scholarly journals Comparison of the structural organisation of reeler hippocampal CA1 region with wild type CA1.

2018 ◽  
Author(s):  
Malikmohamed Yousuf ◽  
Shanting Zhao ◽  
Michael Frotscher
Keyword(s):  
Pyramidal Neurons ◽  
Fluorescent Protein ◽  
Imaging Techniques ◽  
Quantitative Imaging ◽  
Orientation Angle ◽  
Wild Type ◽  
Golgi Impregnation ◽  
Ca1 Pyramidal Neurons ◽  
Ca1 Region ◽  
Dendritic Branches

The dendritic pattern defines the input capacity of a neuron. Existing methods such as Golgi impregnation or intracellular staining only label a small number of neurons. By using high-resolution imaging and 3D reconstruction of green fluorescent protein-expressing neurons, the present study provides an approach to investigate the anatomical organization of dendritic structures in defined brain regions. We characterized the structural organization of dendrites in the CA1 region of the mouse hippocampus by analyzing Sholl intersections, dendritic branches, branching and orientation angles of dendrites, and the different types of spine on the dendritic branches. Utilizing this quantitative imaging approach, we show that there are differences in the number of Sholl intersections and in the orientation of apical and basal dendrites of CA1 pyramidal neurons. Performing 3D reconstructions of the CA1 region of the reeler hippocampus, we show that neurons of this mutant display an arbitrary orientation of apical dendrites at angles ranging from -180 to +180 degrees in contrast to wild-type mice that show a preferred orientation angle. This methodology provides a way of analyzing network organization in wild type and mutant brains using quantitative imaging techniques. Here, we have provided evidence that in reeler a sparse, weakly connected network results from the altered lamination of CA1 pyramidal neurons and the variable orientation of their dendrites.

scholarly journals Increased Calbindin D28k Expression via Long-Term Alternate-Day Fasting Does Not Protect against Ischemia-Reperfusion Injury: A Focus on Delayed Neuronal Death, Gliosis and Immunoglobulin G Leakage

2021 ◽  
Vol 22 (2) ◽  
pp. 644
Author(s):  
Hyejin Sim ◽  
Tae-Kyeong Lee ◽  
Yeon Ho Yoo ◽  
Ji Hyeon Ahn ◽  
Dae Won Kim ◽  
...  
Keyword(s):  
Immunoglobulin G ◽  
Pyramidal Neurons ◽  
Short Term Memory ◽  
Forebrain Ischemia ◽  
Short Term ◽  
Term Memory ◽  
Transient Forebrain Ischemia ◽  
Ca1 Pyramidal Neurons ◽  
Ca1 Region ◽  
Calbindin D28k

Calbindin-D28k (CB), a calcium-binding protein, mediates diverse neuronal functions. In this study, adult gerbils were fed a normal diet (ND) or exposed to intermittent fasting (IF) for three months, and were randomly assigned to sham or ischemia operated groups. Ischemic injury was induced by transient forebrain ischemia for 5 min. Short-term memory was examined via passive avoidance test. CB expression was investigated in the Cornu Ammonis 1 (CA1) region of the hippocampus via western blot analysis and immunohistochemistry. Finally, histological analysis was used to assess neuroprotection and gliosis (microgliosis and astrogliosis) in the CA1 region. Short-term memory did not vary significantly between ischemic gerbils with IF and those exposed to ND. CB expression was increased significantly in the CA1 pyramidal neurons of ischemic gerbils with IF compared with that of gerbils fed ND. However, the CB expression was significantly decreased in ischemic gerbils with IF, similarly to that of ischemic gerbils exposed to ND. The CA1 pyramidal neurons were not protected from ischemic injury in both groups, and gliosis (astrogliosis and microgliosis) was gradually increased with time after ischemia. In addition, immunoglobulin G was leaked into the CA1 parenchyma from blood vessels and gradually increased with time after ischemic insult in both groups. Taken together, our study suggests that IF for three months increases CB expression in hippocampal CA1 pyramidal neurons; however, the CA1 pyramidal neurons are not protected from transient forebrain ischemia. This failure in neuroprotection may be attributed to disruption of the blood–brain barrier, which triggers gliosis after ischemic insults.

