Pathway-Specific Synaptic Plasticity: Activity-Dependent Enhancement and Suppression of Long-Term Heterosynaptic Facilitation at Converging Inputs on a Single Target

Schacher, Samuel; Wu, Fang; Sun, Zhongyi

doi:10.1523/jneurosci.17-02-00597.1997

Cited by 57 publications

(51 citation statements)

References 89 publications

(135 reference statements)

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“…To avoid the possible confusion of terms, we make a distinction between the notions of heterosynaptic plasticity (Dittman & Regehr, 1997;Schacher, Wu, & Sun, 1997;Vogt & Nicoll, 1999) and neuromodulation of plasticity (Bailey, Giustetto, Huang, Hawkins, & Kandel, 2000;Fellous & Linster, 1998). In contrast to the conventionally used monosynaptic Hebbian learning, heterosynaptic Hebbian learning allows for activity-independent modification of synapses such that a synapse can also be updated when only the pre-synaptic or post-synaptic component has been active, and more generally, even when neither have been active.…”

Section: Evolution Of Reinforcement Learning-a Different Approach To mentioning

confidence: 99%

“…Neuromodulation of synaptic plasticity further enhances the learning rule by allowing a three-factor interaction in the learning process: through neuromodulation the activity of a neuron can gate the plasticity of a synapse between two other neurons. Both heterosynaptic plasticity and neuromodulatory gating of synaptic plasticity have been demonstrated in neural tissues (Bailey et al, 2000;Dittman & Regehr, 1997;Fellous & Linster, 1998;Schacher et al, 1997;Vogt & Nicoll, 1999), and have been recognized to increase the computational complexity of synaptic learning (Bailey et al, 2000;Fellous & Linster, 1998;Wickens and Kotter, 1995). By allowing for heterosynaptic learning and neuromodulation of plasticity, we defined a very large search space in which the genetic algorithm could search for optimal synaptic learning rules.…”

Section: Evolution Of Reinforcement Learning-a Different Approach To mentioning

confidence: 99%

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Actor–critic models of the basal ganglia: new anatomical and computational perspectives

2002

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A large number of computational models of information processing in the basal ganglia have been developed in recent years. Prominent in these are actor-critic models of basal ganglia functioning, which build on the strong resemblance between dopamine neuron activity and the temporal difference prediction error signal in the critic, and between dopamine-dependent long-term synaptic plasticity in the striatum and learning guided by a prediction error signal in the actor. We selectively review several actor -critic models of the basal ganglia with an emphasis on two important aspects: the way in which models of the critic reproduce the temporal dynamics of dopamine firing, and the extent to which models of the actor take into account known basal ganglia anatomy and physiology. To complement the efforts to relate basal ganglia mechanisms to reinforcement learning (RL), we introduce an alternative approach to modeling a critic network, which uses Evolutionary Computation techniques to 'evolve' an optimal RL mechanism, and relate the evolved mechanism to the basic model of the critic. We conclude our discussion of models of the critic by a critical discussion of the anatomical plausibility of implementations of a critic in basal ganglia circuitry, and conclude that such implementations build on assumptions that are inconsistent with the known anatomy of the basal ganglia. We return to the actor component of the actor -critic model, which is usually modeled at the striatal level with very little detail. We describe an alternative model of the basal ganglia which takes into account several important, and previously neglected, anatomical and physiological characteristics of basal ganglia -thalamocortical connectivity and suggests that the basal ganglia performs reinforcementbiased dimensionality reduction of cortical inputs. We further suggest that since such selective encoding may bias the representation at the level of the frontal cortex towards the selection of rewarded plans and actions, the reinforcement-driven dimensionality reduction framework may serve as a basis for basal ganglia actor models. We conclude with a short discussion of the dual role of the dopamine signal in RL and in behavioral switching. q

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Section: Evolution Of Reinforcement Learning-a Different Approach To mentioning

confidence: 99%

Section: Evolution Of Reinforcement Learning-a Different Approach To mentioning

confidence: 99%

Actor–critic models of the basal ganglia: new anatomical and computational perspectives

2002

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“…Long-term potentiation (LTP) (Lin & Glanzman, 1994b), as well as several associative forms of learning-related plasticity (Murphy & Glanzman, 1996;Schacher et al 1997;Bao et al 1998), of sensorimotor connections all require a rise in postsynaptic intracellular Ca 2+ . To test whether the effect of 5-HT on the Glu-PSP depends upon intracellular Ca 2+ in the motor neuron, we added BAPTA (100-200 mM) to the standard micropipette solution.…”

Section: Bapta Blocks 5-ht-induced Facilitation Of the Glutamate Respmentioning

confidence: 99%

“…5-HT-induced facilitation of the glutamate response does not depend upon activation of NMDA-type receptors LTP of sensorimotor synapses, as well as some other forms of learning-related enhancement, require activation of N-methyl-D-aspartate (NMDA)-type receptors (Lin & Glanzman, 1994a, b;Murphy & Glanzman, 1997;Schacher et al 1997 of the glutamate response requires activation of NMDAtype receptors in motor neurons, we applied the NMDA receptor antagonist APV (100 µM) to the perfusion medium in conjunction with 5-HT. The presence of APV did not block facilitation of the glutamate response by 5-HT.…”

