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1 aptogenesis and miniature event frequency in excitatory synapses.
2 apses and neuroligin 1 (NLGN1) dominating at excitatory synapses.
3 pocampal CA1 neurons without affecting their excitatory synapses.
4 T is enriched in the postsynaptic density of excitatory synapses.
5 d with an increase in an inward current from excitatory synapses.
6 ompartments and a nanoscopic organization at excitatory synapses.
7 n fragment that accelerates the formation of excitatory synapses.
8 of cytoplasmic vesicle pools in conventional excitatory synapses.
9 of AMPA-type glutamate receptors (AMPARs) at excitatory synapses.
10 as they do not affect spontaneous release at excitatory synapses.
11  in homeostatic synaptic plasticity (HSP) at excitatory synapses.
12 roscopy (STEM) tomography reconstructions of excitatory synapses.
13 ouse CA2 pyramidal neurons and envelop their excitatory synapses.
14 on in dendritic spines, reflecting a loss of excitatory synapses.
15  AMPA receptor (AMPAR) and PSD-95 content at excitatory synapses.
16 D95-positive puncta, indicative of increased excitatory synapses.
17 synaptic plasticity processes in hippocampal excitatory synapses.
18 e formation, organization, and plasticity of excitatory synapses.
19  to synaptic maturation and strengthening of excitatory synapses.
20  specific forms of plasticity at hippocampal excitatory synapses.
21 that modulate their location and function at excitatory synapses.
22 ein localized to the postsynaptic density of excitatory synapses.
23 et produce very different adaptations at NAc excitatory synapses.
24 ing protein that is enriched in postsynaptic excitatory synapses.
25 -term potentiation of lateral-basal amygdala excitatory synapses.
26  features in the physiology and pathology of excitatory synapses.
27 re is essential to the physiology of central excitatory synapses.
28 dant in the brain, where they are present in excitatory synapses.
29 dritic spines-tiny protrusions accommodating excitatory synapses.
30 ry cortex, together with concomitant STDP of excitatory synapses.
31 -dimensional neuropil fragment containing 54 excitatory synapses.
32 flat), anticorrelated to, or correlated with excitatory synapses.
33 gulate transmitter release at inhibitory and excitatory synapses.
34 both structural and functional plasticity at excitatory synapses.
35  glutamate efflux and indirect activation of excitatory synapses.
36 ission and plasticity at both inhibitory and excitatory synapses.
37  hyaluronan preferentially surrounds nascent excitatory synapses.
38 tionality of GABAergic activity over that of excitatory synapses.
39 ains and are essential for different sets of excitatory synapses.
40 tion and loss of both central and peripheral excitatory synapses.
41 rs are used to clear glutamate released from excitatory synapses.
42 ith a glutamate uptake deficit at tripartite excitatory synapses.
43 ntial for Arc's canonical function to weaken excitatory synapses.
44 ade endocannabinoid signaling selectively at excitatory synapses.
45 c morphology and neurotransmitter release at excitatory synapses.
46 has important functions in the maturation of excitatory synapses.
47  that disrupt genes encoding the proteome of excitatory synapses.
48 ell as the number of presynaptic vesicles at excitatory synapses.
49 xpressed in cerebral cortex and localized to excitatory synapses.
50 easing factors that promote the formation of excitatory synapses.
51 e the amplitude and short-term plasticity of excitatory synapses, a result not possible from activati
52 displayed a disturbed morphology of striatal excitatory synapses, accompanied by strongly increased g
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  CSP landscape and interactome of a specific excitatory synapse and reveal IgSF8 as a critical regula
57 levated, consistent with a higher density of excitatory synapses and altered synapse pruning.
58 nd that C1ql3-deficient mice exhibited fewer excitatory synapses and diverse behavioral abnormalities
59 ons with reduced SynGAP protein had stronger excitatory synapses and expressed synaptic activity earl
60                                              Excitatory synapses and fast-spiking properties matured
61 te these deletions in the neurophysiology of excitatory synapses and in ASD-associated synaptic impai
62 tes such as postsynaptic densities (PSDs) in excitatory synapses and in other dense protein meshworks
63 immediate-early gene (IEG) that functions at excitatory synapses and is required for learning and mem
64 ally diminished the ability of NLGN4 to form excitatory synapses and modulate their functional proper
65 hat knockdown of NP1 increases the number of excitatory synapses and neuronal excitability in culture
66 d ion channels that underlie transmission at excitatory synapses and play an important role in regula
67 s located at the postsynaptic compartment of excitatory synapses and plays a role in synapse formatio
68 d role for PNNs in restricting plasticity at excitatory synapses and raise the possibility of an earl
69 key regulator of learning-related changes in excitatory synapses and the acquisition of motor skills.
