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Results for “synaptic plasticity”

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At least 1,207 records · Page 67Linked to original sources
PubMedDate not supplied

The neural cell adhesion molecule in synaptic plasticity and ageing.

By mediating cell adhesion and signal transduction, the neural cell adhesion molecule (NCAM) regulates neurite outgrowth, fasciculation and target recognition in the developing nervous system. In addition, a number of studies suggest an important role for the NCAM in regeneration and learning in the adult nervous system. NCAM-deficient mice are impaired in spatial learning. Moreover, by interfering with normal NCAM function by intracranial injections of NCAM-antibodies, long-term potentiation (LTP) in rat hippocampal slices and learning in rats and chicks have been inhibited. In the vertebrate nervous system, NCAM is the dominant carrier of polysialic acid (PSA), an unusual carbohydrate consisting of long homopolymers of sialic acid. The PSA-NCAM expression decreases markedly during development. However, an upregulation of polysialic acid (PSA) in restricted brain areas including the hippocampus has been observed following learning. Moreover, enzymatic removal of PSA results in impaired LTP and learning. In muscle, the PSA-NCAM expression is upregulated following denervation. This response is weakened in aging rats. The expression of NCAM and PSA have been shown to be regulated by neuronal activity suggesting that the NCAM may promote structural remodelling in an activity dependent manner associated with learning and regeneration.

Aging↗
PubMed2002

mRNA at synapses, synaptic plasticity, and memory consolidation.

Miller et al. (this issue of Neuron) report that deletion of the 3'UTR of alpha-CaMKII mRNA prevents dendritic delivery of the mRNA in transgenic mice and thus local synthesis of alpha-CaMKII protein in dendrites. 3'UTR mutant mice exhibit decreases in alpha-CaMKII protein in postsynaptic densities, and deficits in late phase LTP and in memory consolidation.

3' Untranslated Regions↗
PubMed2003

Narp and NP1 form heterocomplexes that function in developmental and activity-dependent synaptic plasticity.

Narp is a neuronal immediate early gene that plays a role in excitatory synaptogenesis. Here, we report that native Narp in brain is part of a pentraxin complex that includes NP1. These proteins are covalently linked by disulfide bonds into highly organized complexes, and their relative ratio in the complex is dynamically dependent upon the neuron's activity history and developmental stage. Complex formation is dependent on their distinct N-terminal coiled-coil domains, while their closely homologous C-terminal pentraxin domains mediate association with AMPA-type glutamate receptors. Narp is substantially more effective in assays of cell surface cluster formation, coclustering of AMPA receptors, and excitatory synaptogenesis, yet their combined expression results in supraadditive effects. These studies support a model in which Narp can regulate the latent synaptogenic activity of NP1 by forming mixed pentraxin assemblies. This mechanism appears to contribute to both activity-independent and activity-dependent excitatory synaptogenesis.

Amino Acid Sequence↗
PubMedDate not supplied

Active control of spike-timing dependent synaptic plasticity in an electrosensory system.

A spike timing dependent learning rule is present at the synapse between parallel fibers and Purkinje-like medium ganglion cells in the electrosensory lobe of mormyrid electric fish. The synapse is depressed when a postsynaptic dendritic spike occurs within 50 ms of the onset of a parallel fiber excitatory postsynaptic potential, but is enhanced at all other timing relations. Operation of this learning rule results in the cancellation of predictable membrane potential changes, driving the cell towards a constant output frequency. But medium ganglion cells show a strong and predictable response to corollary discharge signals associated with the motor command that initiates the electric organ discharge. The modeling study presented here resolves this conflict by proposing an active control of dendritic spike threshold during the brief period of medium ganglion cell response.

Action Potentials↗
PubMed1996

Postsynaptic calcium and calcium-dependent processes in synaptic plasticity in the developing visual cortex.

In this paper we describe some of the results obtained from recent experiments on mechanisms underlying long-term potentiation (LTP) and long-term depression (LTD) in the visual cortex of young rats. In particular, we focus on experiments which tested the hypotheses that the induction of LTP in the visual cortex is of Hebbian type and that an input-associated Ca2+ rise at postsynaptic sites and subsequent activation of protein kinases or protein phosphatases may play roles in the induction of LTP or LTD in the developing visual cortex.

Animals↗
PubMed1996

Further studies of the role of hippocampal synaptic plasticity in spatial learning: is hippocampal LTP a mechanism for automatically recording attended experience?

Rats trained as normal animals on a delayed matching-to-place task until they were fully familiar with the environment and the strategy required for effective performance were treated with a CSF or D-AP5 at a dose shown to be sufficient to block LTP in vivo. A striking delay-dependent impairment was observed in the AP5-treated animals. These findings indicate that 1-trial event memory depends on NMDA receptors.

