ライフサイエンスコーパス: synaptic strength

1 short-term plasticity dynamically modulates synaptic strength.

2 ipid-dependent control of C1-C2B to modulate synaptic strength.

3 n important synaptic plasticity that weakens synaptic strength.

4 e constants, and reduced GlyR clustering and synaptic strength.

5 , and that conversion level is correlated to synaptic strength.

6 es in the NMDAR to changes in spine size and synaptic strength.

7 AMPA-type glutamate receptors in the PSD and synaptic strength.

8 he role of these vesicular SNAREs in setting synaptic strength.

9 t the postsynaptic density (PSD) to regulate synaptic strength.

10 input, enabling optical readout of relative synaptic strength.

11 to excitatory contacts had little effect on synaptic strength.

12 recordings from the IHCs to measure efferent synaptic strength.

13 ng activity-dependent plasticity to increase synaptic strength.

14 onsolidation and extinction by altering T-LA synaptic strength.

15 t is a presynaptic, long-lasting increase in synaptic strength.

16 rane AMPAR-associated protein that regulates synaptic strength.

17 TP induction but also for the maintenance of synaptic strength.

18 ability in population size, pulse timing and synaptic strength.

19 ization at synapses to regulate function and synaptic strength.

20 , such as receptors, can dramatically change synaptic strength.

21 t cell firing requires a critical inhibitory synaptic strength.

22 nism regulating such long-lasting changes in synaptic strength.

23 ade signaling plays a key role in regulating synaptic strength.

24 s important for the regulation of excitatory synaptic strength.

25 receptors that can be recruited to modulate synaptic strength.

26 osis (CME) is a key mechanism for regulating synaptic strength.

27 lso mediates the more elusive maintenance of synaptic strength.

28 tsynaptic density (PSD) determine excitatory synaptic strength.

29 hodiesterases (PDEs) potential regulators of synaptic strength.

30 e thought to result from specific changes in synaptic strength.

31 or density is a major variable in regulating synaptic strength.

32 t molecular mechanisms to maintain increased synaptic strength.

33 njunction with long-term depression (LTD) of synaptic strength.

34 s, providing a rationale for the increase in synaptic strength.

35 synaptic plasticity that results in enhanced synaptic strength.

36 id receptors (AMPARs) in synapses determines synaptic strength.

37 iated with changes in gamma oscillations and synaptic strength.

38 ses is an important mechanism for regulating synaptic strength.

39 y synapses, where they maintain and modulate synaptic strength.

40 y that was largely responsible for increased synaptic strength.

41 roles for UNC-43/CaMKII in the regulation of synaptic strength.

42 correlated activity patterns into changes in synaptic strength.

43 s and transduce it to homeostatic changes in synaptic strength.

44 ic loss of surface AMPARs and downscaling of synaptic strength.

45 ing recorded in vivo retrogradely influences synaptic strength.

46 s is thought to allow nonlinear summation of synaptic strength.

47 fusion, is a powerful mechanism to regulate synaptic strength.

48 ays a post-developmental role in suppressing synaptic strength.

49 ts that have previously been associated with synaptic strength.

50 wake) leads to widespread reductions in net synaptic strength.

51 s global neurotransmitter output to maintain synaptic strength.

52 synapse numbers but a remarkable decrease in synaptic strength.

53 to stabilize and tune both local and global synaptic strength.

54 frequency (1-4 Hz) may correlate with local synaptic strength.

55 regulated to allow for the precise tuning of synaptic strength.

56 id body axon terminals, resulting in reduced synaptic strength.

57 ostsynaptic action potentials and inhibitory synaptic strength.

58 monitoring energy balance through changes in synaptic strength.

59 neurotransmitter release to restore baseline synaptic strength.

60 y as a novel therapeutic strategy to restore synaptic strength.

61 lization of rewarded STDP and hard limits on synaptic strength.

62 verning cell-class-specific connectivity and synaptic strengths.

63 gnormally distributed, similar to reports of synaptic strengths.

64 associated with homeostatic scaling down of synaptic strengths.

