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

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

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

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

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

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

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

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

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

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

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

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

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

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

26 oduced multiple results including and beyond STDP.

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

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

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

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

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

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

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

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

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

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

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

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

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

40 ing-dependent synaptic plasticity (dendritic STDP).

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

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

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

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

45 and postsynaptic spiking similar to that for STDP.

46 GABAergic STDP is postsynaptic and has an associative component si

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

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

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

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

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

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

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

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

55 However STDP alone produced poorer learning performance.

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

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

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

59 r postsynaptic spiking per se did not induce STDP.

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

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

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

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

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

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

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

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

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

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

70 ith a broad class of experimentally observed STDP rules.

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

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

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

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

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

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

77 dence detector for LTP and LTD components of STDP.

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

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

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

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

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

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

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

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

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

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

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

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

90 or understanding the temporal integration of STDP.

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

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

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

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

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

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

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

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

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

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

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

102 ound it commensurate with the requirement of STDP.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

166 -inspired spike timing dependent plasticity (STDP).

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

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

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

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

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

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

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

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

175 spike-timing dependent synaptic plasticity (STDP).

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

207 subsequently output representations through STDP.

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

209 ich exhibited a temporal specificity akin to STDP.

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

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

212 ithin and across brain regions, and triggers STDP.

213 or-mediated signaling pathway that underlies STDP.

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

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

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

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

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

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

220 osensory neurons in a manner consistent with STDP.

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