scholarly journals Comparing basal dendrite branches in human and mouse hippocampal CA1 pyramidal neurons with Bayesian networks

2020 ◽  
Vol 10 (1) ◽  
Author(s):  
Bojan Mihaljević ◽  
Pedro Larrañaga ◽  
Ruth Benavides-Piccione ◽  
Javier DeFelipe ◽  
Concha Bielza
Keyword(s):  
Bayesian Networks ◽  
Pyramidal Neurons ◽  
Graphical Representation ◽  
Data Set ◽  
Ca1 Region ◽  
Basal Dendrites ◽  
Hippocampal Ca1 ◽  
Dendritic Branches ◽  
Branch Type ◽  
Human And Mouse

Abstract Pyramidal neurons are the most common cell type in the cerebral cortex. Understanding how they differ between species is a key challenge in neuroscience. A recent study provided a unique set of human and mouse pyramidal neurons of the CA1 region of the hippocampus, and used it to compare the morphology of apical and basal dendritic branches of the two species. The study found inter-species differences in the magnitude of the morphometrics and similarities regarding their variation with respect to morphological determinants such as branch type and branch order. We use the same data set to perform additional comparisons of basal dendrites. In order to isolate the heterogeneity due to intrinsic differences between species from the heterogeneity due to differences in morphological determinants, we fit multivariate models over the morphometrics and the determinants. In particular, we use conditional linear Gaussian Bayesian networks, which provide a concise graphical representation of the independencies and correlations among the variables. We also extend the previous study by considering additional morphometrics and by formally testing whether a morphometric increases or decreases with the distance from the soma. This study introduces a multivariate methodology for inter-species comparison of morphology.

Serotonin Modulates Spike Backpropagation and Associated [Ca2+]i Changes in the Apical Dendrites of Hippocampal CA1 Pyramidal Neurons

1999 ◽  
Vol 81 (1) ◽  
pp. 216-224 ◽  
Author(s):  
Vladislav M. Sandler ◽  
William N. Ross
Keyword(s):  
Action Potentials ◽  
Pyramidal Neurons ◽  
Peak Potential ◽  
Fura 2 ◽  
Ca1 Pyramidal Neurons ◽  
Ca1 Region ◽  
Artificial Cerebrospinal Fluid ◽  
Hippocampal Ca1 ◽  
Conductance Increase ◽  
Apical Dendrites

Sandler, Vladislav M. and William N. Ross. Serotonin modulates spike backpropagation and associated [Ca2+]i changes in the apical dendrites of hippocampal CA1 pyramidal neurons. J. Neurophysiol. 81: 216–224, 1999. The effect of serotonin (5-HT) on somatic and dendritic properties was analyzed in pyramidal neurons from the CA1 region in slices from the rat hippocampus. Bath-applied 5-HT (10 μM) hyperpolarized the soma and apical dendrites and caused a conductance increase at both locations. In the dendrites (200–300 μm from the soma) trains of antidromically activated, backpropagating action potentials had lower peak potentials in 5-HT than in normal artificial cerebrospinal fluid. Spike amplitudes were about the same in the two solutions. Similar results were found when the action potentials were evoked synaptically with stimulation in the stratum oriens. In the soma, spike amplitudes increased in 5-HT, with only a small decrease in the peak potential. Calcium concentration measurements, made with bis-fura-2 injected through patch electrodes, showed that the amplitude of the [Ca2+]i changes was reduced at all locations in 5-HT. The reduction of the [Ca2+]i change in the soma was confirmed in slices where cells were loaded with fura-2-AM. The reduction at the soma in 5-HT, where the spike amplitude increased, suggests that the reduction is due primarily to direct modulation of Ca2+ channels. In the dendrites, the reduction is due to a combination of this channel modulation and the lowering of the peak potential of the action potentials.

scholarly journals Barium Plateau Potentials of CA1 Pyramidal Neurons Elicit All-or-None Extracellular Alkaline Shifts Via the Plasma Membrane Calcium ATPase