70 basic structural unit, or building block, of excitatory synapses and their number characterizes synap
71 one-derived ATP can pre-modulate efficacy of excitatory synapses and thereby can have an important ro
72 e encodes a postsynaptic scaffold protein in excitatory synapses, and its disruption is implicated in
73  NL2, the formation and function of cortical excitatory synapses are diminished, whereas inhibitory s
74                                  Frequently, excitatory synapses are formed on dendritic spines.
75     Although it has been proposed that these excitatory synapses are formed onto appendages resemblin
76  hippocampal synapses, but ELKS functions at excitatory synapses are not known.
77 ity mechanisms that decrease the strength of excitatory synapses are preferentially engaged to mainta
78 t the development of circuits containing CA2 excitatory synapses are sensitive to manipulations of th
79 e inhibitory synapses frequently recur while excitatory synapses are stable.
80 s in long-term potentiation (LTP) at central excitatory synapses are thought to contribute to cogniti
81  MNTB neurons through a single calyx of Held excitatory synapse arising from the cochlear nucleus.
82 ong-term depression (NMDA-LTD) at prefrontal excitatory synapses as a synaptic signature of this asso
83 lar and morphological diversity of 5 billion excitatory synapses at single-synapse resolution across
84 ely uniform following minimal stimulation of excitatory synapses at visualized locations along the de
85                                          The excitatory synapse between hippocampal CA3 and CA1 pyram
86 of the recurrent circuit using recordings of excitatory synapses between identified motoneuron and Re
87 amate receptors and induced the formation of excitatory synapses both in vitro and in vivo.
88 , the mGluR agonist did not generate eCBs at excitatory synapses but nevertheless induced burst firin
89 ndicate that both neuroligin-3 and -4 act at excitatory synapses but perform surprisingly distinct fu
90 autism mutation NLGN4-R704C also formed more excitatory synapses but with increased functional synapt
91 have been identified as the Ca(2+) sensor at excitatory synapses, but the Ca(2+) sensor(s) at inhibit
92                            Microglia control excitatory synapses, but their role in inhibitory neurot
93 ilitates a recruitment of P2X receptors into excitatory synapses by Ca(2+)-dependent mechanism.
94 t neuroligin-1 performs two key functions in excitatory synapses by distinct molecular mechanisms.
95 m synaptic potentiation at mouse hippocampal excitatory synapses by inactivating dendritic Kv1.1-cont
96  long-term depression (LTD) of glutamatergic excitatory synapses by increasing inhibitory inputs onto
97 5) is a major regulator in the maturation of excitatory synapses by interacting and trafficking N-met
98       Organization of signaling complexes at excitatory synapses by membrane-associated guanylate kin
99  is a form of synaptic plasticity induced at excitatory synapses by metabotropic glutamate receptors
100 reted glypican 4 induces formation of active excitatory synapses by recruiting AMPA glutamate recepto
101  beta-neurexins control synaptic strength in excitatory synapses by regulating postsynaptic 2-arachid
102 nd functional roles of MAGUKs at hippocampal excitatory synapses by simultaneous knocking down PSD-95
103 ion of spontaneous release at inhibitory and excitatory synapses by stochastic VACC activity that ext
104                                              Excitatory synapses can be potentiated by chemical neuro
105                                  While spiny excitatory synapses can be stable throughout adult life,
106  strength of inhibitory synapses relative to excitatory synapses can be tuned from weak to strong to
107 ors, co-localized with NMDA receptors in the excitatory synapses, can be activated by ATP co-released
108 nd chaperone levels, maintenance of striatal excitatory synapses, clearance of Htt aggregates and pre
109                                         Many excitatory synapses co-express presynaptic GABAA and GAB
110                 The postsynaptic proteome of excitatory synapses comprises 1,000 highly conserved pro
111 esent findings supporting a special role for excitatory synapses connecting pyramidal neurons of the
112                                         Many excitatory synapses contain high levels of mobile zinc w
113 hereby elevating the percentage of Homer1(+) excitatory synapses containing neurexin-1 nanoclusters f
114                                  We observed excitatory synapses contributed more to bursting behavio
115 chanisms for interrupting positive feedback, excitatory synapses could strengthen inexorably, corrupt
116 d short-term plasticity at dentate gyrus-CA3 excitatory synapses culminate in impaired coding of new