65 reveal a rMS-induced reduction in GABAergic synaptic strength (2-4 h after stimulation), which is Ca

66 plicated in the modulation and regulation of synaptic strength, activity, maturation, and axonal rege

67 l cells typically show very small changes in synaptic strength after a pair of presynaptic and postsy

68 s highly plastic, and, therefore, changes in synaptic strength after learning can change the balance

69 p has been hypothesized to rebalance overall synaptic strength after ongoing learning during waking l

70 s stem from its ability to renormalize total synaptic strength, after ongoing learning during wake le

71 absence of cocaine triggered a reduction in synaptic strength akin to that observed with cocaine, an

72 Homeostatic regulation of synaptic strength allows for maintenance of neural activ

73 A decreasing gradient of mossy fiber synaptic strength along the proximodistal axis is mirror

74 A similar activity-dependent reduction in synaptic strength also occurs in the developing brain an

75 NMDA receptors, which regulate synaptic strength and are implicated in learning and mem

76 Astrocytes can control basal synaptic strength and arteriole tone via their resting C

77 (AMPARs) are among the major determinants of synaptic strength and can be trafficked into and out of

78 embryonic spinal cord functions to maintain synaptic strength and challenge the view that scaling ac

79 t not GABAergic, neurons exhibit an enhanced synaptic strength and changes in short-term plasticity b

80 e many forms of brain plasticity, changes in synaptic strength and changes in synapse number are part

81 ver, principles relating gamma oscillations, synaptic strength and circuit computations are unclear.

82 ns between them are important to controlling synaptic strength and circuit functions.

83 Changes in synaptic strength and connectivity are thought to be a m

84 genous activation of CB1Rs modifies afferent synaptic strength and coordinated downstream network sig

85 ation proposes a homeostatic increase in net synaptic strength and cortical excitability along with d

86 cell labeling, we identified an increase of synaptic strength and dendritic spine density specifical

87 tive drug use causes long-lasting changes in synaptic strength and dendritic spine morphology in the

88 lized translation in neurites helps regulate synaptic strength and development.

89 sms by which stress increases amygdala-dmPFC synaptic strength and generates anxiety-like behaviors a

90 ypeptide 38 (PACAP38) alters hippocampal CA1 synaptic strength and GluA1 synaptic localization, its e

91 Npas2 blocked cocaine-induced enhancement of synaptic strength and glutamatergic transmission specifi

92 stimulation, conventionally used to monitor synaptic strength and induce long-term potentiation (LTP

93 mGluR-LTD reduces synaptic strength and is relevant to learning and memory

94 or (NMDAR) stimulation causes a reduction in synaptic strength and is the central mechanism for long-

95 evented the injury-related loss of basal CA1 synaptic strength and key synaptic proteins and reduced

96 ic factor (BDNF), a key player in regulating synaptic strength and learning, is dysregulated followin

97 on synaptic proteins is a major regulator of synaptic strength and long-term plasticity, suggesting t

98 On the other hand, basal synaptic strength and LTP were not affected in slices fr

99 olecular indices to non-invasively study net synaptic strength and LTP-like plasticity in humans afte

100 ce for independent circadian oscillations in synaptic strength and morphology.

101 smitter receptors is crucial for determining synaptic strength and plasticity, but the underlying mec

102 role in postsynaptic protein scaffolding and synaptic strength and plasticity.

103 iverse ways by which HCN1 channels influence synaptic strength and plasticity.

104 synaptic densities and a potent regulator of synaptic strength and plasticity.

105 by clathrin-mediated endocytosis can control synaptic strength and plasticity.

106 ic cocaine use is associated with changes in synaptic strength and resistance to the induction of syn

107 ma 1A, to the Dscam2-dependent regulation of synaptic strength and show that changes in phosphoinosit

108 If so, because synaptic strength and size are correlated, synapses on a

109 ses and play an important role in regulating synaptic strength and stability.

110 We show here that developmental changes in synaptic strength and synaptic plasticity properties at

111 he sensory neuron, is sufficient to increase synaptic strength and that this activity is not isoform-

112 Because evaluation of the determinants of synaptic strength and the extent of connectivity constit

113 ion in PE animals led to enhanced excitatory synaptic strength and the induction of CP-AMPAR-dependen

114 Basal synaptic strength and the maximal attainable t-LTP magni

115 We find that the synaptic strength and timing of excitatory and inhibitor

116 Our study illustrated that the synaptic strength and timing of inhibition relative to e

117 cally adapt to external stimuli and regulate synaptic strength and ultimately network function.

