ライフサイエンスコーパス: STDP

1 STDP disappeared with randomized EPSP/AP pairing or high

2 STDP in entorhinal pyramidal cells is NMDA-receptor-depe

3 STDP in MSNs expressing dopamine D1 receptors shifted fr

4 STDP is widely utilized in models of circuit-level plast

5 STDP occurred at 6-10 Hz but vanished >50 Hz or <1 Hz (w

6 STDP of GABAergic synapses in the VTA provides physiolog

7 STDP strengthens synapses that receive correlated input,

8 STDP with a shifted temporal window such that coincident

9 STDP with the opposite temporal shift functions as a loo

10 STDP, acting alone without further hypothetical global c

11 STDP, combined with these correlations, leads to reinfor

12 STDP-like effects were observed as an increase in spinal

13 risingly enough, very little was known about STDP in the cerebellum, although it is thought to play a

14 The experimentally observed self-adaptive STDP behavior has been complemented with numerical model

15 ule has a selectivity comparable to additive STDP and captures input correlations as well as multipli

16 mentally demonstrate, for the first time, an STDP behavior that ensures self-adaptation of the averag

17 trated behavioral effects consistent with an STDP mechanism; however, many relied on single-unit reco

18 y role in regulating both EPSP amplitude and STDP induction.

19 Our model generalizes across brain areas and STDP rules, allowing broad application to the ubiquitous

20 ivity patterns increases with wave speed and STDP time constants.

21 veral orders of magnitude in wave speeds and STDP time constants, and they provide predictions that c

22 undergo plasticity with both NMDA-spikes and STDP protocols but to a smaller extent compared with LOT

23 he Bienenstock-Cooper-Munro or BCM type) and STDP rules.

24 tory inputs, which displayed an asymmetrical STDP time window.

25 ixed D1/D5R agonist SKF82958 unmasked LTP at STDP pairing intervals that normally fail to alter synap

26 mics can be prevented by precisely balancing STDP rules for potentiation and depression; however, exp

27 a variety of spike patterns, the pair-based STDP model has been augmented to account for multiple pr

28 , which is well characterized for pair-based STDP models, persists in multi-spike models.

29 tion of mossy fiber bursts, probably because STDP expression involved postsynaptic in addition to pre

30 oduced multiple results including and beyond STDP.

31 campal slices show that acetylcholine biases STDP toward synaptic depression, whilst subsequent appli

32 ables the induction of Hebbian bidirectional STDP in FS cells in a manner consistent with a pull-push

33 nimals.(5)(,)(6) In the healthy human brain, STDP-like effects have been shown in the motor cortex, v

34 conduction delays exhibit population bursts, STDP rules exert a strong decoupling force that desynchr

35 Synapses modifiable by STDP compete for control of the timing of postsynaptic a

36 eurons that fire this way can be modified by STDP in a manner that depends on the temporal ordering o

37 ulation delayed connections were modified by STDP.

38 e show in vivo that pre-post pairing causing STDP can, when followed by the local delivery of a reinf

39 However, in pyramidal cells, STDP induction depends on NMDA receptors, whereas in FS

40 al approaches, we show here that the classic STDP rule in which pairs of single pre- and postsynaptic

41 pecific activity regimes restore a classical STDP profile.

42 y depression-biased rSTDP (and not classical STDP) produces stable and diverse top-down weights.

43 e auditory cortex, together with concomitant STDP of excitatory synapses.

44 al investigations suggest that GABA controls STDP polarity through depolarizing effects at distal den

45 We show how conventional STDP acts as a loop-eliminating mechanism and organizes

46 that achieves bidirectional corticostriatal STDP in vivo through modulation by behaviourally relevan

47 ing dendritic and axonal propagation delays, STDP eliminates bidirectional connections between two co

48 ing-dependent synaptic plasticity (dendritic STDP).

49 We also describe STDP in the context of complex spike patterns and its de

50 STDP) interacts with co-activated excitatory STDP to regulate excitatory-inhibitory balance in audito

51 prediction of a model circuit that exhibits STDP at intracortical connections.

