ライフサイエンスコーパス: excitatory synapse

1 specific forms of plasticity at hippocampal excitatory synapses.

2 that modulate their location and function at excitatory synapses.

3 ein localized to the postsynaptic density of excitatory synapses.

4 et produce very different adaptations at NAc excitatory synapses.

5 ing protein that is enriched in postsynaptic excitatory synapses.

6 -term potentiation of lateral-basal amygdala excitatory synapses.

7 features in the physiology and pathology of excitatory synapses.

8 re is essential to the physiology of central excitatory synapses.

9 dant in the brain, where they are present in excitatory synapses.

10 dritic spines-tiny protrusions accommodating excitatory synapses.

11 ry cortex, together with concomitant STDP of excitatory synapses.

12 -dimensional neuropil fragment containing 54 excitatory synapses.

13 gulate transmitter release at inhibitory and excitatory synapses.

14 both structural and functional plasticity at excitatory synapses.

15 ission and plasticity at both inhibitory and excitatory synapses.

16 can result from a synaptic learning rule of excitatory synapses.

17 apses and neuroligin 1 (NLGN1) dominating at excitatory synapses.

18 the central nervous system is the scaling of excitatory synapses.

19 , and dendritic spines are the sites of most excitatory synapses.

20 alize with marker proteins of inhibitory and excitatory synapses.

21 T is enriched in the postsynaptic density of excitatory synapses.

22 reduces the number of spine protrusions and excitatory synapses.

23 ial postsynaptic coordinator in formation of excitatory synapses.

24 rization in postsynaptic dendritic spines at excitatory synapses.

25 apses, producing functional modifications at excitatory synapses.

26 t regulate AMPAR activity and trafficking at excitatory synapses.

27 d with an increase in an inward current from excitatory synapses.

28 g this strengthening is the formation of new excitatory synapses.

29 n CaMKII and NL-1, two primary components of excitatory synapses.

30 l the direction of plasticity at interneuron excitatory synapses.

31 the development and plasticity of classical excitatory synapses.

32 eres with the formation of local clusters of excitatory synapses.

33 pression-like behavior differentially affect excitatory synapses.

34 ompartments and a nanoscopic organization at excitatory synapses.

35 n fragment that accelerates the formation of excitatory synapses.

36 of cytoplasmic vesicle pools in conventional excitatory synapses.

37 of AMPA-type glutamate receptors (AMPARs) at excitatory synapses.

38 as they do not affect spontaneous release at excitatory synapses.

39 in homeostatic synaptic plasticity (HSP) at excitatory synapses.

40 roscopy (STEM) tomography reconstructions of excitatory synapses.

41 ouse CA2 pyramidal neurons and envelop their excitatory synapses.

42 on in dendritic spines, reflecting a loss of excitatory synapses.

43 pocampal CA1 neurons without affecting their excitatory synapses.

44 AMPA receptor (AMPAR) and PSD-95 content at excitatory synapses.

45 D95-positive puncta, indicative of increased excitatory synapses.

46 synaptic plasticity processes in hippocampal excitatory synapses.

47 e formation, organization, and plasticity of excitatory synapses.

48 to synaptic maturation and strengthening of excitatory synapses.

49 e the amplitude and short-term plasticity of excitatory synapses, a result not possible from activati

50 displayed a disturbed morphology of striatal excitatory synapses, accompanied by strongly increased g

51 ON- and OFF-sustained RGCs lost excitatory synapses across an otherwise structurally nor

52 siform cells of the dorsal cochlear nucleus, excitatory synapses activate a TTX-sensitive Na(+) condu

53 DA receptor-containing, AMPA receptor-silent excitatory synapses, albeit in distinct cell types throu

54 ers eCB signaling and impairs eCB-LTD at the excitatory synapses, an important synaptic plasticity th

55 hyperactivity, which triggers increased SPN excitatory synapse and corticostriatal hyperconnectivity

56 nd that C1ql3-deficient mice exhibited fewer excitatory synapses and diverse behavioral abnormalities

57 Excitatory synapses and fast-spiking properties matured

58 d-beta (Abeta) peptides causes early loss of excitatory synapses and impairs synaptic plasticity.

