Learning rules and persistence of dendritic spines

Kasai, Hideaki; Hayama, Tatsuya; Ishikawa, Motoko; Watanabe, Satoshi; Yagishita, Sho; Noguchi, Junjirō

doi:10.1111/j.1460-9568.2010.07344.x

Cited by 111 publications

(86 citation statements)

References 127 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Previous studies have shown that there are structural correlates of synaptic plasticity (Kasai et al, 2010a(Kasai et al, , 2010b. In general, spine size is correlated with the strength of synapses (Kasai et al, 2010a(Kasai et al, , 2010b. Thus, the enlargement of dendritic spines in IT-type neurons of the PD and LID models suggests that there are associated changes in the electrophysiological properties of these neurons.…”

Section: Morphological Changes In Dendritic Spines Of It-type Neuronsmentioning

confidence: 94%

“…The size of dendritic spines in the LID was larger than those in the levodopa-treated control. Previous studies have shown that there are structural correlates of synaptic plasticity (Kasai et al, 2010a(Kasai et al, , 2010b. In general, spine size is correlated with the strength of synapses (Kasai et al, 2010a(Kasai et al, , 2010b.…”

Section: Morphological Changes In Dendritic Spines Of It-type Neuronsmentioning

confidence: 99%

“…The morphological properties of dendritic spines are intimately linked with synaptic functions; i.e., changes in synaptic plasticity are often accompanied by changes in spine size (Kasai et al, 2010a(Kasai et al, , 2010b. Accordingly, morphological examinations of dendritic spines in pyramidal neurons of the motor cortex in animal models should shed light on the mechanisms underlying the cortical synaptic abnormalities observed in PD patients with LID (Morgante et al, 2006;Suppa et al, 2011;Huang et al, 2012;Kishore et al, 2012).…”

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

Morphological and electrophysiological changes in intratelencephalic-type pyramidal neurons in the motor cortex of a rat model of levodopa-induced dyskinesia

Ueno

Yamada

Nishijima

et al. 2014

Neurobiology of Disease

View full text Add to dashboard Cite

Levodopa-induced dyskinesia (LID) is a major complication of long-term dopamine replacement therapy for Parkinson's disease, and becomes increasingly problematic in the advanced stage of the disease. Although the cause of LID still remains unclear, there is accumulating evidence from animal experiments that it results from maladaptive plasticity, resulting in supersensitive excitatory transmission at corticostriatal synapses. Recent work using transcranial magnetic stimulation suggests that the motor cortex displays the same supersensitivity in Parkinson's disease patients with LID. To date, the cellular mechanisms underlying the abnormal cortical plasticity have not been examined. The morphology of the dendritic spines has a strong relationship to synaptic plasticity. Therefore, we explored the spine morphology of pyramidal neurons in the motor cortex in a rat model of LID. We used control rats, 6-hydroxydopamine-lesioned rats  Spine enlargement and hyperexcitability in intratelencephalic-type corticostriatal neurons in M1 may be linked to development of dyskinesia.

show abstract

Section: Morphological Changes In Dendritic Spines Of It-type Neuronsmentioning

confidence: 94%

Section: Morphological Changes In Dendritic Spines Of It-type Neuronsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Morphological and electrophysiological changes in intratelencephalic-type pyramidal neurons in the motor cortex of a rat model of levodopa-induced dyskinesia

Ueno

Yamada

Nishijima

et al. 2014

Neurobiology of Disease

View full text Add to dashboard Cite

show abstract

“…A remarkable feature of excitatory and inhibitory synapses is their high level of structural variability 2 and the fact that their morphologies and stabilities change over time 3 . This phenomenon is regulated by activity, and the size of spine heads correlates with synaptic strength 4 , presynaptic properties 5 and the long-term stability of the synapse 6 .…”

