scholarly journals Elemental characterisation of the pyramidal neuron layer within the rat and mouse hippocampus

Metallomics ◽  
2019 ◽  
Vol 11 (1) ◽  
pp. 151-165 ◽  
Author(s):  
M. J. Hackett ◽  
A. Hollings ◽  
S. Caine ◽  
B. E. Bewer ◽  
M. Alaverdashvili ◽  
...  
Keyword(s):  
Fluorescence Microscopy ◽  
Pyramidal Neuron ◽  
Pyramidal Neurons ◽  
Hippocampal Pyramidal Neurons ◽  
X Ray ◽  
Mouse Hippocampus ◽  
Elemental Characterisation ◽  
Neuron Layer

X-ray fluorescence microscopy reveals unique elemental signatures within sub-populations of hippocampal pyramidal neurons.

scholarly journals Novel application of X-ray fluorescence microscopy (XFM) for the non-destructive micro-elemental analysis of natural mineral pigments on Aboriginal Australian objects

The Analyst ◽  
2016 ◽  
Vol 141 (12) ◽  
pp. 3657-3667 ◽  
Author(s):  
Rachel S. Popelka-Filcoff ◽  
Claire E. Lenehan ◽  
Enzo Lombi ◽  
Erica Donner ◽  
Daryl L. Howard ◽  
...  
Keyword(s):  
Fluorescence Microscopy ◽  
Elemental Analysis ◽  
Natural Mineral ◽  
X Ray ◽  
Elemental Characterisation ◽  
Non Destructive

This manuscript presents the first comprehensive non-destructive micro elemental characterisation of mineral pigments used on Aboriginal Australian objects.

scholarly journals M1 and M4 Receptors Modulate Hippocampal Pyramidal Neurons

2011 ◽  
Vol 105 (2) ◽  
pp. 779-792 ◽  
Author(s):  
Sameera Dasari ◽  
Allan T. Gulledge
Keyword(s):  
Pyramidal Neuron ◽  
Pyramidal Neurons ◽  
Glutamate Release ◽  
Stratum Radiatum ◽  
Cholinergic Modulation ◽  
Schaffer Collateral ◽  
Hippocampal Pyramidal Neurons ◽  
Ca1 Neurons ◽  
Neuron Excitability ◽  
M1 Receptors

Acetylcholine (ACh), acting at muscarinic ACh receptors (mAChRs), modulates the excitability and synaptic connectivity of hippocampal pyramidal neurons. CA1 pyramidal neurons respond to transient (“phasic”) mAChR activation with biphasic responses in which inhibition is followed by excitation, whereas prolonged (“tonic”) mAChR activation increases CA1 neuron excitability. Both phasic and tonic mAChR activation excites pyramidal neurons in the CA3 region, yet ACh suppresses glutamate release at the CA3-to-CA1 synapse (the Schaffer–collateral pathway). Using mice genetically lacking specific mAChRs (mAChR knockout mice), we identified the mAChR subtypes responsible for cholinergic modulation of hippocampal pyramidal neuron excitability and synaptic transmission. Knockout of M1 receptors significantly reduced, or eliminated, most phasic and tonic cholinergic responses in CA1 and CA3 pyramidal neurons. On the other hand, in the absence of other Gq-linked mAChRs (M3 and M5), M1 receptors proved sufficient for all postsynaptic cholinergic effects on CA1 and CA3 pyramidal neuron excitability. M3 receptors were able to participate in tonic depolarization of CA1 neurons, but otherwise contributed little to cholinergic responses. At the Schaffer–collateral synapse, bath application of the cholinergic agonist carbachol suppressed stratum radiatum–evoked excitatory postsynaptic potentials (EPSPs) in wild-type CA1 neurons and in CA1 neurons from mice lacking M1 or M2 receptors. However, Schaffer–collateral EPSPs were not significantly suppressed by carbachol in neurons lacking M4 receptors. We therefore conclude that M1 and M4 receptors are the major mAChR subtypes responsible for direct cholinergic modulation of the excitatory hippocampal circuit.