2010 ◽  
Vol 104 (3) ◽  
pp. 1438-1444 ◽  
Author(s):  
Sachin Makani ◽  
Mitchell Chesler
Keyword(s):  
Plasma Membrane ◽  
High Speed ◽  
Pyramidal Neurons ◽  
Hippocampal Slices ◽  
Brain Regions ◽  
Low Noise ◽  
Body Region ◽  
Pipette Solution ◽  
Ca1 Pyramidal Neurons ◽  
Ca1 Region

In many brain regions, synchronous neural activity causes a rapid rise in extracellular pH. In the CA1 region of hippocampus, this population alkaline transient (PAT) enhances responses from postsynaptic, pH-sensitive N-methyl-d-aspartate (NMDA) receptors. Recently, we showed that the plasma membrane Ca2+-ATPase (PMCA), a ubiquitous transporter that exchanges internal Ca2+ for external H+, is largely responsible for the PAT. It has also been shown that a PAT can be generated after replacing extracellular Ca2+ with Ba2+. The cause of this PAT is unknown, however, because the ability of the mammalian PMCA to transport Ba2+ is unclear. If the PMCA did not carry Ba2+, a different alkalinizing source would have to be postulated. Here, we address this issue in mouse hippocampal slices, using concentric (high-speed, low-noise) pH microelectrodes. In Ba2+-containing, Ca2+-free artificial cerebrospinal fluid, a single antidromic shock to the alveus elicited a large (0.1–0.2 unit pH), “all-or-none” PAT in the CA1 cell body region. In whole cell current clamp of single CA1 pyramidal neurons, the same stimulus evoked a prolonged plateau potential that was similarly all-or-none. Using this plateau as the voltage command in other cells, we recorded Ba2+-dependent surface alkaline transients (SATs). The SATs were suppressed by adding 5 mM extracellular HEPES and abolished when carboxyeosin (a PMCA inhibitor) was in the patch pipette solution. These results suggest that the PAT evoked in the presence of Ba2+ is caused by the PMCA and that this transporter is responsible for the PAT whether Ca2+ or Ba2+ is the charge carrying divalent cation.

scholarly journals Ca2+- and Metabolism-Related Changes of Mitochondrial Potential in Voltage-Clamped CA1 Pyramidal Neurons In Situ

2000 ◽  
Vol 83 (3) ◽  
pp. 1710-1721 ◽  
Author(s):  
S. Schuchmann ◽  
M. Lückermann ◽  
A. Kulik ◽  
U. Heinemann ◽  
K. Ballanyi
Keyword(s):  
Pyramidal Neurons ◽  
Imaging Techniques ◽  
Hippocampal Slices ◽  
Fluorescence Signal ◽  
Mitochondrial Potential ◽  
Ca1 Pyramidal Neurons ◽  
Eosin B ◽  
Intracellular Ca ◽  
Delayed Recovery

In hippocampal slices from rats, dialysis with rhodamine-123 (Rh-123) and/or fura-2 via the patch electrode allowed monitoring of mitochondrial potential (ΔΨ) changes and intracellular Ca2+ ([Ca2+]i) of CA1 pyramidal neurons. Plasmalemmal depolarization to 0 mV caused a mean [Ca2+]i rise of 300 nM and increased Rh-123 fluorescence signal (RFS) by ≤50% of control. The evoked RFS, indicating depolarization of ΔΨ, and the [Ca2+]i transient were abolished by Ca2+-free superfusate or exposure of Ni2+/Cd2+. Simultaneous measurements of RFS and [Ca2+]i showed that the kinetics of both the Ca2+ rise and recovery were considerably faster than those of the ΔΨ depolarization. The plasmalemmal Ca2+/H+ pump blocker eosin-B potentiated the peak of the depolarization-induced RFS and delayed recovery of both the RFS and [Ca2+]i transient. Thus the ΔΨ depolarization due to plasmalemmal depolarization is related to mitochondrial Ca2+ sequestration secondary to Ca2+ influx through voltage-gated Ca2+channels. CN− elevated [Ca2+]iby <50 nM but increased RFS by 221% as a result of extensive depolarization of ΔΨ. Oligomycin decreased RFS by 52% without affecting [Ca2+]i. In the presence of oligomycin, CN− and p-trifluoromethoxy-phenylhydrazone (FCCP) elevated [Ca2+]i by <50 nM and increased RFS by 285 and 290%, respectively. Accordingly, the metabolism-related ΔΨ changes are independent of [Ca2+]i. Imaging techniques revealed that evoked [Ca2+]i rises are distributed uniformly over the soma and primary dendrites, whereas corresponding changes in RFS occur more localized in subregions within the soma. The results show that microfluorometric measurement of the relation between mitochondrial function and intracellular Ca2+ is feasible in whole cell recorded mammalian neurons in situ.