52 Furthermore, our model reveals that the fast STDP learning dynamics during presentation of a given od

53 the diverse time scales of neuronal firing, STDP, and SP, we introduce a simple stochastic SP model,

54 these models, we compare the conditions for STDP and for synaptic strengthening by local dendritic s

55 Our findings provide evidence for STDP in human episodic memory, which builds an important

56 lisecond-precision spike timing required for STDP and the much slower timescales of behavioral learni

57 and postsynaptic spiking similar to that for STDP.

58 GABAergic STDP is postsynaptic and has an associative component si

59 Importantly, GABAergic STDP is heterosynaptic (NMDA receptor dependent): trigge

60 nnel activation by backpropagating APs gated STDP induction during low-frequency AP-EPSP pairing, wit

61 Harnessing STDP, PMCS leads to changes of the synaptic network stru

62 For additive, Hebbian STDP these motif interactions create instabilities in sy

63 e existence of both Hebbian and anti-Hebbian STDP in human long-range connections.

64 Our study demonstrates that driving Hebbian STDP in AON-to-M1 projections induces opposite effects o

65 schemes and a comparison with a hierarchical STDP based ensemble architecture.

66 ion and modulates the outcome of hippocampal STDP even when applied after the plasticity induction pr

67 neuron model implementing both homosynaptic (STDP) and heterosynaptic plasticity with properties matc

68 Here we studied how STDP operates in the context of more natural spike train

69 However STDP alone produced poorer learning performance.

70 lso revealed several layers of complexity in STDP, including its dependence on dendritic location, th

71 eed, exogenous BDNF reversed the deficits in STDP and NMDA receptor transmission in BDNF(Met/Met) neu

72 e variations of spike number or frequency in STDP are sufficient to shift the on-demand fueling from

73 Because a mismatch in STDP rules could impact the maintenance of the excitatio

74 r postsynaptic spiking per se did not induce STDP.

75 P-spike pairing at 6 Hz can optimally induce STDP at the mossy fiber-granule cell synapse in rats.

76 ulation in vivo is a viable method to induce STDP between cortical populations, but that factors beyo

77 tsynaptic spikes at 6-10 Hz reliably induced STDP at the mossy fiber-granule cell synapse, with poten

78 ggests that neurobiological plasticity, like STDP-H, may contribute to reducing the dimensions of inp

79 APs in st-LTP while APs led EPSPs in st-LTD, STDP was Hebbian in nature.

80 receptors were inhibited, a relatively mild STDP protocol induced LTP only within a very narrow timi

81 ptors were activated, however, the same mild STDP protocol induced tLTP over a much broader timing wi

82 o a symmetric combined rule we call Mirrored STDP (mSTDP).

83 th reward modulated and non-reward modulated STDP and implemented multiple mechanisms for homeostatic

84 on of homeostatic mechanisms, multiplicative STDP rules or weak external input to the top neurons.

85 The experimentally observed STDP plasticity curve appears to be designed to adjust s

86 ith a broad class of experimentally observed STDP rules.

87 By varying these parameters, we obtain STDP curves that are long-term potentiation only, bidire

88 e results illustrate the multiple actions of STDP, including a role in associative learning, despite

89 The temporal asymmetry of STDP suppresses strong destabilizing self-excitatory loo

90 c calcium transient and shift the balance of STDP toward LTD.

91 e summarize experimental characterization of STDP at various synapses, the underlying cellular mechan

92 We show that certain classes of STDP rules can stabilize all stored memory patterns desp

93 ing and without STDP, (iii) a combination of STDP and hSP, i.e., without weight-dependent pruning, an

94 dependent pruning, and (iv) a combination of STDP and structural plasticity (SP) that includes hSP an

95 ndicate that a network with a combination of STDP and structural plasticity may require stronger and

96 with only STDP to one with a combination of STDP and structural plasticity.

97 dence detector for LTP and LTD components of STDP.

98 Finally, the functional consequences of STDP have been examined directly in an increasing number

99 wing that, by mapping the time dependence of STDP into spatial interactions, traveling waves can buil

100 The simplest description of STDP only takes into account pairs of pre- and postsynap

101 simulations and by analyzing the effects of STDP on pair-wise interactions of neurons.