scholarly journals CRL5-dependent regulation of Arl4c and Arf6 controls hippocampal morphogenesis

2020 ◽  
Author(s):  
Jisoo S. Han ◽  
Keiko Hino ◽  
Raenier V. Reyes ◽  
Cesar P. Canales ◽  
Adam M. Miltner ◽  
...  
Keyword(s):  
Plasma Membrane ◽  
Pyramidal Neuron ◽  
Pyramidal Neurons ◽  
Small Gtpase ◽  
Knock Out ◽  
Hippocampal Pyramidal Neurons ◽  
Cullin 5 ◽  
Hippocampal Development ◽  
The Stability

SummaryThe small GTPase Arl4c participates in the regulation of cell migration, cytoskeletal rearrangements, and vesicular trafficking in epithelial cells. The Arl4c signaling cascade starts by the recruitment of the Arf-GEF cytohesins to the plasma membrane, which in turn engage the small GTPase Arf6. In the nervous system, Arf6 regulates dendrite outgrowth in vitro and neuronal migration in the developing cortex. However, the role of Arl4c-cytohesin-Arf6 signaling during brain development and particularly during hippocampal development remain elusive. Here, we report that the E3 ubiquitin ligase Cullin 5/Rbx2 (CRL5) controls the stability of Arl4c and its signaling effectors to regulate hippocampal morphogenesis. Rbx2 knock out causes hippocampal pyramidal neuron mislocalization and formation of multiple apical dendrites. The same phenotypes were observed when Cullin 5 was knocked down in pyramidal neurons by in utero electroporation. We used quantitative mass spectrometry to show that Arl4c, Cytohesin-1/3, and Arf6 accumulate in the telencephalon when Rbx2 is absent. Arl4c expression is post-transcriptionally regulated, with a peak in expression at early postnatal stages, and is localized at the plasma membrane and on intracellular vesicles in hippocampal pyramidal neurons. Furthermore, we show that depletion of Arl4c rescues the phenotypes caused by Cullin 5 knock down in the hippocampus, whereas depletion of Arf6 exacerbates over-migration. Finally, we show that Arl4c and Arf6 are necessary for the dendritic outgrowth of pyramidal neurons to the most superficial strata of the hippocampus. Overall, we identified CRL5 as a key regulator of hippocampal development and uncovered Arl4c and Arf6 as novel CRL5-regulated signaling effectors that control pyramidal neuron migration and dendritogenesis.

In vivo dual intra- and extracellular recordings suggest bidirectional coupling between CA1 pyramidal neurons

2012 ◽  
Vol 108 (6) ◽  
pp. 1584-1593 ◽  
Author(s):  
Edith Chorev ◽  
Michael Brecht
Keyword(s):  
Pyramidal Neuron ◽  
Action Potentials ◽  
Pyramidal Neurons ◽  
Hippocampal Pyramidal Neurons ◽  
Voltage Dependent ◽  
Dendritic Spikes ◽  
Discharge Patterns ◽  
Ca1 Pyramidal Neuron ◽  
Neighboring Neuron

Spikelets, small spikelike membrane potential deflections, are prominent in the activity of hippocampal pyramidal neurons in vivo. The origin of spikelets is still a source of much controversy. Somatically recorded spikelets have been postulated to originate from dendritic spikes, ectopic spikes, or spikes in an electrically coupled neuron. To differentiate between the different proposed mechanisms we used a dual recording approach in which we simultaneously recorded the intracellular activity of one CA1 pyramidal neuron and the extracellular activity in its vicinity, thus monitoring extracellularly the activity of both the intracellularly recorded cell as well as other units in its surroundings. Spikelets were observed in a quarter of our recordings ( n = 36). In eight of these nine recordings a second extracellular unit fired in correlation with spikelet occurrences. This observation is consistent with the idea that the spikelets reflect action potentials of electrically coupled nearby neurons. The extracellular spikes of these secondary units preceded the onset of spikelets. While the intracellular spikelet amplitude was voltage dependent, the simultaneously recorded extracellular unit remained unchanged. Spikelets often triggered action potentials in neurons, resulting in a characteristic 1- to 2-ms delay between spikelet onset and firing. Here we show that this relationship is bidirectional, with spikes being triggered by and also triggering spikelets. Secondary units, coupled to pyramidal neurons, showed discharge patterns similar to the recorded pyramidal neuron. These findings suggest that spikelets reflect spikes in an electrically coupled neighboring neuron, most likely of pyramidal cell type. Such coupling might contribute to the synchronization of pyramidal neurons with millisecond precision.