118 follows sensory loss results from changes in synaptic strength and/or unmasking of subthreshold inter

119 works, including homeostatic effects on both synaptic strengths and firing rates.

120 gree of order in the spatial distribution of synaptic strengths and indicates that the relationship b

121 surface AMPARs, dendritic spine density, and synaptic strength, and also alters synaptic plasticity.

122 ion, the resulting enhancement in excitatory synaptic strength, and CP-AMPAR-dependent LTP are simila

123 Abeta-induced reductions in surface AMPARs, synaptic strength, and dendritic spine density.

124 r glutamate, AMPA receptors are critical for synaptic strength, and dysregulation of AMPA receptor-me

125 ion of synapse activity, enhanced excitatory synaptic strength, and early onset of neural network act

126 ol esters and tetanic stimulation potentiate synaptic strength, and lower the energy barrier equally

127 luding regulation of synaptic communication, synaptic strength, and nerve regeneration.

128 o attenuated changes in dendrite morphology, synaptic strength, and NMDAR-dependent responses.

129 tor antagonist messenger RNA, alterations in synaptic strength, and noradrenaline-dependent and persi

130 that synaptic Munc18-1 levels correlate with synaptic strength, and that synapses that recruit more M

131 nt of network excitability and regulation of synaptic strength are both implicated in the homeostatic

132 Bidirectional changes of synaptic strength are crucial for the encoding of new me

133 nt bidirectional modifications of excitatory synaptic strength are essential for learning and storage

134 Dynamic changes in synaptic strength are thought to be critical for higher

135 triatal output, particularly at the level of synaptic strength, are unclear.

136 ecific and spine type-specific comparison of synaptic strength at a single spine level between cocain

137 1 currents and channel numbers and increased synaptic strength at both developmental stages examined.

138 Synaptic strength at excitatory synapses is determined b

139 The regulation of synaptic strength at gamma-aminobutyric acid (GABA)-ergi

140 uncaging and whole-cell recording to examine synaptic strength at individual spines on two distinct t

141 Susceptible mice exhibited increased synaptic strength at intralaminar thalamus (ILT), but no

142 silient animals displayed an upregulation of synaptic strength at large mushroom spines of D1-MSNs an

143 GABA(B) R activation reduced the synaptic strength at P4 and P11.

144 el is associated with transient increases in synaptic strength at prefrontal cortex synapses in the n

145 it remains challenging to connect changes in synaptic strength at specific neural pathways to specifi

146 hat dopamine depletion selectively decreased synaptic strength at thalamic inputs to dMSNs, suggestin

147 How MAGUKs underlie synaptic strength at the molecular level is still not we

148 They mediate enhanced synaptic strength at the onset of burst-like activity, t

149 -timing-dependent plasticity (STDP) modifies synaptic strengths based on the relative timing of pre-

150 Long-term potentiation (LTP) of synaptic strength between hippocampal neurons is associa

151 the rat is sufficient to rapidly facilitate synaptic strength between primary afferent C-fibers and

152 -state propagation determines the changes of synaptic strengths between neurons.

153 y-expressed GABA(B)R decreases glutamatergic synaptic strength by engaging a non-canonical signaling

154 udies have shown that PE enhances excitatory synaptic strength by facilitating an anti-Hebbian form o

155 ocampal brain slices significantly increased synaptic strength by increasing functional synapses.

156 , a form of Hebbian plasticity, both enhance synaptic strength by increasing the abundance of postsyn

157 ne, a key striatal neuromodulator, increases synaptic strength by promoting surface insertion and/or

158 3, the C. elegans homolog of CaMKII, control synaptic strength by regulating motor-driven AMPAR trans

159 t can be converted into long-term changes in synaptic strength by reward-linked neuromodulators.

160 ults showed that the persistent reduction of synaptic strength by transient application of 20 mum tat

161 levels in the AZ are not saturated and that synaptic strength can be modulated by increasing Ca(V)2.