117            Lastly, astrocytic association of excitatory synapses decreases.
118 e caused specifically by inhibitory, but not excitatory, synapse defects.
119                               The density of excitatory synapses, defined by overlapping vesicular gl
120 g of cultured hippocampal neurons, decreased excitatory synapse density in vitro and in vivo, and abo
121 wledge, this is the first demonstration that excitatory synapse density is lower selectively on parva
122        We further show that Sema3G increased excitatory synapse density via neuropilin-2/PlexinA4 sig
123 xpression is activity dependent and supports excitatory synapse density.
124 ng Mef2a Mef2 proteins are key regulators of excitatory synapse density.
125                           The strength of an excitatory synapse depends on its ability to release glu
126  leads to long-term potentiation (LTP) at an excitatory synapse, derived from the posteromedial part
127 orn shortly after SE did not form functional excitatory synapses, despite robust sprouting.
128 hat MT3-MMP loss-of-function interferes with excitatory synapse development in dissociated cortical n
129 a previously unknown mechanism important for excitatory synapse development in the developing perinat
130 large body of accumulated evidence regarding excitatory synapse development, little is known about sy
131                Electrophysiology analysis of excitatory synapse development, starting at P12, showed
132 MMP-dependent shedding of NgR1 in regulating excitatory synapse development.SIGNIFICANCE STATEMENT In
133 age clamp is completely ineffective for most excitatory synapses due to spine electrical compartmenta
134 eins, STEP has been implicated in regulating excitatory synapses during plasticity and playing a role
135 ity, as well as with a transient increase in excitatory synapses during postnatal development.
136  corrects the development of thalamocortical excitatory synapses during the CP.
137                          Inhibitory, but not excitatory, synapse dysfunction underlies cortico-hippoc
138 mbospondin-1 (TSP1) in astrocytes, increased excitatory synapses, enhanced corticostriatal synaptic t
139               We show here that the cleft of excitatory synapses exhibits a distinct density profile
140      Thus, postsynaptic latrophilins promote excitatory synapse formation by simultaneous binding of
141                                              Excitatory synapse formation during development involves
142                               This increased excitatory synapse formation elevates network activity,
143 todomain of NgR1 is sufficient to accelerate excitatory synapse formation in dissociated cortical neu
144 s) with latrophilins (LPHNs/ADGRLs) promotes excitatory synapse formation when LPHNs simultaneously i
145 vitro, teneurin or FLRT alone did not induce excitatory synapse formation, whereas together they pote
146 e addition of purified hyaluronan suppresses excitatory synapse formation.
147 , and two-photon Ca(2+) imaging, we analyzed excitatory synapses formed by climbing fibers on Purkinj
148         Si1 also bilaterally potentiated the excitatory synapse from Si3 to Si2.
149                         Astrocytes depressed excitatory synapses from basolateral amygdala via A1 ade
150              Specifically, DE potentiated FF excitatory synapses from layer 4 (L4) to L2/3 in A1 and
151  from motor outputs, yet the efficacy of the excitatory synapses from single and converging motoneuro
152                   However, how OGT regulates excitatory synapse function is largely unknown.
153 ell-adhesion postsynaptic protein regulating excitatory synapse function, and show increased excitato
154 hare a common underlying neuropathy: altered excitatory synapse function.
155 addition and elimination were interpreted as excitatory synapse gain and loss, respectively.
156 nvolved a new ephaptic coupling, in which an excitatory synapse generated large negative extracellula
157                                           At excitatory synapses, glutamatergic receptors activated b
158 which, like neuroligin-1 is also targeted to excitatory synapses, had no comparable effect.