Section: Molecular Mechanisms Of Synapse Remodellingmentioning

confidence: 99%

Structural plasticity upon learning: regulation and functions

2012

View full text Add to dashboard Cite

The contributions of brain networks to information processing and learning and memory are classically interpreted within the framework of Hebbian plasticity and the notion that synaptic weights can be modified by specific patterns of activity. However, accumulating evidence over the past decade indicates that synaptic networks are also structurally plastic, and that connectivity is remodelled throughout life, through mechanisms of synapse formation, stabilization and elimination 1. This has led to the concept of structural plasticity, which can encompass a variety of morphological changes that have functional consequences. These include on the one hand structural rearrangements at pre-existing synapses, and on the other hand the formation or loss of synapses, of neuronal processes that form synapses or of neurons. In this Review we focus on plasticity that involves gains and/or losses of synapses. Its key potential implication for learning and memory is to physically alter circuit connectivity, thus providing long-lasting memory traces that can be recruited at subsequent retrieval. Detecting this form of plasticity and relating it to its possible functions poses unique challenges, which are in part due to our still limited understanding of how structure relates to function in the nervous system.We review recent studies that relate the structural plasticity of neuronal circuits to behavioural learning and memory and discuss conceptual and mechanistic advances, as well as future challenges. The studies establish a number of strong links between specific behavioural learning processes and the assembly and loss of specific synapses. Further areas of substantial progress include molecular and cellular mechanisms that regulate synapse dynamics in response to alterations in synaptic activity, the specific spatial distribution of the syn aptic changes among identified neurons and dendrites and the relative roles of excitation and inhibition in regulating structural plasticity.The new findings provide exciting early vistas of how learning and memory may be implemented at the level of structural circuit plasticity. At the same time, they highlight major gaps in our understanding of plasticity regulation at the cellular, circuit and systems levels. Accordingly, achieving a better mechanistic understanding of learning and memory processes is likely to depend on the development of more effective techniques and models to investigate ensembles of identified synapses longitudinally, both functionally and structurally. Molecular mechanisms of synapse remodellingA remarkable feature of excitatory and inhibitory synapses is their high level of structural variability 2 and the fact that their morphologies and stabilities change over time 3 . This phenomenon is regulated by activity, and the size of spine heads correlates with synaptic strength 4 , presynaptic properties 5 and the long-term stability of the synapse 6 . The morphological characteristics of synapses thus reveal important features of their function and stabilit...

show abstract

“…Notably, because recent work suggests (24,25) a potential relationship between spine shape, synaptic function, and morphological rearrangements of the spines as forms of developmental or experience-dependent plasticity (26), we performed patch-clamp experiments in Nacc shell slices obtained from ethanol-withdrawn rats to evaluate whether long-term depression (LTD) formation and its underlying synaptic currents are modified by experimental conditions.…”

mentioning

confidence: 99%

Hampered long-term depression and thin spine loss in the nucleus accumbens of ethanol-dependent rats

Spiga

Talani

Mulas

et al. 2014

Proc. Natl. Acad. Sci. U.S.A.

View full text Add to dashboard Cite

Alcoholism involves long-term cognitive deficits, including memory impairment, resulting in substantial cost to society. Neuronal refinement and stabilization are hypothesized to confer resilience to poor decision making and addictive-like behaviors, such as excessive ethanol drinking and dependence. Accordingly, structural abnormalities are likely to contribute to synaptic dysfunctions that occur from suddenly ceasing the use of alcohol after chronic ingestion. Here we show that ethanol-dependent rats display a loss of dendritic spines in medium spiny neurons of the nucleus accumbens (Nacc) shell, accompanied by a reduction of tyrosine hydroxylase immunostaining and postsynaptic density 95-positive elements. Further analysis indicates that "long thin" but not "mushroom" spines are selectively affected. In addition, patch-clamp experiments from Nacc slices reveal that long-term depression (LTD) formation is hampered, with parallel changes in field potential recordings and reductions in NMDA-mediated synaptic currents. These changes are restricted to the withdrawal phase of ethanol dependence, suggesting their relevance in the genesis of signs and/or symptoms affecting ethanol withdrawal and thus the whole addictive cycle. Overall, these results highlight the key role of dynamic alterations in dendritic spines and their presynaptic afferents in the evolution of alcohol dependence. Furthermore, they suggest that the selective loss of long thin spines together with a reduced NMDA receptor function may affect learning. Disruption of this LTD could contribute to the rigid emotional and motivational state observed in alcohol dependence.A lcohol addiction is a major public health problem in the Western world. In the United States alone, about 15% of adults have an alcohol-related disorder at some point in their life, and alcohol abuse costs the economy over $220 billion per y in medical care and productivity loss (1). A general consensus has emerged on drug addiction as a substance-induced, aberrant form of neural plasticity (2, 3). The nucleus accumbens (Nacc) plays a central role in the neural circuits that are responsible for goal-directed behaviors (4, 5) and in addictive states. Its activity is heavily modulated by glutamate-(GLU) and dopamine-(DA) containing projections that originate in cortical and limbic regions and converge on a common postsynaptic target: the medium spiny neuron (MSN). Furthermore, DA modulates GLU inputs to Nacc neurons (6, 7), both by directly influencing synaptic transmission and by modulating voltage-dependent conductances (8). Accordingly, interactions between DA and GLU are involved in druginduced locomotor stimulation and addiction (9, 10) and may represent useful potential therapeutic targets (11,12). In the distal portion of the dendrites of MSNs a significant subpopulation of spines shows a particular synaptic architecture, called the "striatal microcircuit" or "synaptic triad" (13, 14), which is characterized by a double, discrete, and reciprocal interaction between DA and GLU aff...

show abstract

Learning rules and persistence of dendritic spines

Cited by 111 publications

References 127 publications

Morphological and electrophysiological changes in intratelencephalic-type pyramidal neurons in the motor cortex of a rat model of levodopa-induced dyskinesia

Morphological and electrophysiological changes in intratelencephalic-type pyramidal neurons in the motor cortex of a rat model of levodopa-induced dyskinesia

Structural plasticity upon learning: regulation and functions

Hampered long-term depression and thin spine loss in the nucleus accumbens of ethanol-dependent rats

Contact Info

Product

Resources

About