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1 sing out of the climbing fiber-Purkinje cell synaptic clefts ().
2 ha-gamma sequence (counterclockwise from the synaptic cleft).
3 otransmission by removing serotonin from the synaptic cleft.
4 mission by removing their substrate from the synaptic cleft.
5 reasing the number of docked vesicles at the synaptic cleft.
6 on of small transmitter molecules across the synaptic cleft.
7 this molecule across the nascent and mature synaptic cleft.
8 connected by protein complexes spanning the synaptic cleft.
9 to enhanced release of acetylcholine in the synaptic cleft.
10 ium ions, removing neurotransmitter from the synaptic cleft.
11 ptotic serine proteases (granzymes) into the synaptic cleft.
12 vailability, both intracellularly and at the synaptic cleft.
13 serve to regulate GABA concentration in the synaptic cleft.
14 icantly alter activation of receptors in the synaptic cleft.
15 r inability to recruit lytic granules to the synaptic cleft.
16 se and the concentration of glutamate in the synaptic cleft.
17 clearance of excess neurotransmitters at the synaptic cleft.
18 y perform neurotransmitter reuptake from the synaptic cleft.
19 sulting in neurotransmitter release into the synaptic cleft.
20 motor neurons and then escorts it across the synaptic cleft.
21 otemporal profile of neurotransmitter in the synaptic cleft.
22 dulation of the extracellular pH in the cone synaptic cleft.
23 for coordinating signaling events across the synaptic cleft.
24 amount of neurotransmitter released into the synaptic cleft.
25 nduce transient depletion of Ca2+ within the synaptic cleft.
26 robes, consistent with alkalinization of the synaptic cleft.
27 ts of glutamate caused by spillover from the synaptic cleft.
28 glutamate, similar to transients within the synaptic cleft.
29 t of glutamate released per vesicle into the synaptic cleft.
30 s not rely on transmitter spillover from the synaptic cleft.
31 killing by confining cytotoxic agents to the synaptic cleft.
32 rker of changes in levels of dopamine in the synaptic cleft.
33 uptake of glutamate that diffuses out of the synaptic cleft.
34 s, the transporters clear glutamate from the synaptic cleft.
35 altering the flux of transmitter through the synaptic cleft.
36 sporter (DAT) to induce DA overflow into the synaptic cleft.
37 role in these processes on both sides of the synaptic cleft.
38 s, demonstrating the importance of an intact synaptic cleft.
39 ged because of pooling of transmitter in the synaptic cleft.
40 d permeation through ion channels facing the synaptic cleft.
41 phosphoproteins that clear dopamine from the synaptic cleft.
42 mbrane and discharge their contents into the synaptic cleft.
43 epinephrine, dopamine, or serotonin from the synaptic cleft.
44 chain, which is normally concentrated in the synaptic cleft.
45 eptors within the same synapse or across the synaptic cleft.
46 s a neuromodulator upon its release into the synaptic cleft.
47 lpha2, alpha4 and alpha5, are present in the synaptic cleft.
48 rfamily rapidly mediate signaling across the synaptic cleft.
49 of small-molecule neurotransmitters from the synaptic cleft.
50 sequence of events that can affect pH in the synaptic cleft.
51 in the regulation of glutamate levels in the synaptic cleft.
52 ents, but pronounced in glia surrounding the synaptic cleft.
53 o detect even a few molecules of GABA in the synaptic cleft.
54 xist, and that 5-HT escapes readily from the synaptic cleft.
55 can extend its actions beyond the immediate synaptic cleft.
56 ion and removal of neurotransmitter from the synaptic cleft.
57 he concentration profile of glutamate in the synaptic cleft.
58 a constant level of neurotransmitter at the synaptic cleft.
59 lly released glutamate can extend beyond the synaptic cleft.
60 brane by removing neurotransmitters from the synaptic cleft.
61 the synapse function to remove GABA from the synaptic cleft.
62 ric glycoprotein that is concentrated in the synaptic cleft.