159                                           At excitatory synapses, how endogenous AMPARs, NMDARs, and
160                          Here, we propose an excitatory synapse hypothesis of depression in which chr
161 were used to quantify the number of putative excitatory synapses (i.e., the overlap of vesicular glut
162 ponse to action potentials, they differ from excitatory synapses in both structure and function.
163 ease, to be necessary for the development of excitatory synapses in cortical neurons.
164 toskeleton and gates long-term plasticity at excitatory synapses in cortical neurons.
165 orting evidence that dysfunction of multiple excitatory synapses in cortico-mesolimbic reward pathway
166 ically decreased neurotransmitter release at excitatory synapses in cultured cortical neurons.
167  a greater number of morphologically defined excitatory synapses in cultures containing these neurons
168  the hippocampus, and aberrant generation of excitatory synapses in dentate gyrus granule cells.
169 expression of Kal7 restores the reduction of excitatory synapses in HD cortical cultures.
170                               Severe loss of excitatory synapses in key brain regions is thought to b
171 xon 5 of Grin1 leads to an overproduction of excitatory synapses in layer 5 pyramidal neurons in the
172 f the readily releasable pool exclusively at excitatory synapses in mixed sex primary mouse hippocamp
173 e pathway, but did not change the density of excitatory synapses in primary visual cortex.
174 c regulation of miniature synaptic events at excitatory synapses in response to activity deprivation.
175 the protein densin-180 is highly enriched at excitatory synapses in the brain and enhances the cell s
176                              The majority of excitatory synapses in the brain exist on dendritic spin
177 nths) and that loud sounds reversibly modify excitatory synapses in the brain, changing synaptic func
178 mediate neurotransmission at the majority of excitatory synapses in the brain.
179 GTPase activating protein highly enriched at excitatory synapses in the brain.
180       Dendritic spines are the sites of most excitatory synapses in the CNS, and opposing alterations
181 hanced adenosine tone and A1R sensitivity at excitatory synapses in the dorsal horn after nerve injur
182 icroscopy shows that Cdh8 is concentrated at excitatory synapses in the dorsal striatum, and Cdh8 kno
183                                    Damage to excitatory synapses in the hippocampus occurs in associa
184 lone fully accounts for neurotransmission at excitatory synapses in the hippocampus, excluding a role
185 nt sex difference in molecular regulation of excitatory synapses in the hippocampus.
186 unts for the activation of NMDA receptors at excitatory synapses in the hippocampus.
187 duced and activity-dependent potentiation of excitatory synapses in the hippocampus.
188 in Nissl-stained sections so that numbers of excitatory synapses in the inner molecular layer per gra
189 croscopy was used to estimate the numbers of excitatory synapses in the inner molecular layer per hip
190 iled and quantitative map of the features of excitatory synapses in the lumbar spinal cord, detailing
191 pines are the postsynaptic terminals of most excitatory synapses in the mammalian brain.
192                                         Most excitatory synapses in the mammalian CNS are located on
193 e a morphological feature of the majority of excitatory synapses in the mammalian neocortex and are m
194   Here, we demonstrate that, whereas loss of excitatory synapses in the OB is transient after multipl
195                   Increases in the number of excitatory synapses in the superficial dorsal horn of Vc
196 pines are small postsynaptic compartments of excitatory synapses in the vertebrate brain that are mod
197 P2) is a postsynaptic scaffolding protein at excitatory synapses in which mutations and deletions hav
198 sion of inhibitory synapses, decreased it at excitatory synapses in WTs, but had no effect on eCB act
199  Rho-like small GTPases critical to maintain excitatory synapse, in the cortex of HD mice.
200 tion of dendritic spines, principal sites of excitatory synapses, in the motor cortex.
201  at a diverse set of identified and putative excitatory synapses, including a pair of connected neuro
202 , we report that SPARCL1 selectively induces excitatory synapses, increases their efficacy, and enhan
203 that is characterized by its localization at excitatory synapses, interactions with glutamate recepto
204                         Synaptic strength at excitatory synapses is determined by the presence of glu
205                       Glutamate secretion at excitatory synapses is tightly regulated to allow for th
206 (rMS) has been shown to induce plasticity of excitatory synapses, it is unclear whether rMS can also
207 ndent long-term potentiation (LTP) occurs at excitatory synapses made on some inhibitory neurons.