2-Amino-5-phosphonovalerate↗
PubMed1996

Modulation of synaptic plasticity in the hippocampus and piriform cortex by physiologically meaningful olfactory cues in an olfactory association task.

Animals were trained to discriminate two natural odors while another group was trained to discriminate between a patterned electrical stimulation distributed on the lateral olfactory tract (LOT), labelled olfaco-mimetic stimulation (OMS), used as an olfactory cue versus a natural odor. No statistically significant difference was observed in behavioral data between these two groups. The animals trained to learn the meaning of the OMS exhibited a gradual long-term potentiation (LTP) phenomenon in the piriform cortex. When a group of naive animals was pseudo-conditioned, giving the OMS for the the same number of sessions but without any olfactory training, no LTP was recorded. These results indicate that the process of learning olfactory association gradually potentiates cortical synapses in a defined cortical terminal field, and may explain why LTP in the piriform cortex is not elicited by the patterned stimulation itself, but only in and associative context. As olfactory and hippocampus regions are connected via the lateral entorhinal cortex, the olfac-omimetic model was used to study the dynamic of involvement of the dentate gyrus (DG) in learning and memory of this associative olfactory task. Polysynaptic field potentials, evoked by the LOT stimulation, were recorded in the molecular layer of the ipsilateral DG. An early and rapid (2nd session) potentiation was observed when a significant discrimination of the two cues began to be observed. The onset latency of the potential response was 30-40 ms. When a group of naive animals was pseudoconditioned, no change was observed. Taken together, these results support the hypothesis that early activation of the DG during the learning of olfactory cue allows the progressive storage of olfactory information in a defined set of potentiated cortical synapses. The onset latency of the polysynaptic potentiated responses suggests that existence of reactivating hippocampal loops during the processing of olfactory information.

Animals↗
PubMed2002

A pharmacogenetic inducible approach to the study of NMDA/alphaCaMKII signaling in synaptic plasticity.

We recently introduced an inducible pharmacogenetic approach where pharmacological manipulations can be used to reveal recessive mutant phenotypes in a temporally controlled manner. This approach takes advantage of synergisms between pharmacological and genetic manipulations to alter the function of specific signaling pathways. For example, mice heterozygous for a point mutation (T286A) in the alpha-calcium/calmodulin-dependent kinase II (alphaCaMKII) gene show normal learning and memory. However, a concentration of an NMDA receptor antagonist (CPP) that does not affect learning in wild-type (WT) littermates, reveals learning deficits in this heterozygote (alphaCaMKII(T286A+/-)). Here, we show that pretetanic application of a concentration of CPP (0.1 microM) ineffective in WT hippocampal slices induced deficits in alphaCaMKII(T286A+/-) slices in hippocampal long-term potentiation (LTP), a mechanism thought to be involved in learning and memory. Importantly, posttetanic application of CPP (0.1 microM) had no effect on the expression or maintenance of LTP in hippocampal slices from alphaCaMKII(T286A+/-) mice. Thus, this pharmacogenetic approach allowed us to demonstrate that NMDA receptor-dependent autophosphorylation of alphaCaMKII is required during the induction but not maintenance of LTP. This ability to temporally induce recessive mutant phenotypes could be applicable to a broad range of problems and genetic systems.

Animals↗
PubMed2003

Effect of antibodies to morphine on synaptic plasticity of the hippocampus.

Incubation of hippocampal slices with antibodies to morphine did not change the total excitatory postsynaptic potential of mossy fibers, but markedly facilitated long-term posttetanic potentiation. Culturing of the organotypic hippocampal culture in the presence of 10 microM morphine increased the total excitatory postsynaptic potential of mossy fibers and reduced the probability of long-term posttetanic potentiation.

Animals↗
PubMed2005

GluR-A-dependent synaptic plasticity is required for the temporal encoding of nonspatial information.

Four related experiments studied operant performance of mice on differential reinforcement of low rates of responding (DRL) paradigms. Experiment 1 showed that excitotoxic hippocampal lesions impaired performance of a 10-s DRL schedule (DRL-10). Experiments 2 and 3 showed that GluR-A AMPA receptor subunit knockout mice, which are deficient in CA3-CA1 long-term potentiation (LTP), were markedly impaired at 15 s (DRL-15), but less impaired at DRL-10. Experiment 4 compared DRL-15 performance in mice from the 2 strains from which the GluR-A colony was derived and showed that they did not differ. The results show that GluR-A-containing AMPA receptors are required for normal performance on hippocampus-dependent, nonspatial working memory tasks, consistent with a role for GluR-A in the temporal encoding (what happened when) of nonspatial information.

Animals↗