102 re is emerging evidence for the existence of STDP at inhibitory synapses.

103 The decoupling force of STDP may be engaged by the synchronous bursts occurring

104 illatory population discharge), this form of STDP enhances the synchronization of the Kenyon cells' t

105 We found that a Hebbian form of STDP including long-term potentiation (LTP) and long-ter

106 ese results thus show that a Hebbian form of STDP occurs at the cerebellum input stage, providing the

107 ved brain areas and that antithetic forms of STDP-like after-effects result in distinct cortical rhyt

108 However, the impact of STDP at the level of circuits, and the mechanisms govern

109 tion, regulating the inherent instability of STDP in an assembly phase-sequence model.

110 or understanding the temporal integration of STDP.

111 in understanding the cellular mechanisms of STDP at both excitatory and inhibitory synapses and of t

112 with multiplicative, soft-bounded models of STDP.

113 elations as well as multiplicative models of STDP.

114 complex spike trains, and the modulation of STDP by inhibitory and neuromodulatory inputs.

115 monstrate that sequential neuromodulation of STDP by acetylcholine and dopamine offers an efficacious

116 hus, temporally sequenced neuromodulation of STDP enables associations to be made between actions and

117 balance, we examined the neuromodulation of STDP in FS cells of mouse visual cortex.

118 Here, we review neuromodulation of STDP, the underlying mechanisms, functional implications

119 GABA controls the polarity of STDP in both striatopallidal and striatonigral output ne

120 that neuromodulators control the polarity of STDP in different synapses in the same manner, and indep

121 GABAergic signaling governs the polarity of STDP, because blockade of GABAA receptors was able to co

122 ted runaway dynamics for the tested range of STDP and input parameters.

123 GluN2B in the striatum, narrows the range of STDP intervals that cause long term potentiation.

124 ction and reveal an unexpected regulation of STDP in the PFC by BDNF.

125 ound it commensurate with the requirement of STDP.

126 One functional role of STDP might therefore be to facilitate synchronization or

127 dopamine influences the quantitative rule of STDP at glutamatergic synapses of hippocampal neurons.

128 eption and the computational significance of STDP as a synaptic learning rule.

129 um concentration used in in vitro studies of STDP suggests that in vivo plasticity rules may differ s

130 ), compared with the critical time window of STDP in animals.(5)(,)(6) In the healthy human brain, ST

131 Also, DID effects on STDP were accompanied by lower dendritic calcium transie

132 behaviorally relevant activity parameters on STDP and found conditions under which underlying spike-t

133 lasticity, we contrast the network with only STDP to one with a combination of STDP and structural pl

134 lusion, we report new evidence that opposite STDP-like effects induced by corticocortical PAS are ass

135 ively, and combined to implement the overall STDP rule.

136 Spike timing-dependent plasticity (STDP) and other conventional Hebbian-type plasticity rul

137 d modulated spike time dependent plasticity (STDP) are capable of learning simple foraging tasks.

138 (LTD) and spike-timing dependent plasticity (STDP) are demonstrated systematically using a comprehens

139 Spike timing-dependent plasticity (STDP) as a Hebbian synaptic learning rule has been demon

140 rons with spike-timing-dependent plasticity (STDP) as the learning rule.

141 described spike-timing-dependent plasticity (STDP) at a synapse: the connection from neuron A to neur

142 nality in spike-timing dependent plasticity (STDP) at corticostriatal synapses.

143 governing spike-timing-dependent plasticity (STDP) at sensory synapses onto projection neurons remain

144 a form of spike-timing-dependent plasticity (STDP) at the cerebellar inputs stage.

145 ations of spike-timing-dependent plasticity (STDP) at these synapses have been performed largely in b

146 show that spike-timing-dependent plasticity (STDP) can be harnessed from HZO based FTJs.

147 days and spike-timing-dependent plasticity (STDP) effects on a scale of seconds.

