Enhancement of hippocampal LTP, reference memory and sensorimotor gating in mutant mice lacking a telencephalon‐specific cell adhesion molecule

Nakamura, Kazuhiro; Manabe, Toshiya; Watanabe, Masahiko; Mamiya, Takayoshi; Ichikawa, Ryoichi; Kiyama, Yuji; Sanbo, Makoto; Yagi, Takeshi; Inoue, Yoshiro; Nabeshima, Toshitaka; Mori, Hisashi; Mishina, Masayoshi

doi:10.1046/j.0953-816x.2000.01366.x

Cited by 75 publications

(68 citation statements)

References 72 publications

(120 reference statements)

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“…When sorted to the dendritic surface membrane, TLCN plays important roles in the formation and maintenance of the dendritic filopodia (Matsuno, Mori, and Yoshihara, unpublished data), in the generation of long-term potentiation at hippocampal synapses (Sakurai et al, 1998;Nakamura et al, 2001), and in the development and plasticity of neuronal circuit in the visual cortex (M. Faglioni, Matsuno, Mori, Yoshihara, and T. K. Hensch, unpublished data). TLCN has a homophilic binding activity (Tian et al, 2000b).…”

Section: A Transgenic Mouse System For Analysis Of Polarized Targetinmentioning

confidence: 99%

A Novel Phenylalanine-Based Targeting Signal Directs Telencephalin to Neuronal Dendrites

Mitsui

Saito²,

Hayashi³

et al. 2005

J. Neurosci.

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Section: A Transgenic Mouse System For Analysis Of Polarized Targetinmentioning

confidence: 99%

A Novel Phenylalanine-Based Targeting Signal Directs Telencephalin to Neuronal Dendrites

Mitsui

Saito²,

Hayashi³

et al. 2005

J. Neurosci.

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“…Experiments involving the deletion and the overexpression of a gene are strong tests of that gene's function. There are several other transgenic and KO manipulations that facilitate LTP and learning, such as the transgenic expression of the presynaptic Growth Associated Protein 43 (Routtenberg et al, 2000), and the mutation of a telencephalon-specific cell adhesion molecule (Nakamura et al, 2001).…”

Section: Transgenetic Manipulations That Enhance Ltp and Learningmentioning

confidence: 99%

Molecular and cellular cognitive studies of the role of synaptic plasticity in memory

2002

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Synaptic plasticity has a central rolein nearly all models of learning and memory. Besides experiments documenting changes in synaptic function during learning, most of the evidence supporting a role for synaptic plasticity in memory comes from manipulations that either enhance or lesion synaptic processes. In the last decade, mouse transgenetics (knock outs and transgenics) have provided compelling evidence that the molecular mechanisms responsible for the induction and stability of synaptic changes have a critical role in the acquisition and storage of information. Here, I will review this literature, with a special focus on studies of hippocampal-dependent learning and memory.

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confidence: 99%

“…Fragile X syndrome, a common form of mental retardation, exhibits a higher than normal density of spines but more of them exhibit an immature morphology and their turnover is not affected by sensory experience (9,20). Conversely, the protein Telencephalin arrests the maturation of spines and its removal enhances several forms of learning (13,21,22).Although many molecules have been identified that affect synapse number, it is unclear how newly formed spines mature into synapses (13,23,24). On a cellular level, learning and memory are associated with long-term potentiation (LTP) and long-term depression (LTD) of neurotransmission.…”

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confidence: 99%

O-GlcNAc transferase regulates excitatory synapse maturity

Lagerlöf

Hart

Huganir

2017

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

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Experience-driven synaptic plasticity is believed to underlie adaptive behavior by rearranging the way neuronal circuits process information. We have previously discovered that O-GlcNAc transferase (OGT), an enzyme that modifies protein function by attaching β-N-acetylglucosamine (GlcNAc) to serine and threonine residues of intracellular proteins (O-GlcNAc), regulates food intake by modulating excitatory synaptic function in neurons in the hypothalamus. However, how OGT regulates excitatory synapse function is largely unknown. Here we demonstrate that OGT is enriched in the postsynaptic density of excitatory synapses. In the postsynaptic density, O-GlcNAcylation on multiple proteins increased upon neuronal stimulation. Knockout of the OGT gene decreased the synaptic expression of the AMPA receptor GluA2 and GluA3 subunits, but not the GluA1 subunit. The number of opposed excitatory presynaptic terminals was sharply reduced upon postsynaptic knockout of OGT. There were also fewer and less mature dendritic spines on OGT knockout neurons. These data identify OGT as a molecular mechanism that regulates synapse maturity.O-GlcNAc | OGT | excitatory synapses | AMPA receptors N euronal synapses, the cell-cell junctions over which neurons communicate, are formed and eliminated throughout life, and their turnover has for decades been associated with the way neuronal circuits adapt to environmental challenges to optimize behavior (1, 2). In both humans and animals, early development is characterized by massive generation of new synapses. About half of all synapses are then lost during adolescence (2, 3). Most mature excitatory synapses occur on dendritic protrusions called spines and essentially all spines contain an excitatory synapse (4-6). In vivo imaging of individual spines for days to months has shown that adult spines are largely stable but a small subpopulation remains plastic (3, 7) and spine turnover is increased by novel experience (5,(8)(9)(10). Whereas most new spines are thin and withdraw rapidly, some enlarge and form stable synaptic contacts (2,3,7,(11)(12)(13)(14). In fact, the stabilization of a subset of new spines correlates with behavioral performance in several different tasks in multiple animal species (13,(15)(16)(17). Rather than synapse formation or density, the selection of which spines are retained once formed has been suggested to match circuit architecture with behavior (18). Without affecting spine formation, deleting β-adducin, which regulates actin, perturbed the process by which nascent spines establish functional synapses and impaired long-term memory (19). Fragile X syndrome, a common form of mental retardation, exhibits a higher than normal density of spines but more of them exhibit an immature morphology and their turnover is not affected by sensory experience (9,20). Conversely, the protein Telencephalin arrests the maturation of spines and its removal enhances several forms of learning (13,21,22).Although many molecules have been identified that affect synapse number, it is unclear h...

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Enhancement of hippocampal LTP, reference memory and sensorimotor gating in mutant mice lacking a telencephalon‐specific cell adhesion molecule

Cited by 75 publications

References 72 publications

A Novel Phenylalanine-Based Targeting Signal Directs Telencephalin to Neuronal Dendrites

A Novel Phenylalanine-Based Targeting Signal Directs Telencephalin to Neuronal Dendrites

Molecular and cellular cognitive studies of the role of synaptic plasticity in memory

O-GlcNAc transferase regulates excitatory synapse maturity

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