IPSPs modulate spike backpropagation and associated [Ca2+]i changes in the dendrites of hippocampal CA1 pyramidal neurons

1996 ◽  
Vol 76 (5) ◽  
pp. 2896-2906 ◽  
Author(s):  
H. Tsubokawa ◽  
W. N. Ross
Keyword(s):  
Action Potentials ◽  
Pyramidal Neurons ◽  
Time Window ◽  
Proximal Part ◽  
Stratum Radiatum ◽  
Ca1 Pyramidal Neurons ◽  
Hippocampal Ca1 ◽  
Dendritic Branches ◽  
Apical Dendrites ◽  
Stratum Lacunosum Moleculare

1. We studied the effects of synaptic inhibition on backpropagating Na+ spikes in the apical dendrites of CA1 pyramidal neurons in transverse slices from the rat hippocampus. Action potentials were evoked synaptically by stimulation in the stratum radiatum or antidromically by stimulation in the alveus. 2. Inhibitory postsynaptic potentials, evoked by stimulation in the stratum lacunosum moleculare, reduced the amplitude of single spikes in the distal dendrites but did not change the amplitudes in the somatic or proximal regions. Inhibition also reduced the spike-associated [Ca2+]i changes in the distal dendrites but had little effect on the changes in the proximal part of the cell. Both of these results are consistent with inhibition converting actively backpropagating spikes into passively spreading potentials at some point in the arbor. 3. In most cells, the spike amplitude reduction in the distal dendrites was blocked by bicuculline methiodide (10 microM) and inhibition was most effective when evoked in a time window < 10 ms preceding the action potential. This suggests that the amplitude reduction was due to a conductance shunt activated by gamma-aminobuturic acid-A (GABAA) receptors. Synaptically evoked GABAB responses were detected but usually did not block spike propagation. 4. Direct hyperpolarization in the distal dendrites was also effective in blocking antidromically evoked spike backpropagation but probably does not contribute when the action potentials are evoked synaptically. 5. This effect of inhibition is different from its usual function in synaptic integration because spike generation and propagation down the axon are not significantly affected. This kind of inhibition might be important in regulating transient [Ca2+]i changes in the dendrites including individual dendritic branches.

scholarly journals Estradiol Increases Spine Density and NMDA-Dependent Ca2+ Transients in Spines of CA1 Pyramidal Neurons From Hippocampal Slices

1999 ◽  
Vol 81 (3) ◽  
pp. 1404-1411 ◽  
Author(s):  
Lucas D. Pozzo-Miller ◽  
Takafumi Inoue ◽  
Diane Dieuliis Murphy
Keyword(s):  
Pyramidal Neurons ◽  
Hippocampal Slices ◽  
Input Resistance ◽  
Spine Density ◽  
Afferent Stimulation ◽  
Α Subunit ◽  
Ca1 Neurons ◽  
Ca1 Pyramidal Neurons ◽  
Ca1 Region