59 immediate-early gene (IEG) that functions at excitatory synapses and is required for learning and mem

60 hat knockdown of NP1 increases the number of excitatory synapses and neuronal excitability in culture

61 d ion channels that underlie transmission at excitatory synapses and play an important role in regula

62 s located at the postsynaptic compartment of excitatory synapses and plays a role in synapse formatio

63 d role for PNNs in restricting plasticity at excitatory synapses and raise the possibility of an earl

64 y, S783A mice exhibited increased numbers of excitatory synapses and surface AMPA receptors, effects

65 ty drives tau to the postsynaptic density of excitatory synapses and that Abetao-driven tau transloca

66 key regulator of learning-related changes in excitatory synapses and the acquisition of motor skills.

67 A deficit in pruning of cortical excitatory synapses and the resulting hyperconnectivity

68 basic structural unit, or building block, of excitatory synapses and their number characterizes synap

69 one-derived ATP can pre-modulate efficacy of excitatory synapses and thereby can have an important ro

70 s accompanied by a decrease in the number of excitatory synapses and, consequently, by a reduction of

71 is localized in the vicinity of hippocampal excitatory synapses, and that its activation increases d

72 NL2, the formation and function of cortical excitatory synapses are diminished, whereas inhibitory s

73 Frequently, excitatory synapses are formed on dendritic spines.

74 Although it has been proposed that these excitatory synapses are formed onto appendages resemblin

75 Developmental alterations of excitatory synapses are implicated in autism spectrum di

76 hippocampal synapses, but ELKS functions at excitatory synapses are not known.

77 mpairment of synaptic plasticity and loss of excitatory synapses are only beginning to be unraveled.

78 Excitatory synapses are polarized structures that primar

79 t the development of circuits containing CA2 excitatory synapses are sensitive to manipulations of th

80 e inhibitory synapses frequently recur while excitatory synapses are stable.

81 s in long-term potentiation (LTP) at central excitatory synapses are thought to contribute to cogniti

82 Although the disruptions in excitatory synapses are well documented in fragile X, th

83 d its recovery by antidepressants, implicate excitatory synapses as a locus of plasticity in depressi

84 ong-term depression (NMDA-LTD) at prefrontal excitatory synapses as a synaptic signature of this asso

85 ombospondin interactions known to facilitate excitatory synapse assembly.

86 used automated methods to construct maps of excitatory synapses associated with high concentrations

87 at medial layer V entorhinal neurons receive excitatory synapses at distal dendritic locations, which

88 ely uniform following minimal stimulation of excitatory synapses at visualized locations along the de

89 hese cellular locales is its localization to excitatory synapses between excitatory neurons, presynap

90 of the recurrent circuit using recordings of excitatory synapses between identified motoneuron and Re

91 , the mGluR agonist did not generate eCBs at excitatory synapses but nevertheless induced burst firin

92 ndicate that both neuroligin-3 and -4 act at excitatory synapses but perform surprisingly distinct fu

93 have been identified as the Ca(2+) sensor at excitatory synapses, but the Ca(2+) sensor(s) at inhibit

94 Microglia control excitatory synapses, but their role in inhibitory neurot

95 NMDARs) are essential for the development of excitatory synapses, but their role in synaptic refineme

96 ilitates a recruitment of P2X receptors into excitatory synapses by Ca(2+)-dependent mechanism.

97 m synaptic potentiation at mouse hippocampal excitatory synapses by inactivating dendritic Kv1.1-cont

98 long-term depression (LTD) of glutamatergic excitatory synapses by increasing inhibitory inputs onto

99 itative ultrastructural analysis of cortical excitatory synapses by mean of a new, efficient method,

100 Organization of signaling complexes at excitatory synapses by membrane-associated guanylate kin

101 is a form of synaptic plasticity induced at excitatory synapses by metabotropic glutamate receptors

102 ortant role in regulating the development of excitatory synapses by promoting local activity-dependen

103 reted glypican 4 induces formation of active excitatory synapses by recruiting AMPA glutamate recepto

104 beta-neurexins control synaptic strength in excitatory synapses by regulating postsynaptic 2-arachid

105 nd functional roles of MAGUKs at hippocampal excitatory synapses by simultaneous knocking down PSD-95

106 ion of spontaneous release at inhibitory and excitatory synapses by stochastic VACC activity that ext

107 ic transmission was unaffected, showing that excitatory synapses can be dissociated from spines.

