Nectin-dependent localization of ZO-1 at puncta adhaerentia junctions between the mossy fiber terminals and the dendrites of the pyramidal cells in the CA3 area of adult mouse hippocampus

2003 ◽  
Vol 460 (4) ◽  
pp. 514-524 ◽  
Author(s):  
Maiko Inagaki ◽  
Kenji Irie ◽  
Maki Deguchi-Tawarada ◽  
Wataru Ikeda ◽  
Toshihisa Ohtsuka ◽  
...  
Keyword(s):  
Adult Mouse ◽  
Mossy Fiber ◽  
Pyramidal Cells ◽  
Mouse Hippocampus

scholarly journals Nectin

2002 ◽  
Vol 156 (3) ◽  
pp. 555-565 ◽  
Author(s):  
Akira Mizoguchi ◽  
Hiroyuki Nakanishi ◽  
Kazushi Kimura ◽  
Kaho Matsubara ◽  
Kumi Ozaki-Kuroda ◽  
...  
Keyword(s):  
Hippocampal Neurons ◽  
Adult Mouse ◽  
Mossy Fiber ◽  
Pyramidal Cells ◽  
Concomitant Increase ◽  
Adhesion System ◽  
Mouse Hippocampus ◽  
Synaptic Junctions ◽  
Trans Dimer

The nectin–afadin system is a novel cell–cell adhesion system that organizes adherens junctions cooperatively with the cadherin–catenin system in epithelial cells. Nectin is an immunoglobulin-like adhesion molecule, and afadin is an actin filament–binding protein that connects nectin to the actin cytoskeleton. Nectin has four isoforms (-1, -2, -3, and -4). Each nectin forms a homo-cis-dimer followed by formation of a homo-trans-dimer, but nectin-3 furthermore forms a hetero-trans-dimer with nectin-1 or -2, and the formation of each hetero-trans-dimer is stronger than that of each homo-trans-dimer. We show here that at the synapses between the mossy fiber terminals and dendrites of pyramidal cells in the CA3 area of adult mouse hippocampus, the nectin–afadin system colocalizes with the cadherin–catenin system, and nectin-1 and -3 asymmetrically localize at the pre- and postsynaptic sides of puncta adherentia junctions, respectively. During development, nectin-1 and -3 asymmetrically localize not only at puncta adherentia junctions but also at synaptic junctions. Inhibition of the nectin-based adhesion by an inhibitor of nectin-1 in cultured rat hippocampal neurons results in a decrease in synapse size and a concomitant increase in synapse number. These results indicate an important role of the nectin–afadin system in the formation of synapses.

scholarly journals Kainate Receptor–Mediated Inhibition of Glutamate Release Involves Protein Kinase A in the Mouse Hippocampus

2006 ◽  
Vol 96 (4) ◽  
pp. 1829-1837 ◽  
Author(s):  
José V. Negrete-Díaz ◽  
Talvinder S. Sihra ◽  
José M. Delgado-García ◽  
Antonio Rodríguez-Moreno
Keyword(s):  
Protein Kinase ◽  
Protein Kinase A ◽  
Mossy Fiber ◽  
Glutamate Release ◽  
Pyramidal Cells ◽  
Kainate Receptors ◽  
Mouse Hippocampus ◽  
Ca3 Pyramidal Cells ◽  
Kinase A ◽  
Stimulation Of

The mechanisms involved in the inhibition of glutamate release mediated by the activation of presynaptic kainate receptors (KARs) at the hippocampal mossy fiber–CA3 synapse are not well understood. We have observed a long-lasting inhibition of CA3 evoked excitatory postsynaptic currents (eEPSCs) after a brief application of kainate (KA) at concentrations ranging from 0.3 to 10 μM. The inhibition outlasted the change in holding current caused by the activation of ionotropic KARs in CA3 pyramidal cells, indicating that this action is not contingent on the opening of the receptor channels. The inhibition of the eEPSCs by KA was prevented by G protein and protein kinase A (PKA) inhibitors and was enhanced after stimulation of the adenylyl cyclase (AC) with forskolin. We conclude that KARs present at mossy fiber terminals mediate the inhibition of glutamate release through a metabotropic mechanism that involves the activation of an AC-second messenger cAMP-PKA signaling cascade.