162 Alterations in synaptic strength can result from modulation of AMPA rec

163 duces a selective increase in the excitatory synaptic strength, characterized by enhanced synchronous

164 y strong input, followed by the decrement in synaptic strength coinciding with the pruning of climbin

165 NCE STATEMENT: Activity-dependent changes in synaptic strength constitute a basic mechanism for memor

166 hat there is a minimum of 26 distinguishable synaptic strengths, corresponding to storing 4.7 bits of

167 zation of AMPARs and reduces corticostriatal synaptic strength, dephosphorylates DARPP-32 and GluA1,

168 tatic mechanisms can be harnessed to restore synaptic strength despite C9orf72 pathogenesis.

169 o illuminate three mechanisms that stabilize synaptic strength despite major disparities in synaptic

170 urrents between neuron types can explain why synaptic strength does not predict firing reliability/in

171 ynapses is a major mechanism for controlling synaptic strength during homeostatic scaling in response

172 ction is a fundamental mechanism controlling synaptic strength during long-term potentiation/depressi

173 operties and trafficking events that control synaptic strength during NMDA receptor-dependent synapti

174 ptor activation, and contributes to adapting synaptic strength during plasticity and neuromodulation.

175 is offset by a homoeostatic reduction in net synaptic strength during sleep.

176 y expressed afferent CB1Rs regulate afferent synaptic strength during synaptogenesis, which enables c

177 s hypothesis, has emphasized the increase in synaptic strength during waking, and compensatory downsi

178 me system (UPS), which is known to influence synaptic strength, dynamically regulates Tomo-1 protein

179 We derive an expression for the synaptic strength dynamics showing that, by mapping the

180 dendrites, impairing synaptic plasticity and synaptic strength, even when Na(V)1.2 expression was dis

181 As a result, synaptic strength exceeds acceptable levels and damages

182 One homeostatic response is the increase in synaptic strength following a chronic block of activity.

183 How neurons stabilize their overall synaptic strength following conditions that alter synapt

184 tex that incorporates heterogeneity of local synaptic strengths, following a hierarchical axis inferr

185 These results were confirmed by decreased synaptic strength from sensory, but not from contralater

186 Enhanced synaptic strength from the intact cortex via the corpus

187 Rapid frequency-dependent changes in synaptic strength have key roles in sensory adaptation,

188 at spontaneous release functions to regulate synaptic strength homeostatically in vivo SIGNIFICANCE S

189 The DG ligand agrin increases GABAergic synaptic strength in a DG-dependent manner that mimics h

190 pool size and release probability normalize synaptic strength in a hierarchical fashion upon acute p

191 long-term depression (DCS-LTD) of excitatory synaptic strength in both human and mouse neocortical sl

192 nd activity-dependent neuromodulation alters synaptic strength in both male and female brains, yet fe

193 Changes in glutamatergic synaptic strength in brain are dependent on AMPA-type gl

194 fine the isoform specificity for maintaining synaptic strength in distinct facilitation paradigms.

195 gest that presynaptic beta-neurexins control synaptic strength in excitatory synapses by regulating p

196 of cocaine-dependent increases in NAc shell synaptic strength in male mice.

197 that, despite similar magnitude increases in synaptic strength in males and females, the roles of cAM

198 e C (PKC), can maintain long-term changes in synaptic strength in many systems, including the hermaph

199 mulation of heart cells, and potentiation of synaptic strength in neurons.

200 Augmentation of synaptic strength in nociceptive pathways represents a c

201 ptor (GLP-1R) activation augments excitatory synaptic strength in PVN corticotropin-releasing hormone

202 aptic currents, exhibits enhanced excitatory synaptic strength in pyramidal cells that is induced pos

203 presynaptic Ca(2+) levels to maintain stable synaptic strength in response to diverse challenges, wit

204 lead to homeostatic adaptation of excitatory synaptic strength in sensory cortices.

205 and quantal size were unaltered, the reduced synaptic strength in the absence of Cplx1 is most likely

206 ates activity-dependent long-term changes of synaptic strength in the CNS.

