Developmental Remodeling of the Retinogeniculate Synapse

Chen, Chinfei; Regehr, Wade G.

doi:10.1016/s0896-6273(00)00166-5

Cited by 394 publications

(536 citation statements)

References 82 publications

(4 reference statements)

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“…Numerous studies have revealed developmentally regulated synaptic maturation during periods when the expression of LTP is also robust (Crair and Malenka, 1995;Rumpel et al, 1998;Chen and Regehr, 2000), and this synaptic maturation is correlated with axon remodeling during map refinement (Meyer and Smith, 2006;Ruthazer et al, 2006). Whether the experimentally induced LTP is physiologically relevant to circuit formation is unclear, however, because of the wide variety of induction protocols used and the lack of information about natural activity patterns during development.…”

Section: Resultsmentioning

confidence: 99%

“…These results were seen during a period of significant refinement and maturation of retinogeniculate synapses, including increases in AMPA/ NMDA ratios and decreases in the presence of silent synapses (Chen and Regehr, 2000). By varying the timings of presynaptic and postsynaptic burst onsets, Butts et al (2007) also demonstrated that LTP did not depend on burst order, and that longterm depression (LTD) could be induced by separating burst onsets by hundreds to thousands of milliseconds.…”

Section: Model Of Retinal-wave-dependent Synaptic Plasticitymentioning

confidence: 93%

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Retinocollicular Synapse Maturation and Plasticity Are Regulated by Correlated Retinal Waves

Shah¹,

Crair²

2008

J. Neurosci.

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During development, spontaneous retinal waves are thought to provide an instructive signal for retinotopic map formation in the superior colliculus. In mice lacking the ␤2 subunit of nicotinic ACh receptors (␤2 Ϫ/Ϫ ), correlated retinal waves are absent during the first postnatal week, but return during the second postnatal week. In control retinocollicular synapses, in vitro analysis reveals that AMPA/ NMDA ratios and AMPA quantal amplitudes increase during the first postnatal week while the prevalence of silent synapses decreases. In age-matched ␤2 Ϫ/Ϫ mice, however, these parameters remain unchanged through the first postnatal week in the absence of retinal waves, but quickly mature to control levels by the end of the second week, suggesting that the delayed onset of correlated waves is able to drive synapse maturation. To examine whether such a mechanistic relationship exists, we applied a "burst-based" plasticity protocol that mimics coincident activity during retinal waves. We find that this pattern of activation is indeed capable of inducing synaptic strengthening [long-term potentiation (LTP)] on average across genotypes early in the first postnatal week [postnatal day 3 (P3) to P4] and, interestingly, that the capacity for LTP at the end of the first week (P6 -P7) is significantly greater in immature ␤2 Ϫ/Ϫ synapses than in mature control synapses. Together, our results suggest that retinal waves drive retinocollicular synapse maturation through a learning rule that is physiologically relevant to natural wave statistics and that these synaptic changes may serve an instructive role during retinotopic map refinement.

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Section: Resultsmentioning

confidence: 99%

Section: Model Of Retinal-wave-dependent Synaptic Plasticitymentioning

confidence: 93%

Retinocollicular Synapse Maturation and Plasticity Are Regulated by Correlated Retinal Waves

Shah¹,

Crair²

2008

J. Neurosci.

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“…Synaptic inputs from the ipsilateral and contralateral eyes compete for territory [30][31][32][33]. To achieve mature projection patterns, synaptic remodeling occurs, including synapse elimination as well as stabilization and elaboration of remaining synapses [34,35].…”