108 ors, co-localized with NMDA receptors in the excitatory synapses, can be activated by ATP co-released

109 nd chaperone levels, maintenance of striatal excitatory synapses, clearance of Htt aggregates and pre

110 Many excitatory synapses co-express presynaptic GABAA and GAB

111 The postsynaptic proteome of excitatory synapses comprises 1,000 highly conserved pr

112 esent findings supporting a special role for excitatory synapses connecting pyramidal neurons of the

113 Many excitatory synapses contain high levels of mobile zinc w

114 We observed excitatory synapses contributed more to bursting behavio

115 d short-term plasticity at dentate gyrus-CA3 excitatory synapses culminate in impaired coding of new

116 e caused specifically by inhibitory, but not excitatory, synapse defects.

117 The density of excitatory synapses, defined by overlapping vesicular gl

118 g of cultured hippocampal neurons, decreased excitatory synapse density in vitro and in vivo, and abo

119 that absence of NO prevents the increase in excitatory synapse density induced by environmental enri

120 wledge, this is the first demonstration that excitatory synapse density is lower selectively on parva

121 xpression is activity dependent and supports excitatory synapse density.

122 tatory synapses with the capacity to enhance excitatory synapses dependent on synaptic activity or Ca

123 orn shortly after SE did not form functional excitatory synapses, despite robust sprouting.

124 Rem2 is a positive regulator of functional, excitatory synapse development and a negative regulator

125 LRRTM4 positively regulates excitatory synapse development in cultured neurons and i

126 hat MT3-MMP loss-of-function interferes with excitatory synapse development in dissociated cortical n

127 localization, thus revealing a mechanism for excitatory synapse development in the mammalian CNS.

128 ction in inhibitory synapse numbers, whereas excitatory synapse development was normal.

129 large body of accumulated evidence regarding excitatory synapse development, little is known about sy

130 Electrophysiology analysis of excitatory synapse development, starting at P12, showed

131 y for proper filopodia, dendritic spine, and excitatory synapse development.

132 nd a Rac-GAP (Bcr) that cooperate to control excitatory synapse development.

133 MMP-dependent shedding of NgR1 in regulating excitatory synapse development.SIGNIFICANCE STATEMENT In

134 Thus, the action of RA at inhibitory and excitatory synapses diverges significantly after the ste

135 age clamp is completely ineffective for most excitatory synapses due to spine electrical compartmenta

136 Inhibitory, but not excitatory, synapse dysfunction underlies cortico-hippoc

137 We show here that the cleft of excitatory synapses exhibits a distinct density profile

138 Functionally silent (non-AMPAR-mediated) excitatory synapses exist in several systems during deve

139 ial neuropathic pain states through abnormal excitatory synapse formation and enhanced presynaptic ex

140 l conditional knock-outs, we found excessive excitatory synapse formation and maturation in the corti

141 AP-1 expression or induced activity prior to excitatory synapse formation disrupts dendritic growth.

142 ic Sema5A/PlexinA2 interactions that inhibit excitatory synapse formation in developmentally born and

143 todomain of NgR1 is sufficient to accelerate excitatory synapse formation in dissociated cortical neu

144 orphological changes that initiate spine and excitatory synapse formation.

145 tions with additional ligands to orchestrate excitatory synapse formation.

146 function was silenced, cortical and striatal excitatory synapses formed and matured at an accelerated

147 , and two-photon Ca(2+) imaging, we analyzed excitatory synapses formed by climbing fibers on Purkinj

148 Four excitatory synapses formed by two distinct inputs, audit

149 Astrocytes depressed excitatory synapses from basolateral amygdala via A1 ade

150 We examined the structural plasticity of excitatory synapses from corticostriatal and thalamostri

151 Specifically, DE potentiated FF excitatory synapses from layer 4 (L4) to L2/3 in A1 and

152 from motor outputs, yet the efficacy of the excitatory synapses from single and converging motoneuro

153 c cell adhesion molecule N-cadherin controls excitatory synapse function and stabilizes dendritic spi

154 However, how OGT regulates excitatory synapse function is largely unknown.

155 ell-adhesion postsynaptic protein regulating excitatory synapse function, and show increased excitato

156 hare a common underlying neuropathy: altered excitatory synapse function.

157 addition and elimination were interpreted as excitatory synapse gain and loss, respectively.