Estradiol increases spine density and NMDA-dependent Ca2+transients in spines of CA1 pyramidal neurons from hippocampal slices. To investigate the physiological consequences of the increase in spine density induced by estradiol in pyramidal neurons of the hippocampus, we performed simultaneous whole cell recordings and Ca2+ imaging in CA1 neuron spines and dendrites in hippocampal slices. Four- to eight-days in vitro slice cultures were exposed to 17β-estradiol (EST) for an additional 4- to 8-day period, and spine density was assessed by confocal microscopy of DiI-labeled CA1 pyramidal neurons. Spine density was doubled in both apical and basal dendrites of the CA1 region in EST-treated slices; consistently, a reduction in cell input resistance was observed in EST-treated CA1 neurons. Double immunofluorescence staining of presynaptic (synaptophysin) and postsynaptic (α-subunit of CaMKII) proteins showed an increase in synaptic density after EST treatment. The slopes of the input/output curves of both α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) and N-methyl-d-aspartate (NMDA) postsynaptic currents were steeper in EST-treated CA1 neurons, consistent with the observed increase in synapse density. To characterize NMDA-dependent synaptic currents and dendritic Ca2+ transients during Schaffer collaterals stimulation, neurons were maintained at +40 mV in the presence of nimodipine, picrotoxin, and 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX). No differences in resting spine or dendritic Ca2+ levels were observed between control and EST-treated CA1 neurons. Intracellular Ca2+transients during afferent stimulation exhibited a faster slope and reached higher levels in spines than in adjacent dendrites. Peak Ca2+ levels were larger in both spines and dendrites of EST-treated CA1 neurons. Ca2+ gradients between spine heads and dendrites during afferent stimulation were also larger in EST-treated neurons. Both spine and dendritic Ca2+transients during afferent stimulation were reversibly blocked byd,l-2-amino-5-phosphonovaleric acid (d,l-APV). The increase in spine density and the enhanced NMDA-dependent Ca2+ signals in spines and dendrites induced by EST may underlie a threshold reduction for induction of NMDA-dependent synaptic plasticity in the hippocampus.

ERK/MAPK regulates the Kv4.2 potassium channel by direct phosphorylation of the pore-forming subunit

2006 ◽  
Vol 290 (3) ◽  
pp. C852-C861 ◽  
Author(s):  
Laura A. Schrader ◽  
Shari G. Birnbaum ◽  
Brian M. Nadin ◽  
Yajun Ren ◽  
Duy Bui ◽  
...  
Keyword(s):  
Opposite Effect ◽  
Pyramidal Neurons ◽  
Wild Type ◽  
Activation Curve ◽  
Dynamic Regulation ◽  
Interacting Protein ◽  
Ca1 Pyramidal Neurons ◽  
Erk Mapk ◽  
Outward Currents ◽  
Hippocampal Ca1

Kv4.2 is the primary pore-forming subunit encoding A-type currents in many neurons throughout the nervous system, and it also contributes to the transient outward currents of cardiac myocytes. A-type currents in the dendrites of hippocampal CA1 pyramidal neurons are regulated by activation of ERK/MAPK, and Kv4.2 is the likely pore-forming subunit of that current. We showed previously that Kv4.2 is directly phosphorylated at three sites by ERK/MAPK (T602, T607, and S616). In this study we determined whether direct phosphorylation of Kv4.2 by ERK/MAPK is responsible for the regulation of the A-type current observed in neurons. We made site-directed mutants, changing the phosphosite serine (S) or threonine (T) to aspartate (D) to mimic phosphorylation. We found that the T607D mutation mimicked the electrophysiological changes elicited by ERK/MAPK activation in neurons: a rightward shift of the activation curve and an overall reduction in current compared with wild type (WT). Surprisingly, the S616D mutation caused the opposite effect, a leftward shift in the activation voltage. K+ channel-interacting protein (KChIP)3 ancillary subunit coexpression with Kv4.2 was necessary for the T607D effect, as the T607D mutant when expressed in the absence of KChIP3 was not different from WT Kv4.2. These data suggest that direct phosphorylation of Kv4.2 at T607 is involved in the dynamic regulation of the channel function by ERK/MAPK and an interaction of the primary subunit with KChIP is also necessary for this effect. Overall these studies provide new insights into the structure-function relationships for MAPK regulation of membrane ion channels.