148 rate that spike-timing dependent plasticity (STDP) enhances synchronization (entrainment) in a hybrid

149 the induction of spike-dependent plasticity (STDP) follows a simple Hebbian rule in which the order o

150 Such spike-timing-dependent plasticity (STDP) follows rules that govern how patterns of neural a

151 e through spike-timing-dependent plasticity (STDP) has been missing.

152 This spike-timing-dependent plasticity (STDP) has been studied by systematically varying the int

153 l actions.Spike timing dependent plasticity (STDP) has been studied extensively in slices but whether

154 ndings of spike timing-dependent plasticity (STDP) have stimulated much interest among experimentalis

155 on of the spike-timing-dependent plasticity (STDP) Hebbian learning rule by phenomenological modeling

156 ffects on spike timing-dependent plasticity (STDP) in medium spiny neurons (MSNs) of the core nucleus

157 ncy (ULF) spike-timing-dependent plasticity (STDP) in mouse models of AUD to reduce DMS D1/D2 MSN sig

158 s exhibit spike timing-dependent plasticity (STDP) in which the precise timing of presynaptic and pos

159 inhibitory spike-time-dependent plasticity (STDP) interacts with co-activated excitatory STDP to reg

160 ies, such spike timing-dependent plasticity (STDP) introduces the desirable features of competition a

161 Spike-timing-dependent plasticity (STDP) is a form of long-term synaptic plasticity exploit

162 Spike timing-dependent plasticity (STDP) is a learning rule important for synaptic refineme

163 Spike-timing dependent plasticity (STDP) is a widespread plasticity mechanism in the nervou

164 omenon of spike-timing-dependent plasticity (STDP) is believed to arise by nonlinear processes that l

165 Spike-timing-dependent plasticity (STDP) is considered a physiologically relevant form of H

166 Spike-timing-dependent plasticity (STDP) is considered as a primary mechanism underlying fo

167 uction of spike-timing dependent plasticity (STDP) is not clear.

168 hs due to spike-timing-dependent plasticity (STDP) is sensitive to correlations between pre- and post

169 Spike timing-dependent plasticity (STDP) is under neuromodulatory control, which is correla

170 nderlying spike timing-dependent plasticity (STDP) may be separated into functional modules that are

171 Spike-timing-dependent plasticity (STDP) modifies synaptic strengths based on the relative

172 Spike timing-dependent plasticity (STDP) modifies synaptic strengths based on timing inform

173 e examine spike-timing-dependent plasticity (STDP) of inhibitory synapses onto layer 5 neurons in sli

174 regulates spike timing-dependent plasticity (STDP) of the medial perforant path (mPP) synapse onto de

175 o hebbian spike-timing dependent plasticity (STDP) on a +/-25 ms timescale.

176 f ongoing spike-timing-dependent plasticity (STDP) on the stability of memory patterns stored in syna

177 a single spike-timing-dependent plasticity (STDP) pairing once per circuit reactivation.

178 uced with spike-timing-dependent plasticity (STDP) protocol at a long pre-post interval that was subt

179 in vivo a spike-timing-dependent plasticity (STDP) protocol-consisting of pairing a postsynaptic AP w

180 le global spike timing-dependent plasticity (STDP) protocols failed to induce LTP in these distal syn

181 sponse to spike timing dependent plasticity (STDP) protocols, and thereby shape synaptic integration

182 a single spike-timing-dependent plasticity (STDP) rule alone can fully describe the mapping between

183 a Hebbian spike-timing-dependent plasticity (STDP) rule.

184 y derived spike-timing-dependent plasticity (STDP) rules, suggesting that STDP is key to drive these

185 luence of spike-timing-dependent plasticity (STDP) rules.

