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Jun Noguchi

Publications and source records attributed to Jun Noguchi.

6 recordsLinked to original sources
PubMed2005

Spine-neck geometry determines NMDA receptor-dependent Ca2+ signaling in dendrites.

Increases in cytosolic Ca2+ concentration ([Ca2+]i) mediated by NMDA-sensitive glutamate receptors (NMDARs) are important for synaptic plasticity. We studied a wide variety of dendritic spines on rat CA1 pyramidal neurons in acute hippocampal slices. Two-photon uncaging and Ca2+ imaging revealed that NMDAR-mediated currents increased with spine-head volume and that even the smallest spines contained a significant number of NMDARs. The fate of Ca2+ that entered spine heads through NMDARs was governed by the shape (length and radius) of the spine neck. Larger spines had necks that permitted greater efflux of Ca2+ into the dendritic shaft, whereas smaller spines manifested a larger increase in [Ca2+]i within the spine compartment as a result of a smaller Ca2+ flux through the neck. Spine-neck geometry is thus an important determinant of spine Ca2+ signaling, allowing small spines to be the preferential sites for isolated induction of long-term potentiation.

Animals↗
PubMed2005

[Case of primary antiphospholipid antibody syndrome with repeated renal biopsies].

Antiphospholipid antibody syndrome (APS) is characterized by the presence of repeated arterial and venous thrombosis, recurrent fetal loss and thrombocytopenia. Recently, renal involvement associated with APS is being increasingly recognized and discussed. In most cases, there has been a vascular nephropathy characterized by small vessel vaso-occulusive lesions associated with fibrous intimal hyperplasia of the interlobular arteries, thrombosis and focal cortical atrophy. We report a case of a 38-year-old patient with primary APS. Renal biopsies were performed three times in 26 years. Various glomerular and vascular lesions associated with APS were observed and discussed.

Abortion, Habitual↗
PubMed2003

Structure-stability-function relationships of dendritic spines.

Dendritic spines, which receive most of the excitatory synaptic input in the cerebral cortex, are heterogeneous with regard to their structure, stability and function. Spines with large heads are stable, express large numbers of AMPA-type glutamate receptors, and contribute to strong synaptic connections. By contrast, spines with small heads are motile and unstable and contribute to weak or silent synaptic connections. Their structure-stability-function relationships suggest that large and small spines are "memory spines" and "learning spines", respectively. Given that turnover of glutamate receptors is rapid, spine structure and the underlying organization of the actin cytoskeleton are likely to be major determinants of fast synaptic transmission and, therefore, are likely to provide a physical basis for memory in cortical neuronal networks. Characterization of supramolecular complexes responsible for synaptic memory and learning is key to the understanding of brain function and disease.

Animals↗
PubMed2002

[Dendritic spine structures and functions].

Glutamate sensitivities of single dendritic spines were investigated with a two-photon photolysis of a caged-glutamate compound and the patch-clamp method in mouse hippocampal slice preparations. We found that the fast glutamate responses mediated by AMPA receptors were proportional to the volume of the spine head, but the slow responses induced by NMDA receptors displayed only weak correlation with the spine head volume and were independently regulated with the expression of AMPA receptors. This indicates that the strength of synaptic connection is stored as the spine structures, but that its plasticity may be regulated by independent factors. Abnormalities in spine shapes and distributions are commonly detected in most brain dysfunctions, including metal retardations, where structural consolidation phase may be impaired. These observations suggest that a physical basis of the memory in the cerebral cortex resides in the alteration and maintenance of spine structures.

Animals↗
PubMedDate not supplied

Nicotinic cholinergic synaptic mechanisms in the ventral tegmental area contribute to nicotine addiction.

Tobacco use is a major health problem that is estimated to cause 4 million deaths a year worldwide. Nicotine is the main addictive component of tobacco. It acts as an agonist to activate and desensitize nicotinic acetylcholine receptors (nAChRs). A component of nicotine's addictive power is attributable to actions on the mesolimbic dopaminergic system, which serves a fundamental role in the acquisition of behaviors that are inappropriately reinforced by addictive drugs. Here we show that nicotine, in the same concentration and time ranges as obtained from tobacco, has three main actions that regulate the activity of midbrain dopamine (DA) neurons. Nicotine first activates and then desensitizes nAChRs on the DA neurons. This process directly excites the DA neurons for a short period of time before the nAChRs desensitize. Nicotine also enhances glutamatergic excitation and decreases GABAergic inhibition onto DA neurons. These events increase the probability for synaptic plasticity, such as long-term potentiation. The short-lived direct excitation of the DA neurons coupled with the enhanced glutamatergic afferent activity provides the presynaptic and postsynaptic coincidence necessary to initiate synaptic potentiation. In total, these synaptic events lead to a relatively long-lasting heightened activity of midbrain DA neurons. Consistent with other summarized studies, this work indicates that the synaptic changes normally associated with learning and memory can be influenced and commandeered during the nicotine addiction process.

Acetylcholine↗