Scanning x-ray fluorescence microscopy and principal component analysis

1992 ◽  
Vol 50 (2) ◽  
pp. 1752-1753
Author(s):  
Brian Cross
Keyword(s):  
Principal Component Analysis ◽  
Fluorescence Microscopy ◽  
Spatial Resolution ◽  
High Speed ◽  
Image Acquisition ◽  
Principal Component ◽  
Fluorescence Microscope ◽  
Acquisition Rate ◽  
X Ray ◽  
Speed Up

A relatively new entry, in the field of microscopy, is the Scanning X-Ray Fluorescence Microscope (SXRFM). Using this type of instrument (e.g. Kevex Omicron X-ray Microprobe), one can obtain multiple elemental x-ray images, from the analysis of materials which show heterogeneity. The SXRFM obtains images by collimating an x-ray beam (e.g. 100 μm diameter), and then scanning the sample with a high-speed x-y stage. To speed up the image acquisition, data is acquired "on-the-fly" by slew-scanning the stage along the x-axis, like a TV or SEM scan. To reduce the overhead from "fly-back," the images can be acquired by bi-directional scanning of the x-axis. This results in very little overhead with the re-positioning of the sample stage. The image acquisition rate is dominated by the x-ray acquisition rate. Therefore, the total x-ray image acquisition rate, using the SXRFM, is very comparable to an SEM. Although the x-ray spatial resolution of the SXRFM is worse than an SEM (say 100 vs. 2 μm), there are several other advantages.

scholarly journals X-ray fluorescence microscopy scanning of Drosophila oocytes and eggs

2021 ◽  
Vol 2 (1) ◽  
pp. 100247
Author(s):  
Qinan Hu ◽  
Olga A. Antipova ◽  
Thomas V. O’Halloran ◽  
Mariana F. Wolfner
Keyword(s):  
Fluorescence Microscopy ◽  
X Ray

scholarly journals Prenatal treatment with rapamycin restores enhanced hippocampal mGluR-LTD and mushroom spine size in a Down’s syndrome mouse model

2021 ◽  
Vol 14 (1) ◽  
Author(s):  
Jesús David Urbano-Gámez ◽  
Juan José Casañas ◽  
Itziar Benito ◽  
María Luz Montesinos
Keyword(s):  
Intellectual Disability ◽  
Pyramidal Neurons ◽  
Metabotropic Glutamate Receptor ◽  
Therapeutic Potential ◽  
Mammalian Target Of Rapamycin ◽  
Memory Deficits ◽  
Prenatal Treatment ◽  
Hippocampal Pyramidal Neurons ◽  
Metabotropic Glutamate ◽  
Mushroom Spines

AbstractDown syndrome (DS) is the most frequent genetic cause of intellectual disability including hippocampal-dependent memory deficits. We have previously reported hippocampal mTOR (mammalian target of rapamycin) hyperactivation, and related plasticity as well as memory deficits in Ts1Cje mice, a DS experimental model. Here we characterize the proteome of hippocampal synaptoneurosomes (SNs) from these mice, and found a predicted alteration of synaptic plasticity pathways, including long term depression (LTD). Accordingly, mGluR-LTD (metabotropic Glutamate Receptor-LTD) is enhanced in the hippocampus of Ts1Cje mice and this is correlated with an increased proportion of a particular category of mushroom spines in hippocampal pyramidal neurons. Remarkably, prenatal treatment of these mice with rapamycin has a positive pharmacological effect on both phenotypes, supporting the therapeutic potential of rapamycin/rapalogs for DS intellectual disability.

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