186 tion with spike-timing-dependent plasticity (STDP) that runs on a longer time scale than neuronal spi

187 a Hebbian spike-timing-dependent plasticity (STDP) to test their functional relevance to automatic an

188 nd shifts spike timing-dependent plasticity (STDP) toward LTD at GABAergic synapses onto VTA DA neuro

189 port that spike timing-dependent plasticity (STDP) was absent in the IL-mPFC pyramidal neurons from B

190 rning rule, spike time-dependent plasticity (STDP) which codifies the temporal sequence of pre- and p

191 (i) only spike-timing-dependent plasticity (STDP), (ii) only homeostatic structural plasticity (hSP)

192 rate that spike-timing dependent plasticity (STDP), a form of Hebbian learning, acting on temporally

193 The spike-timing-dependent plasticity (STDP), a synaptic learning rule for encoding learning an

194 ponses is spike-timing-dependent plasticity (STDP), an up- or downregulation of synaptic efficacy con

195 dynamics, spike-timing-dependent plasticity (STDP), and acetylcholine modulation; detailed laminar th

196 n Hebbian spike-timing-dependent plasticity (STDP), best explains PF shifting dynamics.

197 h we call spike-timing-dependent plasticity (STDP), depends on the relative timing of pre- and postsy

198 rsions of spike-timing dependent plasticity (STDP), leading to a symmetric combined rule we call Mirr

199 ther with spike timing-dependent plasticity (STDP), reconfigures neuronal firing rates across the net

200 yer through Spike-Time-Dependent Plasticity (STDP), resulting in separate translation-invariant repre

201 cifically spike-timing-dependent plasticity (STDP), such that it was expressed either independently p

202 e form of spike timing-dependent plasticity (STDP), the manner by which STDP responds to binge alcoho

203 In spike-timing-dependent plasticity (STDP), the order and precise temporal interval between p

204 strate that spike-time-dependent plasticity (STDP), the primary known mechanism for temporal order le

205 nement is spike-timing dependent plasticity (STDP), which translates correlated activity patterns int

206 cuits via spike timing-dependent plasticity (STDP).

207 y through spike-timing-dependent plasticity (STDP).

208 rons with spike-timing-dependent plasticity (STDP).

209 , such as spike timing-dependent plasticity (STDP).

210 ons such as spike-time dependent plasticity (STDP).

211 additive spike-timing-dependent plasticity (STDP).

212 y through spike-timing-dependent plasticity (STDP).

213 to elicit spike timing-dependent plasticity (STDP).

214 -inspired spike timing dependent plasticity (STDP).

215 le called spike-timing-dependent plasticity (STDP).

216 support the spike-time-dependent plasticity (STDP).

217 gm termed spike timing-dependent plasticity (STDP).

218 nections [spike-timing-dependent plasticity (STDP)], but how the precise temporal relationship of the

219 ppocampal Spike-Timing-Dependent-Plasticity (STDP) that is sequentially modulated by acetylcholine an

220 forms of spike-timing-dependent-plasticity (STDP) when paired pulses are repeatedly applied with dif

221 spike-timing-dependent synaptic plasticity (STDP) as the underlying mechanism, it remains unclear wh

222 Spike-timing-dependent synaptic plasticity (STDP) is a leading cellular model for behavioral learnin

223 spike-timing dependent synaptic plasticity (STDP) rules may be required at top-down synapses.

224 Spike timing-dependent synaptic plasticity (STDP) serves as a key cellular correlate of associative

225 spike-timing dependent synaptic plasticity (STDP).

226 termed "spike-timing-dependent plasticity" (STDP).(4) Evidence found in human in vitro studies sugge

227 Spike timing-dependent plasticity, STDP, has attracted considerable attention primarily due

228 tional correlation-based Hebbian plasticity, STDP opens up new avenues for understanding information

229 pike-timing-dependent synaptic potentiation (STDP) in PFC slices derived from BDNF-KIV, but not wild-

230 showing the existence of temporally reversed STDP in synapses that are distal to the post-synaptic ce

231 owing layer of neurons implementing rewarded STDP, the network was able to learn, despite the absence

232 dden layer of neurons employing non-rewarded STDP created neurons that responded to the specific comb

233 alancing, activity normalization of rewarded STDP and hard limits on synaptic strength.

234 latta), and also show that, like in rodents, STDP is gated by neuromodulators.

235 plasticity and homeostatic synaptic scaling (STDP-H) learning rules.

236 n spine calcium concentration during several STDP protocols in a model of a striatal medium spiny pro

237 ntral role for GABAergic circuits in shaping STDP and suggest that GABA could operate as a Hebbian/an

238 from in vitro experiments, especially since STDP depends strongly on calcium for induction.