63 delay in transmitting information across the synaptic cleft.
64 but remains elevated for longer than in the synaptic cleft.
65 ctivation of 5-HT after its release into the synaptic cleft.
66 forming trans-synaptic bridges spanning the synaptic cleft.
67 g's enhancement of available dopamine at the synaptic cleft.
68 cializations once dopamine diffuses from the synaptic cleft.
69 ed that transporters buffer glutamate in the synaptic cleft.
70 for the reuptake of biogenic amines from the synaptic cleft.
71 ad to spillover of neurotransmitter from the synaptic cleft.
72 to account for transmitter removal from the synaptic cleft.
73 the transmitter concentration profile in the synaptic cleft.
74 ion from multiple release sites into a large synaptic cleft.
75 on and reuptake of neurotransmitter from the synaptic cleft.
76 ly, blocks neurotransmitter release into the synaptic cleft.
77 anized by the basal lamina that occupies the synaptic cleft.
78 by failing to clear excess glutamate at the synaptic cleft.
79 minants of a slow "tail" of glutamate in the synaptic cleft.
80 ferent and creates resistive coupling at the synaptic cleft.
81 y of the neurotransmitter glutamate from the synaptic cleft.
82 ibition and increased dopamine levels in the synaptic cleft.
83 d permeation through ion channels facing the synaptic cleft.
84 aptic glutamate receptor proteins across the synaptic cleft.
85 some polarization and actin clearance at the synaptic cleft.
86 heir presynaptic partner neurexin across the synaptic cleft.
87 g kinetics and motion, and fluid flow in the synaptic cleft.
88 responsible for acetylcholine release to the synaptic cleft.
89 adhesive proteins, and the fluid flow in the synaptic cleft.
90 ing within the brain occurs across the 20-nm synaptic cleft.
91 lecules and intercellular signals across the synaptic cleft.
92 ed uptake and clearance of dopamine from the synaptic cleft.
93 e removal of excitatory amino acids from the synaptic cleft.
94 a(+)-dependent removal of glutamate from the synaptic cleft.
95 neurotransmitters, such as glutamate, in the synaptic cleft.
96 ion via rapid reuptake of serotonin from the synaptic cleft.
97 form when activated by ACh released into the synaptic cleft.
98 e and/or recycling of neurotransmitters from synaptic clefts.
99 any place within or immediately surrounding synaptic clefts.
100 ble for the rapid clearance of dopamine from synaptic clefts.
101 plays a major role in glutamate clearance in synaptic clefts.
102 structure, and (4) morphological changes in synaptic clefts.
103 ion of the contents of the vesicles into the synaptic cleft (a process known as exocytosis), the vesi
104 er glutamate concentration transients in the synaptic cleft, a result indicative of MVR, and suggests
110 neural synapses share properties such as the synaptic cleft, adhesion molecules, stability, and polar
112 ptake of 5-hydroxytryptamine (5-HT) from the synaptic cleft after release from serotonergic neurons.
113 eft protons involved in HC feedback but that synaptic cleft alkalization during light-evoked hyperpol
114 ensity that was aligned with a 17-20 nm-wide synaptic cleft and a thicker post-synaptic density.
