Learning-Induced Structural Plasticity in the Cerebellum

Nishiyama, Hiroshi

doi:10.1016/b978-0-12-420247-4.00001-4

Cited by 12 publications

(3 citation statements)

References 88 publications

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“…Changes in synaptic strength have been shown to be an important determinant of the subsequent physical restructuring and maintenance of synaptic connections in multiple brain areas (Andreae and Burrone, 2014; Kwon and Sabatini, 2011; Nishiyama, 2014; Sorra and Harris, 1998; Yuste and Bonhoeffer, 2001). We found that after hearing onset the developing intrinsic properties of MSO neurons drive down AP amplitudes and decrease AP backpropagation into the dendrites (Fig.…”

Section: Discussionmentioning

confidence: 99%

Glycinergic Inhibitory Plasticity in Binaural Neurons Is Cumulative and Gated by Developmental Changes in Action Potential Backpropagation

Winters

Golding

2018

Neuron

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Utilization of timing-based sound localization cues by neurons in the medial superior olive (MSO) depends critically on glycinergic inhibitory inputs. After hearing onset, the strength and subcellular location of these inhibitory inputs are dramatically altered, but the cellular processes underlying this experience-dependent refinement are unknown. Here we reveal a form of inhibitory long-term potentiation (iLTP) in MSO neurons that is dependent on spiking and synaptic activation but is not affected by their fine-scale relative timing at higher frequencies prevalent in auditory circuits. We find that iLTP reinforces inhibitory inputs coactive with binaural excitation in a cumulative manner, likely well suited for networks featuring persistent high-frequency activity. We also show that a steep drop in action potential size and backpropagation limits induction of iLTP to the first 2 weeks of hearing. These intrinsic changes would deprive more distal inhibitory synapses of reinforcement, conceivably establishing the mature, soma-biased pattern of inhibition.

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Section: Discussionmentioning

confidence: 99%

Glycinergic Inhibitory Plasticity in Binaural Neurons Is Cumulative and Gated by Developmental Changes in Action Potential Backpropagation

Winters

Golding

2018

Neuron

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“…Several types of behavioral plasticity are associated with changes in dendritic spines, the primary sites of excitatory synapses in the brain. For example, many forms of learning and memory are accompanied by dendritic spinogenesis (Moser et al, 1994;Leuner et al, 2003;Restivo et al, 2009;Vetere et al, 2011a,b;Bock et al, 2014;Kuhlman et al, 2014;Nishiyama, 2014;González-Tapia et al, 2015Mahmmoud et al, 2015;Jasinska et al, 2016;Ma et al, 2016) or spine elimination (Vetere et al, 2011b;Sanders et al, 2012;Jasinska et al, 2016;Ma et al, 2016;Swanson et al, 2017). Spine plasticity is also associated with proficiency of certain motor tasks (Fu et al, 2012;Liston et al, 2013;Hayashi-Takagi et al, 2015;Gonzalez-Tapia et al, 2016) and potentially, action-outcome expectation, given that drugs that enhance action-outcome learning can trigger spine elimination in certain brain regions (Swanson et al, 2017).…”

Section: Introductionmentioning

confidence: 99%

Reward-Related Expectations Trigger Dendritic Spine Plasticity in the Mouse Ventrolateral Orbitofrontal Cortex

et al. 2019

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An essential aspect of goal-directed decision-making is selecting actions based on anticipated consequences, a process that involves the orbitofrontal cortex (OFC) and potentially, the plasticity of dendritic spines in this region. To investigate this possibility, we trained male and female mice to nose poke for food reinforcers, or we delivered the same number of food reinforcers non-contingently to separate mice. We then decreased the likelihood of reinforcement for trained mice, requiring them to modify action-outcome expectations. In a separate experiment, we blocked action-outcome updating via chemogenetic inactivation of the OFC. In both cases, successfully selecting actions based on their likely consequences was associated with fewer immature, thin-shaped dendritic spines and a greater proportion of mature, mushroom-shaped spines in the ventrolateral OFC. This pattern was distinct from spine loss associated with aging, and we identified no effects on hippocampal CA1 neurons. Given that the OFC is involved in prospective calculations of likely outcomes, even when they are not observable, constraining spinogenesis while preserving mature spines may be important for solidifying durable expectations. To investigate causal relationships, we inhibited the RNA-binding protein fragile X mental retardation protein (encoded by Fmr1), which constrains dendritic spine turnover. Ventrolateral OFC-selective Fmr1 knockdown recapitulated the behavioral effects of inducible OFC inactivation (and lesions; also shown here), impairing action-outcome conditioning, and caused dendritic spine excess. Our findings suggest that a proper balance of dendritic spine plasticity within the OFC is necessary for one's ability to select actions based on anticipated consequences.

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“…Here, we review the recent literature devoted to delineating the cellular and molecular mechanisms of dendritic spine elimination in the cerebral cortex. Mechanisms of spine structural plasticity and synapse elimination in the cerebellum have been reviewed recently elsewhere (Hashimoto and Kano, 2013; Nishiyama 2014). We have highlighted those studies that investigate the molecular mechanisms driving the dynamic processes of spine shrinkage and elimination, rather than those that report static spine density changes, as it is not possible to link decreases in spine density to increased spine elimination rather than to decreased spine formation or stabilization, and vice versa.…”

Section: Introductionmentioning

confidence: 99%

Dendritic Spine Elimination: Molecular Mechanisms and Implications

Stein

Zito

2018

Neuroscientist

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Dynamic modification of synaptic connectivity in response to sensory experience is a vital step in the refinement of brain circuits as they are established during development and modified during learning. In addition to the well-established role for new spine growth and stabilization in the experience-dependent plasticity of neural circuits, dendritic spine elimination has been linked to improvements in learning, and dysregulation of spine elimination has been associated with intellectual disability and behavioral impairment. Proper brain function requires a tightly regulated balance between spine formation and spine elimination. Although most studies have focused on the mechanisms of spine formation, considerable progress has been made recently in delineating the neural activity patterns and downstream molecular mechanisms that drive dendritic spine elimination. Here, we review the current state of knowledge concerning the signaling pathways that drive dendritic spine shrinkage and elimination and we discuss their implication in neuropsychiatric and neurodegenerative disease.

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Learning-Induced Structural Plasticity in the Cerebellum

Cited by 12 publications

References 88 publications

Glycinergic Inhibitory Plasticity in Binaural Neurons Is Cumulative and Gated by Developmental Changes in Action Potential Backpropagation

Glycinergic Inhibitory Plasticity in Binaural Neurons Is Cumulative and Gated by Developmental Changes in Action Potential Backpropagation

Reward-Related Expectations Trigger Dendritic Spine Plasticity in the Mouse Ventrolateral Orbitofrontal Cortex

Dendritic Spine Elimination: Molecular Mechanisms and Implications

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