208   An anti-Hebbian form of LTP is observed at excitatory synapses made with some hippocampal interneur
209 al of hyaluronan increases the expression of excitatory synapse markers and results in a correspondin
210 l activation, BDNF-dependent increase in the excitatory synapse markers synaptophysin and PSD-95, and
211 rites together with reduced NMDAR content in excitatory synapses may be the cause.
212 tient antibodies do not alter the density of excitatory synapses, N-methyl-D-aspartate receptor (NMDA
213                                           At excitatory synapses, NLGN1 mediates transsynaptic bindin
214 sults indicate that NP1 negatively regulates excitatory synapse number by modulating neuronal excitab
215 r 2 (MEF2) transcription factors suppress an excitatory synapse number by promoting degradation of th
216  major, but not the minor, variant increased excitatory synapse number on PV interneurons and display
217                                      Because excitatory synapse number on PV interneurons is regulate
218          Mice lacking GRASP1 showed abnormal excitatory synapse number, synaptic plasticity, and hipp
219 l-derived neurons resulted in an increase in excitatory synapse numbers but a remarkable decrease in
220                During synaptic plasticity at excitatory synapses, numerous structural, signaling, and
221 perience-dependent homeostatic plasticity of excitatory synapses observed in superficial layers of vi
222 our results demonstrate that NPAS2 regulates excitatory synapses of D1R-MSNs in the NAc and cocaine r
223 ogether, PE leads to impaired eCB-LTD at the excitatory synapses of VTA DA neurons primarily due to C
224 -protein receptors (GPCRs) agonists enhanced excitatory synapses on direct pathway striatal spiny pro
225 neurons (dSPNs), whereas rapid production of excitatory synapses on indirect pathway neurons (iSPNs)
226 s, we describe a novel form of plasticity of excitatory synapses on inhibitory neurons, weight-depend
227 nges at both inhibitory synapses, as well as excitatory synapses on inhibitory neurons.
228 l cells, comparatively little is known about excitatory synapses on interneurons.
229 ding mouse primary visual cortex (V1), where excitatory synapses on layer 2/3 (L2/3) neurons undergo
230                    Drug-evoked plasticity at excitatory synapses on medium spiny neurons (MSNs) of th
231 ction in glutamate transport and potentiated excitatory synapses on medium spiny neurons.
232  for VTA glutamatergic neurons through local excitatory synapses on mesoaccumbens dopaminergic neuron
233 rd, and the first pathway shown to establish excitatory synapses on nAcc parvalbumin GABAergic intern
234 emonstrate that LH(PV) axons form functional excitatory synapses on neurons in the ventrolateral peri
235 hat neuroligin-3 specifies the properties of excitatory synapses on parvalbumin-containing interneuro
236                                              Excitatory synapses on PV interneurons are dependent on
237     Therefore, we tested the hypothesis that excitatory synapses on PV interneurons are pruned during
238 t ErbB4 splicing may regulate the pruning of excitatory synapses on PV interneurons during adolescenc
239 ng, we tested the hypothesis that pruning of excitatory synapses on PV interneurons is associated wit
240 h is known about the molecular properties of excitatory synapses on pyramidal cells, comparatively li
241                    Long-term potentiation of excitatory synapses on pyramidal neurons in the stratum
242 g fibers from the inferior olive make strong excitatory synapses onto cerebellar Purkinje cell (PC) d
243 ritic distributions of these corticocortical excitatory synapses onto CSPs in both areas also showed
244 ynaptic strength of ventral hippocampus (VH) excitatory synapses onto D1 medium spiny neurons (D1-MSN
245 st that microglia promote the development of excitatory synapses onto developing abGCs, which may imp
246                NRG1 enhanced the strength of excitatory synapses onto FS INs, which inhibited ocular
247 period timing by controlling the strength of excitatory synapses onto FS INs.
248 e model of Rett syndrome, we show that naive excitatory synapses onto hippocampal pyramidal neurons o
249  We confirm that the AON forms glutamatergic excitatory synapses onto piriform pyramidal neurons; and
250  (NMDAR) subunit composition and kinetics at excitatory synapses onto pyramidal cells; however, littl
251                                              Excitatory synapses onto somatostatin (SOM) interneurons
252 e, we tested synaptic plasticity of cortical excitatory synapses onto striatal spiny projection neuro
253 fibre axons (PFs) form approximately 180,000 excitatory synapses onto the dendritic tree of a Purkinj
254                       In the CA1 hippocampus excitatory synapses onto these cells comprise GluA2-lack
255                                         This excitatory synapse originates in secondary motor cortex,
256  the major postsynaptic elements of cortical excitatory synapses, our understanding of the synaptic o
257  In mature neurons AMPA receptors cluster at excitatory synapses primarily on dendritic spines, where
258 , PSD-95, and SAP102 differentially regulate excitatory synapse properties in the NAc.