115 he CA1 region of the hippocampus escapes the synaptic cleft and activates extrasynaptic targets; it a
116 released at one synapse can escape from the synaptic cleft and affect receptors at other synapses ne
117 cy is that NMDARs are located outside of the synaptic cleft and are activated only when extrasynaptic
118 diate reuptake of neurotransmitters from the synaptic cleft and are targets for several therapeutics
119 ) control neurotransmitter levels within the synaptic cleft and are the site of action for amphetamin
120 icles release their acidic contents into the synaptic cleft and chronically during ischemia and seizu
121 ntitative assessment of zinc dynamics in the synaptic cleft and clarify its role in the regulation of
122 n) increases serotonin (5-HT) content in the synaptic cleft and exerts anorexigenic effects in animal
126 The concentration of transmitter in the synaptic cleft and its clearance time are one of the mai
127 we investigate the substrate uptake from the synaptic cleft and its release in the intracellular medi
128 ponsible for clearance of glutamate from the synaptic cleft and loss of EAAT2 has been previously rep
129 ial cells enhanced residual glutamate in the synaptic cleft and markedly increased the extent of depr
131 ime, glutamate release can spill outside the synaptic cleft and possibly stimulate extrasynaptic NMDA
132 AChE is clustered by the collagen Q in the synaptic cleft and prevents the repetitive activation of
133 of the neurotransmitter dopamine (DA) in the synaptic cleft and recycles DA for storage in the presyn
134 s a lower concentration than attained in the synaptic cleft and remains elevated in the extrasynaptic
135 to be in the process of withdrawing from the synaptic cleft and some boutons were fully enwrapped in
136 hip between adhesive interactions across the synaptic cleft and synaptic function has remained elusiv
137 coupling the glutamate concentration in the synaptic cleft and the ATP hydrolysis, thus accounting f
138 ning the amount of glutamate efflux from the synaptic cleft and the distance it diffuses is critical
139 ctors, including the detailed anatomy of the synaptic cleft and the time course of transmitter cleara
140 the diffusion of neurotransmitters from the synaptic cleft and the volume transmission of transmitte
141 utamate is transported postsynaptically from synaptic clefts and increased lactate availability for n
142 leased from climbing fiber terminals escapes synaptic clefts and reaches glial membranes shortly afte
143 sine triphosphate (ATP) is secreted into the synaptic cleft, and a 48 kDa/50 kDa protein duplex becom
144 is expressed neuronally and detected in the synaptic cleft, and is required to form the specialized
145 tions in the extracellular space outside the synaptic cleft, and neither the origin nor the function
146 nal signaling by rapid NE clearance from the synaptic cleft, and NET is a target for cocaine and amph
147 of synapses, the presynaptic nerve terminal, synaptic cleft, and postsynaptic specialization form a t
148 , Schwann cell processes were present in the synaptic cleft, and secondary folds were often misaligne
149 tates, variance of GABA concentration in the synaptic cleft, and some of the presynaptic factors regu
151 afferent could also elevate potassium in the synaptic cleft, and would depolarize other hair cells en
152 ts in docked vesicles presynaptically, wider synaptic clefts, and simpler secondary folds postsynapti
153 s, in which elementary modules that span the synaptic cleft are added or removed as a function of exp
154 ers, which act to clear transmitter from the synaptic cleft, are regulated by multiple second messeng
156 king of signaling components to and from the synaptic cleft, as well as in the directed delivery and
157 is to facilitate cytokine secretion into the synaptic cleft, as well as provide important insights in
158 with respect to ionotropic receptors to the synaptic cleft, as well as regulate glutamate levels in
159 -serine (and possibly glycine) levels in the synaptic cleft, Asc-1 may play an important role in cont
161 show that laminin beta2, a component of the synaptic cleft at the neuromuscular junction, binds dire
163 ls, are actively inhibited from entering the synaptic cleft between the motor nerve terminal and the
166 plete clearance of neurotransmitter from the synaptic cleft between vesicle-fusion events need not be
167 at cholinergic synapses, was present in the synaptic clefts between the retinotopic units and along
168 peptide-MHC directly exporting TCR into the synaptic cleft, but incorporation of other effectors is
170 heir neurotransmitter content fully into the synaptic cleft by flattening out and becoming part of th
172 ) control the glutamate concentration in the synaptic cleft by glial and neuronal glutamate uptake.