207 Therefore, we examined synaptic strength in the DH during prolonged abstinence

208 mechanisms underlying persistent changes in synaptic strength in the hippocampus, specifically long-

209 rimarily by evoking changes in glutamatergic synaptic strength in the mesocorticolimbic dopamine circ

210 ated cocaine exposure in vivo does not alter synaptic strength in the mouse prefrontal cortex during

211 ne activates a signaling cascade that alters synaptic strength in the NAc shell and triggers a behavi

212 elf promoted reinstatement and depotentiated synaptic strength in the NAc shell.

213 e of memory does not lead to a net change in synaptic strength in the ventral hippocampal output to t

214 J and utilized several approaches to restore synaptic strength in this model.

215 ich could be mediated by enhanced excitatory synaptic strength in ventral tegmental area (VTA) dopami

216 and the maintenance of augmented excitatory synaptic strength in VTA DA neurons and increased addict

217 Increased excitatory synaptic strength in VTA DA neurons is a critical cellul

218 st that, in PE animals, increased excitatory synaptic strength in VTA DA neurons might be susceptible

219 lt in the maintenance of enhanced excitatory synaptic strength in VTA DA neurons, which in turn contr

220 ondeterministic neuronal spiking and dynamic synaptic strengths in a randomly connected network are s

221 the essential homeostatic task of modifying synaptic strengths in the opposite direction of the acti

222 nge through activity-dependent modulation of synaptic strength, in older animals may augment TBI-indu

223 ts neighbors) and Hebbian learning (in which synaptic strength, in this case divisive normalization,

224 ic plasticity to induce long-term changes in synaptic strength, including long-term potentiation (LTP

225 function of sleep is to renormalize overall synaptic strength increased by wake.

226 now demonstrate that glial cells can control synaptic strength independent of neuronal activity.

227 egative feedback response to fluctuations in synaptic strength induced by developmental or learning-r

228 gly, we show that homeostatic downscaling of synaptic strength is accompanied by an increase and decr

229 In a presynaptic nerve terminal, synaptic strength is determined by the pool of readily r

230 t has been known for more than 70 years that synaptic strength is dynamically regulated in a use-depe

231 mice, RIM1/2 protein levels are reduced and synaptic strength is impaired.

232 In sharp contrast, alteration of inhibitory synaptic strength is independent of postsynaptic activat

233 minals grow and retract throughout life, yet synaptic strength is maintained within stable physiologi

234 Although it is known that inhibitory synaptic strength is malleable, induction of long-term p

235 This enhanced synaptic strength is mediated by a long-lasting increase

236 Synaptic strength is modulated by multiple factors inclu

237 hereas the spaced 5-HT-dependent increase in synaptic strength is partially dependent on translation

238 ession (LTD) at synapses in the adult brain, synaptic strength is reduced in an experience-dependent

239 commonly assumed that homeostasis modulates synaptic strength, membrane excitability, and firing rat

240 uronal processes is key to the alteration of synaptic strength necessary for long-term potentiation,

241 n of KIBRA is neither sufficient to increase synaptic strength, nor to prolong a form of PKM-dependen

242 ,' and showed that drug-induced decreases in synaptic strength occur rapidly (within 30 min) and requ

243 wn as synaptic scaling, maintains the global synaptic strength of individual neurons in response to s

244 Up-scaling increased the synaptic strength of respiratory motoneurons and acted t

245 sessed the effect of mAChR activation on the synaptic strength of specific PFC inputs.

246 R deletion in iMSNs causes a decrease in the synaptic strength of striatopallidal neurons, which in t

247 hese phenomena are associated with increased synaptic strength of ventral hippocampus (VH) excitatory

248 P innervation of mPFC neurons, and increased synaptic strength of vHIP inputs onto layer five pyramid

249 ion of abGCs may be to regulate the relative synaptic strengths of LEC-driven contextual information

250 not exhibit a significant overall change in synaptic strength on D1-MSNs or D2-MSNs, we observed a s

251 uingly, the CaMKII inhibitor tatCN21 reduces synaptic strength only at high concentrations necessary

252 ion, we found that leptin reduces excitatory synaptic strength onto both melanin-concentrating hormon

253 havior are causally linked to alterations of synaptic strength onto nucleus accumbens (NAc) medium sp

254 Autaptic strength was greater than synaptic strength onto PNs as a result of a larger quant

255 tional range through compensatory changes in synaptic strength or intrinsic cellular excitability.

