more than electric
257 also predicts accurately the faster decay of synaptic currents that is observed in spasmodic mice.
258 m the interplay of excitatory and inhibitory synaptic currents that it receives.
259 d could both contribute in different ways to synaptic currents that mediate feedback signaling.
260 o spines, and potentiation of AMPAR-mediated synaptic currents that occur during LTP.
261                           Here, we study the synaptic currents that process ILD in vivo and use stimu
262 cells in the guinea pig retina and monitored synaptic currents that were evoked by visual stimulation
263 results to generate simulated M/T population synaptic currents that were injected into real cortical
264                The time course of excitatory synaptic currents, the major means of fast communication
265 nd depression, which modify the amplitude of synaptic currents, this activity-induced change in AMPA
266 f short-term synaptic depression relative to synaptic current time constant.
267           These changes alter the ability of synaptic currents to evoke an action potential and there
268 in the significant reduction of disinhibited synaptic currents to healthy control levels, suggesting
269 ral interaction of excitatory and inhibitory synaptic currents to shape the firing pattern of the neu
270 s the amplitude of excitatory and inhibitory synaptic currents to the MSO and, moreover, show that th
271 activity reduced the LTP of these excitatory synaptic currents triggered by high-frequency stimulatio
272 ma receptor isoform produces slowly decaying synaptic currents typical of SCS that transit to a much
273                      Fluctuation analysis of synaptic currents uncovered an increase in conductance a
274 ng potentiation of NMDAR- and AMPAR-mediated synaptic currents via glucocorticoid receptors (GRs) sel
275 peak of the population discharge, the inward synaptic current was essentially mediated by glutamate r
276                    Linearity of summation of synaptic currents was similar to WT.
277                       By direct recording of synaptic currents, we also show that motoneurons are act
278         Inhibitory GABAergic and glycinergic synaptic currents were also significantly increased by D
279                 Both AMPA- and NMDA-mediated synaptic currents were enhanced, and analysis of AMPA-me
280                    Unexpectedly, cholinergic synaptic currents were entirely absent from both inner a
281                                        These synaptic currents were mediated by a decrease in an outw
282                              Whole-cell GABA synaptic currents were recorded in magnocellular neurons
283 elopment of the behavioral phenotype, evoked synaptic currents were reduced.
284 s (PC-->DCN), light- and electrically evoked synaptic currents were remarkably similar for ChR2 expre
285                          Although inhibitory synaptic currents were similar between the two neuronal
286  slightly reduced, miniature inhibitory post synaptic currents were unaffected, and intrinsic membran
287  dramatic increase in tonic current, whereas synaptic currents were unaffected.
288  a TH(+) neuron evoked a brief GABA-mediated synaptic current, whereas evoked dopamine release was as
289 apses selectively prolongs the decay time of synaptic currents, whereas a switch from GluR2-lacking t
290 n in AMPA- and NMDA-mediated excitatory post-synaptic currents, whereas the control peptide, TAT-myc,
291 ic responses as detected in larger miniature synaptic currents which are caused by enlarged presynapt
292 h other, generating negative correlations in synaptic currents which cancel the effect of shared inpu
293 ne receptor-mediated inhibitory postsynaptic synaptic currents, which were prevalent in preterm MNTB
294 r of recruitment is defined by scaling their synaptic current with their input resistance.
295 tch-clamp recordings demonstrated excitatory synaptic currents with strikingly long duration and epil
296 ng-term plasticity of NMDA receptor-mediated synaptic currents with the polarity of plasticity determ
297 lockade of Cl- currents (including tonic and synaptic currents) with picrotoxin reduced interspike in
298 stsynaptic apparatus and generate functional synaptic currents within 4-6 h when cocultured with matu
299 s may provide a powerful means of amplifying synaptic currents without incurring plateau potentials o
300 in gene dramatically increased NR2A-mediated synaptic currents, without affecting AMPA receptor curre

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