Section: Bapta Blocks 5-ht-induced Facilitation Of the Glutamate Respmentioning

confidence: 99%

Serotonin facilitates AMPA‐type responses in isolated siphon motor neurons of Aplysia in culture

Chitwood

Glanzman

2001

The Journal of Physiology

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1. Serotonin (5-HT) facilitates the connections between sensory and motor neurons in Aplysia during behavioural sensitization. The effect of 5-HT on sensorimotor synapses is believed to be primarily presynaptic. Here we tested whether 5-HT can have an exclusively postsynaptic facilitatory effect.2. Siphon motor neurons were individually dissociated from the abdominal ganglion of Aplysia and placed into cell culture. Brief pulses of glutamate, the putative sensory neuron transmitter, were focally applied (0.1 Hz) to solitary motor neurons in culture, and the glutamate-evoked postsynaptic potentials (Glu-PSPs) were recorded.3. When 5-HT was perfused over the motor neuron for 10 min, the amplitude of the Glu-PSPs was significantly increased. The 5-HT-induced enhancement of the Glu-PSPs persisted for at least 40 min after washout.4. Prior injection into the motor neuron of the calcium chelator BAPTA, GDP-b-S or GTP-y-S blocked the 5-HT-induced facilitation of the Glu-PSPs. However, the facilitation was not blocked when APV, an NMDA receptor antagonist, was applied together with the 5-HT.5. The enhancement of the Glu-PSPs by 5-HT was reversed by the AMPA receptor antagonist DNQX, indicating that 5-HT increased the functional expression of AMPA-type receptors in the motor neuron.6. The presence of botulinum toxin in the motor neuron blocked the 5-HT-induced enhancement of the Glu-PSPs. As botulinum toxin prevents exocytosis we hypothesize that during sensitization 5-HT causes the insertion of additional AMPA-type receptors into the postsynaptic membrane of sensorimotor synapses via exocytosis. This postsynaptic mechanism may contribute to facilitation of the synapses.

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“…One mechanism that could account for our results is a homeostatic process in which the strength of multiple synaptic inputs onto a single target is regulated, such that overall synaptic strength is conserved. Evidence for the operation of such a homeostatic process has come mostly from studies of cell culture systems or development (Glanzman et al, 1991;Schacher et al, 1997;Turrigiano and Nelson, 2004); there is a paucity of evidence for homeostatic regulation of synaptic strength in studies of learning-related systems. Interpreted as the effect of homeostatic regulation, the decrement we observed in the anticorrelated CSϪ pathway reflects a competitive loss of synaptic strength because of the increase in strength in the coactive CSϩ pathway.…”

Section: Discussionmentioning

confidence: 99%

Differential Classical Conditioning of the Gill-Withdrawal Reflex inAplysiaRecruits Both NMDA Receptor-Dependent Enhancement and NMDA Receptor-Dependent Depression of the Reflex

Jami¹,

Wright²,

Glanzman³

2007

J. Neurosci.

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Differential classical conditioning of the gill-withdrawal response (GWR) in Aplysia can be elicited by training in which a conditioned stimulus (CS) delivered to one side of the siphon (the CSϩ) is paired with a noxious unconditioned stimulus (US; tail shock), while a second conditioned stimulus (the CSϪ), delivered to a different siphon site, is unpaired with the US. NMDA receptor (NMDAR) activation has been shown previously to be critical for nondifferential classical conditioning in Aplysia. Here, we used a semi-intact preparation to test whether differential classical conditioning of the GWR also depends on activation of NMDARs. Differential training produced conditioned enhancement of the reflexive response to the CSϩ and a reduction in the response to the CSϪ. Comparison of the results after differential training with those after training in which only the two CSs were presented (CS-alone experiments) indicated that the decrement in the response to CSϪ after differential training was not caused by habituation. Surprisingly, differential training in the NMDAR antagonist APV (DL-2-amino-5-phosphonovalerate) blocked not only the conditioned enhancement of the GWR, but also the conditioning-induced depression of the GWR. We suggest that differential conditioning involves an NMDAR-dependent, competitive interaction between the separate neural pathways activated by the CSϩ and CSϪ.

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Pathway-Specific Synaptic Plasticity: Activity-Dependent Enhancement and Suppression of Long-Term Heterosynaptic Facilitation at Converging Inputs on a Single Target

Cited by 57 publications

References 89 publications

Actor–critic models of the basal ganglia: new anatomical and computational perspectives

Actor–critic models of the basal ganglia: new anatomical and computational perspectives

Serotonin facilitates AMPA‐type responses in isolated siphon motor neurons of Aplysia in culture

Differential Classical Conditioning of the Gill-Withdrawal Reflex inAplysiaRecruits Both NMDA Receptor-Dependent Enhancement and NMDA Receptor-Dependent Depression of the Reflex

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