256 been understood to arise through changes in synaptic strength or synaptic connectivity.

257 ticity is inactive at stable states and that synaptic strength overshoots during recovery from visual

258 form new GABAergic synapses that have little synaptic strength plasticity.

259 e ability of L-655,708 to restore excitatory synaptic strength rapidly may underlie its ability to re

260 However, how Shank3 regulates synaptic strength remains unclear.

261 tentiation (LTP) is a persistent increase in synaptic strength required for many behavioral adaptatio

262 d that the massed 5-HT-dependent increase in synaptic strength requires translation elongation, but n

263 We show that synaptic strength scales with the number of connections

264 lus-specific long-term potentiation (LTP) of synaptic strength selectively at the GABAergic component

265 Thus, basal synaptic strength, short-term plasticity, and homeostasi

266 to promote their internalization and weaken synaptic strength, similar to what occurs in Nedd4-1's e

267 ator that can effect long-lasting changes in synaptic strength such as long-term potentiation (LTP),

268 This protein loss also caused an increase in synaptic strength, suggesting that spontaneous neurotran

269 ceptor expression, and structural markers of synaptic strength, suggesting these EB neurons undergo "

270 insic noise massively increases the range of synaptic strengths supporting gamma oscillations and gri

271 zinc-sensitive signaling system, regulating synaptic strength that may be impaired in ASD.

272 tion of surface AMPARs and the scaling up of synaptic strength that occur in response to chronic acti

273 ingly, spontaneous neurotransmitter release, synaptic strength, the time course of evoked release, re

274 LTP, LTD, and homeostatic scaling alter synaptic strength through changes in postsynaptic AMPA-t

275 ly regulates long-term potentiation (LTP) of synaptic strength through inhibition of AMPA receptor tr

276 Modulation of synaptic strength through trafficking of AMPA receptors

277 We demonstrate indices of increased net synaptic strength (TMS intensity to elicit a predefined

278 ynaptic release collectively serve to reduce synaptic strength to levels that fall below the threshol

279 tic plasticity could normalize and stabilize synaptic strengths to achieve any possible excitatory-in

280 noise, variation in excitatory or inhibitory synaptic strength tunes the amplitude and frequency of g

281 though it is widely accepted that changes in synaptic strength underlie many forms of learning and me

282 tial framework for coordinating post-and pre-synaptic strength, using retrograde regulation of axonal

283 hes to study how ongoing activity influences synaptic strength, using voltage- and current-clamp reco

284 signaling may play a role in fine-tuning of synaptic strengths via presynaptically-expressed CB1 rec

285 ncreased with maturation, whereas individual synaptic strength was constant.

286 Increased synaptic strength was not due to changes in voltage-gate

287 In animals treated with cocaine, average synaptic strength was reduced specifically at large mush

288 ative effects differed between muscle types: synaptic strength was rescued only in slow-twitch muscle

289 lectrophysiological recordings revealed that synaptic strength was unchanged in all but one of these

290 e in nervous system function is equilibrium: synaptic strengths wax and wane, neuronal firing rates a

291 quire normal long-term potentiation (LTP) of synaptic strength, which in turn requires binding of the

292 c function of the NMDAR in the regulation of synaptic strength, which relies on glutamate binding but

293 rinsic excitability and recurrent excitatory synaptic strength, while E/I ratio, local output strengt

294 le in determining receptor concentration and synaptic strength, with known links between changes in b

295 rgrown synapses yet express stable levels of synaptic strength, with three specific compensatory mech

296 ress exposure leads to a lasting increase in synaptic strength within a reciprocal BLA-plPFC-BLA subc

297 or, in part due to alterations in excitatory synaptic strength within cortical-accumbens pathways.

298 atal day (p)17] or CP (p22-p25), and FS-->SP synaptic strength within layer 4 was assessed using conf

299 iated by activity-dependent modifications of synaptic strength within neuronal circuits.

300 gulation is essential for the maintenance of synaptic strength within the physiological range.