158 N1), a postsynaptic protein found in central excitatory synapses, governs excitatory synaptic efficac

159 which, like neuroligin-1 is also targeted to excitatory synapses, had no comparable effect.

160 Different from RA action at excitatory synapses, however, RA at inhibitory synapses

161 Here, we propose an excitatory synapse hypothesis of depression in which chr

162 were used to quantify the number of putative excitatory synapses (i.e., the overlap of vesicular glut

163 astin-deficient (Np(-/-)) mice the number of excitatory synapses in CA1 and DG, but not CA3 regions i

164 ease, to be necessary for the development of excitatory synapses in cortical neurons.

165 toskeleton and gates long-term plasticity at excitatory synapses in cortical neurons.

166 orting evidence that dysfunction of multiple excitatory synapses in cortico-mesolimbic reward pathway

167 ically decreased neurotransmitter release at excitatory synapses in cultured cortical neurons.

168 Kalirin-7 and X11alpha co-localize at excitatory synapses in cultured cortical neurons.

169 the hippocampus, and aberrant generation of excitatory synapses in dentate gyrus granule cells.

170 expression of Kal7 restores the reduction of excitatory synapses in HD cortical cultures.

171 under control by promoting the maturation of excitatory synapses in interneurons.

172 le in these processes, as the major sites of excitatory synapses in neuronal communication.

173 caine seeking is associated with potentiated excitatory synapses in nucleus accumbens.

174 c regulation of miniature synaptic events at excitatory synapses in response to activity deprivation.

175 Dendritic spines establish most excitatory synapses in the brain and are located in Purk

176 the protein densin-180 is highly enriched at excitatory synapses in the brain and enhances the cell s

177 The majority of excitatory synapses in the brain exist on dendritic spin

178 nths) and that loud sounds reversibly modify excitatory synapses in the brain, changing synaptic func

179 GTPase activating protein highly enriched at excitatory synapses in the brain.

180 mediate neurotransmission at the majority of excitatory synapses in the brain.

181 B receptors (GABABRs) can down-regulate most excitatory synapses in the CNS by reducing postsynaptic

182 Dendritic spines are the sites of most excitatory synapses in the CNS, and opposing alterations

183 hanced adenosine tone and A1R sensitivity at excitatory synapses in the dorsal horn after nerve injur

184 icroscopy shows that Cdh8 is concentrated at excitatory synapses in the dorsal striatum, and Cdh8 kno

185 or acute knockdown in vivo results in fewer excitatory synapses in the hippocampal formation as asse

186 Damage to excitatory synapses in the hippocampus occurs in associa

187 lone fully accounts for neurotransmission at excitatory synapses in the hippocampus, excluding a role

188 nt sex difference in molecular regulation of excitatory synapses in the hippocampus.

189 unts for the activation of NMDA receptors at excitatory synapses in the hippocampus.

190 in Nissl-stained sections so that numbers of excitatory synapses in the inner molecular layer per gra

191 croscopy was used to estimate the numbers of excitatory synapses in the inner molecular layer per hip

192 pines are the postsynaptic terminals of most excitatory synapses in the mammalian brain.

193 Most excitatory synapses in the mammalian CNS are located on

194 e a morphological feature of the majority of excitatory synapses in the mammalian neocortex and are m

195 s sufficient to potentiate layer 4-layer 2/3 excitatory synapses in the mouse somatosensory (barrel)

196 lapse to cocaine use necessitates remodeling excitatory synapses in the nucleus accumbens and synapti

197 trolling activity-dependent strengthening of excitatory synapses in the rat hippocampus.

198 Increases in the number of excitatory synapses in the superficial dorsal horn of Vc

199 pines are small postsynaptic compartments of excitatory synapses in the vertebrate brain that are mod

200 on of ectopic Nxph1 at the synaptic cleft of excitatory synapses in transgenic mice and revealed an e

201 P2) is a postsynaptic scaffolding protein at excitatory synapses in which mutations and deletions hav

202 sion of inhibitory synapses, decreased it at excitatory synapses in WTs, but had no effect on eCB act

203 Rho-like small GTPases critical to maintain excitatory synapse, in the cortex of HD mice.

204 tion of dendritic spines, principal sites of excitatory synapses, in the motor cortex.