175 itter in the CNS, and it is removed from the synaptic cleft by sodium-dependent glutamate transport a
176 ntral nervous system and is removed from the synaptic cleft by sodium-dependent glutamate transporter
177 y of proteins that remove glutamate from the synaptic cleft by transporting it into surrounding glial
178 amics and kinetics of protein binding in the synaptic cleft can describe the short-time formation and
179 riments suggesting that acidification of the synaptic cleft can reduce Ca2+ channel activity and ther
180 in increased acetylcholine levels within the synaptic cleft causing loss of muscle control, seizures,
181 hibitory interaction between glial cells and synaptic cleft components may contribute to synaptic rea
182 recent reports have suggested that the peak synaptic cleft concentration of the inhibitory neurotran
183 mbrane adhesion molecules interlinked in the synaptic cleft, connected via their intracytoplasmic dom
184 Next, we simulated diffusion of GABA in the synaptic cleft, constrained by previous electron microsc
185 portion of the muscle's BL that occupies the synaptic cleft contains at least three alpha chains and
186 that a higher glutamate concentration in the synaptic cleft contributes to the large size of mEPSCs.
189 variations of glutamate concentration in the synaptic cleft (Deltaq), and differences in the potency
190 t included diffusion of glutamate within the synaptic cleft, different kinetic properties of AMPA and
191 t that the concentration of glutamate in the synaptic cleft does not attain levels previously suggest
192 synaptic terminal to shape the extracellular synaptic cleft domain, and that the cleft domain functio
193 smission, suggesting an acidification of the synaptic cleft due to the corelease of neurotransmitter
194 ince the Zn2+ concentrations released in the synaptic cleft during excitatory synaptic activity are s
195 increased endogenous endocannabinoids in the synaptic cleft during high frequency, but not low, TS st
198 ease their neurotransmitter content into the synaptic cleft, eliciting a response in the postsynaptic
199 igin (NLG), which bind each other across the synaptic cleft, enabled sensitive visualization of synap
200 omeostatic concentration of glutamate in the synaptic cleft ensures a correct signal transduction alo
201 ically secreted Mind the gap (Mtg) molds the synaptic cleft extracellular matrix, leading us to hypot
205 , a significant amount of variability in the synaptic cleft GABA transient had to be present to accou
206 ion of this presynaptic GPCR lowers the peak synaptic cleft glutamate concentration independently of
207 ebellum was not associated with changes in a synaptic cleft glutamate transient, indicating that this
212 th changes in glutamate concentration in the synaptic cleft, indicating that single synapses can rele
215 ules and assemble with each other across the synaptic cleft into a specific, transsynaptic SynCAM 1/2
217 e of the neurotransmitter glutamate from the synaptic cleft into the cytoplasm of glia and neuronal c
218 at catalyse neurotransmitter uptake from the synaptic cleft into the cytoplasm of glial cells and neu
219 he level of neurotransmitters present in the synaptic cleft is a function of the delicate balance amo
220 Once released, its rapid removal from the synaptic cleft is critical for preventing excitotoxicity
223 neurotransmitter norepinephrine (NE) in the synaptic cleft is insufficient to maintain blood pressur
227 The reduced rate of GABA clearance from the synaptic cleft is probably responsible for the slower de
230 inally isolated from the basal lamina of the synaptic cleft, is synthesized and secreted by motoneuro
231 redicted to result in dopamine excess in the synaptic cleft, it likely also causes depletion of presy
232 circular canal epithelia, the [K(+) ] in the synaptic cleft ([K(+) ](c) ) contributes to setting the
233 odulating the potassium concentration in the synaptic cleft, [K(+) ](c) , which regulates potassium-s
234 hat neurotransmission itself can acidify the synaptic cleft, likely due to the corelease of protons a
235 ations in the glutamate concentration in the synaptic cleft may change the apparent unitary conductan
236 , which would reduce serotonin levels in the synaptic cleft, may cause or contribute to the increase
237 show that potassium ions accumulating in the synaptic cleft modulated membrane potentials and extende
238 hese sites, receptors not located within the synaptic cleft must be activated by transmitter that dif
239 d neither by depletion of Ca2+ ions from the synaptic cleft nor by metabotropic feedback inhibition,
240 se results suggest that acidification of the synaptic cleft occurs physiologically during GABAergic t
243 ted the localization of ectopic Nxph1 at the synaptic cleft of excitatory synapses in transgenic mice
244 Adenosine triphosphate is released into the synaptic cleft of the neuromuscular junction during norm
246 We found that this enzyme is located in synaptic clefts of L-neurons in both of the brain region
249 outons and on their surfaces, but not in the synaptic clefts or in their immediate vicinity, a distri
250 ther neurotransmitters are restricted to the synaptic cleft (participating only in hard-wired neurotr
251 (HCs) to photoreceptors involves changes in synaptic cleft pH accompanying light-evoked changes in H
252 els, our data support earlier proposals that synaptic cleft pH changes are more likely responsible.