239 result, a number of different "multi-spike" STDP models have been proposed based on different experi

240 We compared pair-based standard STDP models and a biologically tuned triplet STDP model,

241 shaping neural function and strongly suggest STDP as a relevant mechanism for plasticity in the matur

242 shold for WT mice, although a suprathreshold STDP protocol at a short pre-post interval resulted in s

243 We demonstrate that STDP outcome is controlled by eCB levels and dynamics: p

244 et al. and Mu and Poo provide evidence that STDP contributes to the effects of sensory stimuli in re

245 ere is now strong experimental evidence that STDP is under neuromodulatory control by acetylcholine,

246 We tested the hypothesis that STDP could be induced via prolonged paired stimulation a

247 These findings indicate that STDP is not a unitary process and suggest that endocanna

248 We show instead that STDP at layer 4 to layer 2/3 synapses in somatosensory (

249 ferroelectric tunnel junctions and show that STDP can be harnessed from inhomogeneous polarization sw

250 important insights about the structures that STDP can produce in large networks.

251 Together, these findings suggest that STDP can mediate sensory experience-dependent circuit re

252 ent plasticity (STDP) rules, suggesting that STDP is key to drive these changes.

253 hermore, experimental evidence suggests that STDP is not the only learning rule available to neurons.

254 This SNN model suggests that STDP-H observed in the nervous system may be performing

255 In conclusion, the STDP rule is profoundly altered in physiological Ca(2+),

256 aptic and postsynaptic inputs determines the STDP effects in humans is poorly understood.

257 A major challenge for the STDP implementation is that, in contrast to some simplis

258 ynchronization of synchronized states in the STDP-only model (i) with the desynchronization of models

259 than in randomly structured networks in the STDP-only model.

260 e GluN2 subunit to modulate the shape of the STDP curve could underlie the role that GluN2 subunits p

261 nsory reinforcement signal within 2 s of the STDP pairing, thus revealing a timing-dependent eligibil

262 only, the change is a transformation of the STDP rule itself.

263 ing, but whether GABAergic circuits rule the STDP remained unknown.

264 nce-dependent suppression also sharpened the STDP curve, with reliable synaptic potentiation induced

265 lies of neurons emerge automatically through STDP in a simple cortical microcircuit model.

266 subsequently output representations through STDP.

267 decoupling of the two-module system through STDP, i.e., by unlearning pathologically strong synaptic

268 Thus, STDP can bind plasticity to the mossy fiber burst phase

269 ich exhibited a temporal specificity akin to STDP.

270 he learning of such temporal associations to STDP, we must account for this large discrepancy in time

271 l neuron with excitatory synapses subject to STDP described by three different proposed multi-spike m

272 ithin and across brain regions, and triggers STDP.

273 STDP models and a biologically tuned triplet STDP model, and investigated the outcomes in a minimal s

274 Our data suggest that GPi/ACC ULF-STDP selectively decreases DMS D1-MSN hyperactivity lead

275 or-mediated signaling pathway that underlies STDP.

276 associate with contextual IC information via STDP mechanisms to provide cognitive and emotional value

277 ndent plasticity (STDP), the manner by which STDP responds to binge alcohol drinking, and its sensiti

278 at in MSPNs, GluN2A and GluN2B control which STDP intervals allow for substantial calcium elevation i

279 r neural network model and investigate which STDP rules can lead to a distribution of top-down synapt

280 amined the interaction of wave activity with STDP rules in simple, biologically plausible models of s

281 on within single neurons, when combined with STDP, organizes networks to generate long unary activity

282 oduced robust effects in EPs consistent with STDP, but only at 2/15 tested pairs.

283 osensory neurons in a manner consistent with STDP.

284 ization with fewer links than a network with STDP alone.

285 witch between the states than a network with STDP only.

286 perties of the spiking neuronal network with STDP that was sufficient to solve a complex foraging tas

287 lving spike-timing-dependent plasticity with STDP-H parameters of the connections between then middle

288 without weight-dependent pruning and without STDP, (iii) a combination of STDP and hSP, i.e., without