205 that is characterized by its localization at excitatory synapses, interactions with glutamate recepto

206 Synaptic strength at excitatory synapses is determined by the presence of glu

207 Plasticity of cortical excitatory synapses is thought to be important for learn

208 (rMS) has been shown to induce plasticity of excitatory synapses, it is unclear whether rMS can also

209 ontribute to the plasticity and integrity of excitatory synapses, leading to selective loss of dendri

210 In cortical tissue, ErbB4 associates with excitatory synapses located on inhibitory interneurons.

211 ndent long-term potentiation (LTP) occurs at excitatory synapses made on some inhibitory neurons.

212 An anti-Hebbian form of LTP is observed at excitatory synapses made with some hippocampal interneur

213 Disrupted excitatory synapse maturation in GABAergic interneurons

214 dea that an imbalance between inhibitory and excitatory synapses may contribute to these disorders.

215 tory changes in the number of inhibitory and excitatory synapses may serve as a novel mechanism to re

216 ow long-term potentiation (LTP) of different excitatory synapses modifies the flow of information.

217 tient antibodies do not alter the density of excitatory synapses, N-methyl-D-aspartate receptor (NMDA

218 Our analysis was based on 79 excitatory synapses, nonperforated (NPSs) and perforated

219 sults indicate that NP1 negatively regulates excitatory synapse number by modulating neuronal excitab

220 r 2 (MEF2) transcription factors suppress an excitatory synapse number by promoting degradation of th

221 major, but not the minor, variant increased excitatory synapse number on PV interneurons and display

222 Because excitatory synapse number on PV interneurons is regulate

223 Mice lacking GRASP1 showed abnormal excitatory synapse number, synaptic plasticity, and hipp

224 During synaptic plasticity at excitatory synapses, numerous structural, signaling, and

225 Excitatory synapses occur mainly on dendritic spines, an

226 However, whether HDAC2 regulation of excitatory synapses occurs in a cell-autonomous manner a

227 d by Ca2+ signals of different amplitudes at excitatory synapses of interneurons.

228 the region of interest, serial sections from excitatory synapses of medial prefrontal cortex (mPFC) o

229 rophysiologically, plasticity was altered at excitatory synapses of the striatal circuitry that is kn

230 ogether, PE leads to impaired eCB-LTD at the excitatory synapses of VTA DA neurons primarily due to C

231 -protein receptors (GPCRs) agonists enhanced excitatory synapses on direct pathway striatal spiny pro

232 neurons (dSPNs), whereas rapid production of excitatory synapses on indirect pathway neurons (iSPNs)

233 l cells, comparatively little is known about excitatory synapses on interneurons.

234 Drug-evoked plasticity at excitatory synapses on medium spiny neurons (MSNs) of th

235 ction in glutamate transport and potentiated excitatory synapses on medium spiny neurons.

236 for VTA glutamatergic neurons through local excitatory synapses on mesoaccumbens dopaminergic neuron

237 rd, and the first pathway shown to establish excitatory synapses on nAcc parvalbumin GABAergic intern

238 hat neuroligin-3 specifies the properties of excitatory synapses on parvalbumin-containing interneuro

239 Excitatory synapses on PV interneurons are dependent on

240 Therefore, we tested the hypothesis that excitatory synapses on PV interneurons are pruned during

241 t ErbB4 splicing may regulate the pruning of excitatory synapses on PV interneurons during adolescenc

242 ng, we tested the hypothesis that pruning of excitatory synapses on PV interneurons is associated wit

243 h is known about the molecular properties of excitatory synapses on pyramidal cells, comparatively li

244 Long-term potentiation of excitatory synapses on pyramidal neurons in the stratum

245 Whereas excitatory synapses on spines can be imaged with a fluor

246 MEC form predominantly asymmetrical, likely excitatory, synapses on dendritic spines (90%) or shafts

247 ed behavioral state-dependent changes in the excitatory synapses onto a subset of mPFC neurons: those

248 sible for the remote AC-mediated recovery of excitatory synapses onto axotomized motor neurons in adu

249 ritic distributions of these corticocortical excitatory synapses onto CSPs in both areas also showed

250 NRG1 enhanced the strength of excitatory synapses onto FS INs, which inhibited ocular

251 period timing by controlling the strength of excitatory synapses onto FS INs.