254 We also examined mechanisms for changing synaptic cleft pH in response to changes in HC membrane
255 ibitory feedback from HCs involve changes in synaptic cleft pH that modulate photoreceptor calcium cu
256 domain (NTD), which projects midway into the synaptic cleft, plays a fundamental role in this process
257 -H(+) exchangers are the principal source of synaptic cleft protons involved in HC feedback but that
259 e widening and accumulation of debris in the synaptic cleft, resulting in loss of efficacy of release
261 sion behavior indicates that sQDs access the synaptic clefts significantly more often than commercial
263 nervous system, including regulation of the synaptic cleft structure and neuroprotection against inj
264 cytic processes are sometimes present at the synaptic cleft, suggesting that they might act directly
268 y result in a transient acidification of the synaptic cleft that can block Ca(2+) channels located cl
269 requires bidirectional signaling across the synaptic cleft that directs the differentiation of pre-
270 strate the proteomic characterization of the synaptic clefts that exist at both excitatory and inhibi
271 antity of neurotransmitter released into the synaptic cleft, the reliability with which it is release
272 ) to block the removal of serotonin from the synaptic cleft, thereby enhancing serotonin signals.
273 This contrasts with the concentration in the synaptic cleft, thought to rapidly rise above 1 mM, but
274 CR regulates the profile of glutamate in the synaptic cleft through altering the mechanism of vesicle
276 he reuptake of the neurotransmitter from the synaptic cleft, thus controlling the glutamate concentra
278 sequently transfer these trophins across the synaptic cleft to afferent synapses (transsynaptic trans
280 amate transporters remove glutamate from the synaptic cleft to maintain efficient synaptic communicat
281 amate transporters remove glutamate from the synaptic cleft to maintain efficient synaptic communicat
282 by which horizontal cells control pH in the synaptic cleft to modulate photoreceptor neurotransmitte
283 actions assemble SynCAM complexes within the synaptic cleft to promote synapse induction and modulate
284 e for reuptake of neurotransmitters from the synaptic cleft to terminate a neuronal signal and enable
286 sponsible for removing excess glutamate from synaptic clefts to prevent excitotoxic neuronal death.
288 ter hEAAT1, which removes glutamate from the synaptic cleft via stoichiometrically coupled Na(+)-K(+)
289 and temporal activity of DA release into the synaptic cleft via the rapid reuptake of DA into presyna
290 tic density (a measure for synaptic size and synaptic cleft volume) nor with the total number of SVs
291 sporters in clearing free glutamate from the synaptic cleft was studied in rat CA1 hippocampal neuron
292 rgmann glial membranes are excluded from the synaptic cleft, we propose that exocytosis can occur fro
293 imulation, synaptic zinc diffuses beyond the synaptic cleft where it inhibits extrasynaptic NMDARs.
294 stimulates the release of glutamate into the synaptic cleft, where it activates postsynaptic glutamat
295 AChE is anchored to the basal lamina of the synaptic cleft, where it hydrolyzes acetylcholine to ter
296 In adults, alpha4 is restricted to primary synaptic clefts whereas alpha5 is present in both primar
297 idly removed by reuptake before escaping the synaptic cleft, whereas increased population activity mo
298 flets and reduced astrocyte contact with the synaptic cleft, which consequently boosted extrasynaptic
299 ransmitter-filled vesicles released into the synaptic cleft with each action potential dictates the r
300 stsynaptic receptors and is cleared from the synaptic cleft within a few milliseconds by diffusion an