Size Does Matter: Generation of Intrinsic Network Rhythms in Thick Mouse Hippocampal Slices

2005 ◽  
Vol 93 (4) ◽  
pp. 2302-2317 ◽  
Author(s):  
Chiping Wu ◽  
Wah Ping Luk ◽  
Jesse Gillis ◽  
Frances Skinner ◽  
Liang Zhang
Keyword(s):  
In Vitro Model ◽  
Adult Mouse ◽  
Hippocampal Slices ◽  
Network Connectivity ◽  
Slice Preparation ◽  
Fundamental Properties ◽  
Mouse Hippocampus ◽  
Hippocampal Network ◽  
Vitro Model

Rodent hippocampal slices of ≤0.5 mm thickness have been widely used as a convenient in vitro model since the 1970s. However, spontaneous population rhythmic activities do not consistently occur in this preparation due to limited network connectivity. To overcome this limitation, we develop a novel slice preparation of 1 mm thickness from adult mouse hippocampus by separating dentate gyrus from CA3/CA1 areas but preserving dentate–CA3-CA1 connectivity. While superfused in vitro at 32 or 37°C, the thick slice exhibits robust spontaneous network rhythms of 1–4 Hz that originate from the CA3 area. Via assessing tissue O2, K+, pH, synaptic, and single-cell activities of superfused thick slices, we verify that these spontaneous rhythms are not a consequence of hypoxia and nonspecific experimental artifacts. We suggest that the thick slice contains a unitary circuitry sufficient to generate intrinsic hippocampal network rhythms and this preparation is suitable for exploring the fundamental properties and plasticity of a functionally defined hippocampal “lamella” in vitro.

scholarly journals Connectivity and network state-dependent recruitment of long-range VIP-GABAergic neurons in the mouse hippocampus

2018 ◽  
Author(s):  
Ruggiero Francavilla ◽  
Vincent Villette ◽  
Xiao Luo ◽  
Simon Chamberland ◽  
Einer Muñoz-Pino ◽  
...  
Keyword(s):  
Molecular Diversity ◽  
Pyramidal Cells ◽  
Functional Specialization ◽  
Gabaergic Interneurons ◽  
Long Distance ◽  
State Dependent ◽  
Mouse Hippocampus ◽  
Ca1 Area ◽  
New Evidence

AbstractGABAergic interneurons in the hippocampus provide for local and long-distance coordination of neurons in functionally connected areas. Vasoactive intestinal peptide-expressing (VIP+) interneurons occupy a distinct niche in circuitry as many of them specialize in innervating GABAergic cells, thus providing network disinhibition. In the CA1 hippocampus, VIP+ interneuron-selective cells target local interneurons. Here, we discovered a novel type of VIP+ neuron whose axon innervates CA1 and also projects to the subiculum (VIP-LRPs). VIP-LRPs showed specific molecular properties and targeted interneurons within the CA1 area but both interneurons and pyramidal cells within subiculum. They were interconnected through gap junctions but demonstrated sparse spike coupling in vitro. In awake mice, VIP-LRPs decreased their activity during theta-run epochs and were more active during quiet wakefulness but not coupled to sharp-wave ripples. Together, the data provide new evidence for VIP interneuron molecular diversity and functional specialization in controlling cell ensembles along the hippocampo-subicular axis.

scholarly journals Separable actions of acetylcholine and noradrenaline on neuronal ensemble formation in hippocampal CA3 circuits

2021 ◽  
Vol 17 (10) ◽  
pp. e1009435
Author(s):  
Luke Y. Prince ◽  
Travis Bacon ◽  
Rachel Humphries ◽  
Krasimira Tsaneva-Atanasova ◽  
Claudia Clopath ◽  
...  
Keyword(s):  
Granule Cells ◽  
Mossy Fiber ◽  
Pyramidal Cells ◽  
Recurrent Network ◽  
Memory Storage ◽  
Neuronal Ensembles ◽  
Hippocampal Ca3 ◽  
Ca3 Pyramidal Cells ◽  
Episodic Memories ◽  
Mossy Fiber Pathway

In the hippocampus, episodic memories are thought to be encoded by the formation of ensembles of synaptically coupled CA3 pyramidal cells driven by sparse but powerful mossy fiber inputs from dentate gyrus granule cells. The neuromodulators acetylcholine and noradrenaline are separately proposed as saliency signals that dictate memory encoding but it is not known if they represent distinct signals with separate mechanisms. Here, we show experimentally that acetylcholine, and to a lesser extent noradrenaline, suppress feed-forward inhibition and enhance Excitatory–Inhibitory ratio in the mossy fiber pathway but CA3 recurrent network properties are only altered by acetylcholine. We explore the implications of these findings on CA3 ensemble formation using a hierarchy of models. In reconstructions of CA3 pyramidal cells, mossy fiber pathway disinhibition facilitates postsynaptic dendritic depolarization known to be required for synaptic plasticity at CA3-CA3 recurrent synapses. We further show in a spiking neural network model of CA3 how acetylcholine-specific network alterations can drive rapid overlapping ensemble formation. Thus, through these distinct sets of mechanisms, acetylcholine and noradrenaline facilitate the formation of neuronal ensembles in CA3 that encode salient episodic memories in the hippocampus but acetylcholine selectively enhances the density of memory storage.

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