259 itory synapses as well as the development of excitatory synapses received by these cells.
260 es where the postsynaptic components of most excitatory synapses reside.
261 c assemblies of Abeta peptide associate with excitatory synapses resulting in synapse elimination thr
262 at neurexin-1 forms discrete nanoclusters at excitatory synapses, revealing a novel organizational fe
263 ensures efficient Cav1.2 Ca(2+) signaling at excitatory synapses.SIGNIFICANCE STATEMENT The number an
264 ivity-dependent and independent processes to excitatory synapse size diversity, we studied glutamater
265               The extraordinary diversity of excitatory synapse sizes is commonly attributed to activ
266 m potentiation (LTP) and depression (LTD) of excitatory synapse strength require the Ca(2+)/calmoduli
267 have shown that Syngap1 regulates developing excitatory synapse structure and function, with loss-of-
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 ction is not seen at kappaORs at neighboring excitatory synapses, suggesting distinct time courses an
271 t neocortical inhibitory synapses but not at excitatory synapses, suggesting fundamental differences
272 ficant increase in the paired-pulse ratio at excitatory synapses, suggestive of a decrease in presyna
273                    However, in comparison to excitatory synapses, the structural and functional alter
274            Abeta triggers the elimination of excitatory synapses through a mechanism that requires NM
275 ermine which factors impact the diversity of excitatory synapses throughout the lumbar spinal cord.
276 lasticity may counteract runaway dynamics at excitatory synapses to inhibitory neurons imposed by Heb
277 ange coincides with increased sensitivity of excitatory synapses to monocular deprivation (MD).
278 city requires interactions with co-activated excitatory synapses to properly regulate excitatory-inhi
279            Individual ganglion cells receive excitatory synapses tuned to different orientations, but
280 rmissive for activity-dependent sculpting of excitatory synapses via the mechanism of NMDAR-dependent
281 ntaining NMDA receptors (NMDARs) at immature excitatory synapses, via a transcription-dependent mecha
282 e BDNF Val66Met polymorphism affects the CEm excitatory synapses, we examined basal glutamatergic syn
283  of proteins that are critical components of excitatory synapses were not associated with GABAARs.
284 (+) terminals forming asymmetrical (putative excitatory) synapses were dendritic spines, most of whic
285                     RNF10 is enriched at the excitatory synapse where it associates with the GluN2A s
286                  KCC2 is highly localized to excitatory synapses where it regulates spine morphogenes
287 an extracellular matrix surrounds developing excitatory synapses, where it critically regulates synap
288 me carries through to the molecular level at excitatory synapses, where protein function is controlle
289 folding proteins at the PSD in glutamatergic excitatory synapses, where they maintain and modulate sy
290 eptor (R) synaptic transmission, or silenced excitatory synapses, whereas more prolonged (24 hr) firi
291 ics, we studied AMPA receptor (AMPAR)-silent excitatory synapses, which are generated in the nucleus
292 a corresponding increase in the formation of excitatory synapses, while also decreasing inhibitory sy
293 all of the CPG neurons and made monosynaptic excitatory synapses with both Si3s.
294 ed with changes in the strength or number of excitatory synapses with MCs but was instead associated
295 hat RMS led to layer-specific elimination of excitatory synapses with the most pronounced loss observ
296 ons (OSNs) are chemoreceptors that establish excitatory synapses within glomeruli of the olfactory bu
297 ation generates AMPA receptor (AMPAR)-silent excitatory synapses within the basolateral amygdala (BLA
298                                              Excitatory synapses within the NAc undergo synaptic plas
299  of autoantibodies into the CNS, and loss of excitatory synapses within the olfactory bulb (OB).
300  ELKS, we find that ELKS enhances the RRP at excitatory synapses without affecting P.

 
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