Section: Synaptic Pruning and Neuronal Developmentmentioning

confidence: 99%

Neuroinflammation: Ways in Which the Immune System Affects the Brain

et al. 2015

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Neuroinflammation is the response of the central nervous system (CNS) to disturbed homeostasis and typifies all neurological diseases. The main reactive components of the CNS include microglial cells and infiltrating myeloid cells, astrocytes, oligodendrocytes, and the blood-brain b a r r i e r , c y t o k i n e s , a n d c y t o k i n e s i g n a l i n g . Neuroinflammatory responses may be helpful or harmful, as mechanisms associated with neuroinflammation are involved in normal brain development, as well as in neuropathological processes. This review examines the roles of various cell types that contribute to the immune dysregulation associated with neuroinflammation. Microglia enter the CNS very early in embryonic development and, as such, play an essential role in both the healthy and diseased brain. B-cell diversity contributes to CNS disease through both antibody-dependent and antibody-independent mechanisms. The influences of these B-cell mechanisms on other cell types, including myeloid cells and T cells, are reviewed in relationship to antibody-mediated CNS disorders, paraneoplastic neurological diseases, and multiple sclerosis. New insights into neuroinflammation offer exciting opportunities to investigate potential therapeutic targets for debilitating CNS diseases.

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“…D uring early development in vertebrates, neurons in many parts of the nervous system form weak synapses with a large number of target cells (1)(2)(3)(4)(5)(6)(7). This early pattern of connectivity is refined through two processes: synapse elimination that removes many initial connections and synapse maturation whereby the remaining connections are strengthened (8,9).…”

mentioning

confidence: 99%

Essential role of postsynaptic NMDA receptors in developmental refinement of excitatory synapses

Zhang

Peterson

Liu

2012

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

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Neurons in the brains of newborns are usually connected with many other neurons through weak synapses. This early pattern of connectivity is refined through pruning of many immature connections and strengthening of the remaining ones. NMDA receptors (NMDARs) are essential for the development of excitatory synapses, but their role in synaptic refinement is controversial. Although chronic application of blockers or global knockdown of NMDARs disrupts developmental refinement in many parts of the brain, the ubiquitous presence of NMDARs makes it difficult to dissociate direct effects from indirect ones. We addressed this question in the thalamus by using genetic mosaic deletion of NMDARs. We demonstrate that pruning and strengthening of immature synapses are blocked in neurons without NMDARs, but occur normally in neighboring neurons with NMDARs. Our data support a model in which activation of NMDARs in postsynaptic neurons initiates synaptic refinement.D uring early development in vertebrates, neurons in many parts of the nervous system form weak synapses with a large number of target cells (1-7). This early pattern of connectivity is refined through two processes: synapse elimination that removes many initial connections and synapse maturation whereby the remaining connections are strengthened (8,9). This refinement of immature synapses is essential for the formation of neural circuits, and provides the basis for behavioral development. Many studies, in particular those conducted at the neuromuscular junction, in the cerebellum and visual pathways, have demonstrated that activity plays a central role in synaptic refinement (10-12). However, the mechanisms of synaptic refinement remain incompletely understood. At the neuromuscular junction, silencing of synaptic transmission disrupted the refinement process (13,14). The role of synaptic transmission in the refinement of central synapses seems more complex. Although manipulations of presynaptic activity disrupted the refinement of connections in the visual pathway (15-17), some of the effects were independent of synaptic transmission (18,19).The vast majority of excitatory synapses in the brain use glutamate as neurotransmitter; synaptic transmission is usually mediated by AMPA receptors (AMPARs) and NMDA receptors (NMDARs) in postsynaptic neurons. NMDARs play an important role in the development of neural circuits. In the brains of neonates, glutamatergic synapses have few or no AMPARs, and synaptic transmission is primarily mediated by NMDARs (20-23). Activation of NMDARs by correlated activity is thought to be a key mechanism underlying synaptic refinement during development (24, 25). Consistent with this idea, chronic application of NMDAR antagonists or global knockdown of NMDARs disrupts developmental refinement of neuronal circuits in many parts of the brain (26-28). However, recent studies in the hippocampus have shown that single-cell deletion of NMDARs in newborn mice has no effect on the number or density of synaptic spines (29). These findings raised the...

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Developmental Remodeling of the Retinogeniculate Synapse

Cited by 394 publications

References 82 publications

Retinocollicular Synapse Maturation and Plasticity Are Regulated by Correlated Retinal Waves

Retinocollicular Synapse Maturation and Plasticity Are Regulated by Correlated Retinal Waves

Neuroinflammation: Ways in Which the Immune System Affects the Brain

Essential role of postsynaptic NMDA receptors in developmental refinement of excitatory synapses

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