Electrotonic architecture of hippocampal CA1 pyramidal neurons based on three-dimensional reconstructions

1996 ◽  
Vol 76 (3) ◽  
pp. 1904-1923 ◽  
Author(s):  
Z. F. Mainen ◽  
N. T. Carnevale ◽  
A. M. Zador ◽  
B. J. Claiborne ◽  
T. H. Brown
Keyword(s):  
Pyramidal Neurons ◽  
Three Dimensional ◽  
Dendritic Tree ◽  
Membrane Resistance ◽  
Electrical Signals ◽  
Spatial Gradients ◽  
Time To Peak ◽  
Ca1 Pyramidal Neurons ◽  
Ca1 Region ◽  
Cylinder Model

1. The spread of electrical signals in pyramidal neurons from the CA1 field of rat hippocampus was investigated through multicompartmental modeling based on three-dimensional morphometric reconstructions of four of these cells. These models were used to dissect the electrotonic architecture of these neurons, and to evaluate the equivalent cylinder approach that this laboratory and others have previously applied to them. Robustness of results was verified by the use of wide ranges of values of specific membrane resistance (Rm) and cytoplasmic resistivity. 2. The anatomy exhibited extreme departures from a key assumption of the equivalent cylinder model, the so-called "3/2 power law." 3. The compartmental models showed that the frequency distribution of steady-state electrotonic distances between the soma and the dendritic terminations was multimodal, with a large range and a sizeable coefficient of variation. This violated another central assumption of the equivalent cylinder model, namely, that all terminations are electronically equidistant from the soma. This finding, which was observed both for "centrifugal" (away from the soma) and "centripetal" (toward the soma) spread of electrical signals, indicates that the concept of an equivalent electrotonic length for the whole dendritic tree is not appropriate for these neurons. 4. The multiple peaks in the electrotonic distance distributions, whether for centrifugal or centripetal voltage transfer, were clearly related to the laminar organization of synaptic afferents in the CA1 region. 5. The results in the three preceding paragraphs reveal how little of the electrotonic architecture of these neurons is captured by a simple equivalent cylinder model. The multicompartmental model is more appropriate for exploring synaptic signaling and transient events in CA1 pyramidal neurons. 6. There was significant attenuation of synaptic potential, current, and charge as they spread from the dendritic tree to the soma. Charge suffered the least and voltage suffered the most attenuation. Attenuation depended weakly on Rm and strongly on synaptic location. Delay of time to peak was more distorted for voltage than for current and was more affected by Rm. 7. Adequate space clamp is not possible for most of the synapses on these cells. Application of a somatic voltage clamp had no significant effect on voltage transients in the subsynaptic membrane. 8. The possible existence of steep voltage gradients within the dendritic tree is consistent with the idea that there can be some degree of local processing and that different regions of the neuron may function semiautonomously. These spatial gradients are potentially relevant to synaptic plasticity in the hippocampus, and they also suggest caution in interpreting some neurophysiological results.

scholarly journals Comparing basal dendrite branches in human and mouse hippocampal CA1 pyramidal neurons with Bayesian networks

2020 ◽  
Author(s):  
Bojan Mihaljević ◽  
Pedro Larrañaga ◽  
Ruth Benavides-Piccione ◽  
Javier DeFelipe ◽  
Concha Bielza
Keyword(s):  
Bayesian Networks ◽  
Pyramidal Neurons ◽  
Graphical Representation ◽  
Data Set ◽  
Ca1 Region ◽  
Basal Dendrites ◽  
Hippocampal Ca1 ◽  
Dendritic Branches ◽  
Branch Type ◽  
Human And Mouse

ABSTRACTPyramidal neurons are the most common cell type in the cerebral cortex. Understanding how they differ between species is a key challenge in neuroscience. A recent study provided a unique set of human and mouse pyramidal neurons of the CA1 region of the hippocampus, and used it to compare the morphology of apical and basal dendritic branches of the two species. The study found inter-species differences in the magnitude of the morphometrics and similarities regarding their variation with respect to morphological determinants such as branch type and branch order. We use the same data set to perform additional comparisons of basal dendrites. In order to isolate the heterogeneity due to intrinsic differences between species from the heterogeneity due to differences in morphological determinants, we fit multivariate models over the morphometrics and the determinants. In particular, we use conditional linear Gaussian Bayesian networks, which provide a concise graphical representation of the independencies and correlations among the variables. We also extend the previous study by considering additional morphometrics and by formally testing test whether a morphometric increases or decreases with the distance from the soma. This study introduces a multivariate methodology for inter-species comparison of morphology.

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