252 e model of Rett syndrome, we show that naive excitatory synapses onto hippocampal pyramidal neurons o

253 (NMDAR) subunit composition and kinetics at excitatory synapses onto pyramidal cells; however, littl

254 e, we tested synaptic plasticity of cortical excitatory synapses onto striatal spiny projection neuro

255 fibre axons (PFs) form approximately 180,000 excitatory synapses onto the dendritic tree of a Purkinj

256 This occurs, not by direct effect on excitatory synapses or postsynaptic neurons, but rather

257 This excitatory synapse originates in secondary motor cortex,

258 the major postsynaptic elements of cortical excitatory synapses, our understanding of the synaptic o

259 In mature neurons AMPA receptors cluster at excitatory synapses primarily on dendritic spines, where

260 al deprivation that causes maximal change in excitatory synapses produces minimal change in inhibitor

261 , PSD-95, and SAP102 differentially regulate excitatory synapse properties in the NAc.

262 Compared with excitatory synapses, relatively little is known about th

263 d a reduced short-term facilitation at these excitatory synapses, representing an inverse phenotype t

264 es where the postsynaptic components of most excitatory synapses reside.

265 c assemblies of Abeta peptide associate with excitatory synapses resulting in synapse elimination thr

266 ensures efficient Cav1.2 Ca(2+) signaling at excitatory synapses.SIGNIFICANCE STATEMENT The number an

267 m potentiation (LTP) and depression (LTD) of excitatory synapse strength require the Ca(2+)/calmoduli

268 og Trio play critical and redundant roles in excitatory synapse structure and function.

269 s of an integrate-and-fire model neuron with excitatory synapses subject to STDP described by three d

270 3,5)P2 synthesis complex, is concentrated at excitatory synapses, suggesting a potential role for PI(

271 ction is not seen at kappaORs at neighboring excitatory synapses, suggesting distinct time courses an

272 t neocortical inhibitory synapses but not at excitatory synapses, suggesting fundamental differences

273 trolling ADAM10 localization and activity at excitatory synapses that is relevant to AD pathogenesis.

274 dritic spines, the receptive regions of most excitatory synapses that play a crucial role in higher b

275 However, in comparison to excitatory synapses, the structural and functional alter

276 Abeta triggers the elimination of excitatory synapses through a mechanism that requires NM

277 ange coincides with increased sensitivity of excitatory synapses to monocular deprivation (MD).

278 anism that aims at adjusting the strength of excitatory synapses to persisting changes in network act

279 city requires interactions with co-activated excitatory synapses to properly regulate excitatory-inhi

280 in ganglion cells and its colocalization at excitatory synapses to their dendrites, whereas chronic

281 These excitatory synapse types included AN synapses on bushy c

282 Among the four excitatory synapse types, the AN-BC synapses were the sm

283 rmissive for activity-dependent sculpting of excitatory synapses via the mechanism of NMDAR-dependent

284 ntaining NMDA receptors (NMDARs) at immature excitatory synapses, via a transcription-dependent mecha

285 orm the SA and to homeostatically strengthen excitatory synapses was rescued.

286 e BDNF Val66Met polymorphism affects the CEm excitatory synapses, we examined basal glutamatergic syn

287 of proteins that are critical components of excitatory synapses were not associated with GABAARs.

288 (+) terminals forming asymmetrical (putative excitatory) synapses were dendritic spines, most of whic

289 RNF10 is enriched at the excitatory synapse where it associates with the GluN2A s

290 KCC2 is highly localized to excitatory synapses where it regulates spine morphogenes

291 me carries through to the molecular level at excitatory synapses, where protein function is controlle

292 folding proteins at the PSD in glutamatergic excitatory synapses, where they maintain and modulate sy

293 eptor (R) synaptic transmission, or silenced excitatory synapses, whereas more prolonged (24 hr) firi

294 ed with changes in the strength or number of excitatory synapses with MCs but was instead associated

295 -1 (NL-1, also called NLGN1) are specific to excitatory synapses with the capacity to enhance excitat

296 Experience-dependent plasticity at excitatory synapses within dopamine neurons of the ventr

297 ons (OSNs) are chemoreceptors that establish excitatory synapses within glomeruli of the olfactory bu

298 ation generates AMPA receptor (AMPAR)-silent excitatory synapses within the basolateral amygdala (BLA

299 o, network activity preferentially regulated excitatory synapses within the proximal dendrites of CA3

300 ELKS, we find that ELKS enhances the RRP at excitatory synapses without affecting P.