scholarly journals Morphometric Analysis of Hippocampal Pyramidal Neuronsin situand in Grafts Developing in the Anterior Eye Chambers of Young and Aged Wistar Rats

1997 ◽  
Vol 6 (1) ◽  
pp. 49-57 ◽  
Author(s):  
Z. N. Zhuravleva ◽  
V. N. Saifullina ◽  
C. I. Zenchenko
Keyword(s):  
Morphometric Analysis ◽  
Growth And Development ◽  
Wistar Rats ◽  
Pyramidal Neurons ◽  
Pyramidal Cells ◽  
Ca1 Neurons ◽  
Ca3 Pyramidal Neurons ◽  
The Mean ◽  
Ca3 Neurons

We performed a morphometric analysis of the somatic and nuclear areas in the pyramidal neurons of the hippocampal fields CA1 and CA3in situand in grafts developing for six weeks in the anterior eye chambers of young (3-to-9 wk.) and of aged (18-to-19.5 mos.) Wistar rats. The mean areas of the CA1 pyramidal somata and nuclei were significantly decreased in the aged animalsin situ. The mean parameters of the CA3 pyramidal neurons were not changed, although their distribution was different (bimodalversusunimodal in the young animals). In both groups of recipients, the areas of CA1 neurons and of their nuclei were significantly larger in the grafted tissue than those foundin situ. The areas of CA3 neurons did not show any difference in aged recipients and demonstrated only slight hypertrophy in young recipients. We concluded that the area sizes of the pyramidal cell bodies and nuclei in CA1 neurons are more sensitive than those of CA3 neurons to both aging and transplantation. The age of recipients did not significantly influence the growth and development of grafted pyramidal cells.

scholarly journals Synapse type-specific proteomic dissection identifies IgSF8 as a hippocampal CA3 microcircuit organizer

2019 ◽  
Author(s):  
Nuno Apóstolo ◽  
Samuel N. Smukowski ◽  
Jeroen Vanderlinden ◽  
Giuseppe Condomitti ◽  
Vasily Rybakin ◽  
...  
Keyword(s):  
Cell Surface ◽  
Pyramidal Neurons ◽  
Mossy Fiber ◽  
Surface Protein ◽  
Guidance Cue ◽  
Hippocampal Ca3 ◽  
Cell Surface Interactions ◽  
Ca3 Pyramidal Neurons ◽  
Ca3 Neurons ◽  
Multiple Ligand

SummarySynaptic diversity is a key feature of neural circuits. The structural and functional diversity of closely spaced inputs converging on the same neuron suggests that cell-surface interactions are essential in organizing input properties. Here, we analyzed the cell-surface protein (CSP) composition of hippocampal mossy fiber (MF) inputs on CA3 pyramidal neurons to identify regulators of MF-CA3 synapse properties. We uncover a rich cell-surface repertoire that includes adhesion proteins, guidance cue receptors, extracellular matrix (ECM) proteins, and uncharacterized CSPs. Interactome screening reveals multiple ligand-receptor modules and identifies ECM protein Tenascin-R (TenR) as a ligand of the uncharacterized neuronal receptor IgSF8. Presynaptic Igsf8 deletion impairs MF-CA3 synaptic architecture and robustly decreases the density of bouton filopodia that provide feedforward inhibition of CA3 neurons. Consequently, loss of IgSF8 increases CA3 neuron excitability. Our findings identify IgSF8 as a regulator of CA3 microcircuit development and suggest that combinations of CSP modules define input identity.

Calcium Currents in Retrogradely Labeled Pyramidal Cells From Rat Sensorimotor Cortex

2000 ◽  
Vol 83 (4) ◽  
pp. 2349-2354 ◽  
Author(s):  
Ansalan Stewart ◽  
Robert C. Foehring
Keyword(s):  
Pyramidal Neurons ◽  
Pyramidal Cells ◽  
Cell Types ◽  
Calcium Currents ◽  
Patch Clamp Technique ◽  
Whole Cell ◽  
Multiple Populations ◽  
Whole Cell Patch Clamp ◽  
The Mean ◽  
P Type

Our previous studies of calcium (Ca2+) currents in cortical pyramidal cells revealed that the percentage contribution of each Ca2+ current type to the whole cell Ca2+ current varies from cell to cell. The extent to which these currents are modulated by neurotransmitters is also variable. This study was directed at testing the hypothesis that a major source of this variability is recording from multiple populations of pyramidal cells. We used the whole cell patch-clamp technique to record from dissociated corticocortical, corticostriatal, and corticotectal projecting pyramidal cells. There were significant differences between the three pyramidal cell types in the mean percentage of L-, P-, and N-type Ca2+ currents. For both N- and P-type currents, the range of percentages expressed was small for corticostriatal and corticotectal cells as compared with cells which project to the corpus callosum or to the general population. The variance was significantly different between cell types for N- and P-type currents. These results suggest that an important source of the variability in the proportions of Ca2+ current types present in neocortical pyramidal neurons is recording from multiple populations of pyramidal cells.

scholarly journals Early Ischemia Enhances Action Potential-Dependent, Spontaneous Glutamatergic Responses in CA1 Neurons

2009 ◽  
Vol 30 (3) ◽  
pp. 555-565 ◽  
Author(s):  
Hui Ye ◽  
Shirin Jalini ◽  
Liang Zhang ◽  
Milton Charlton ◽  
Peter L Carlen
Keyword(s):  
Action Potential ◽  
Pyramidal Neurons ◽  
Glutamate Release ◽  
Brain Slices ◽  
Spontaneous Release ◽  
Ca1 Neurons ◽  
Relative Contribution ◽  
Hippocampal Ca1 ◽  
Ca3 Neurons

Two types of quantal spontaneous neurotransmitter release are present in the nervous system, namely action potential (AP)-dependent release and AP-independent release. Previous studies have identified and characterized AP-independent release during hypoxia and ischemia. However, the relative contribution of AP-dependent spontaneous release to the overall glutamate released during transient ischemia has not been quantified. Furthermore, the neuronal activity that mediates such release has not been identified. Using acute brain slices, we show that AP-dependent release constitutes approximately one-third of the overall glutamate-mediated excitatory postsynaptic potentials/currents (EPSPs/EPSCs) measured onto hippocampal CA1 pyramidal neurons. However, during transient (2 mins) in vitro hypoxia–hypoglycemia, large-amplitude, AP-dependent spontaneous release is significantly enhanced and contributes to 74% of the overall glutamatergic responses. This increased AP-dependent release is due to hyper-excitability in the presynaptic CA3 neurons, which is mediated by the activity of NMDA receptors. Spontaneous glutamate release during ischemia can lead to excitotoxicity and perturbation of neural network functions.

Role of EPSPs in initiation of spontaneous synchronized burst firing in rat hippocampal neurons bathed in high potassium

1990 ◽  
Vol 64 (3) ◽  
pp. 1000-1008 ◽  
Author(s):  
N. L. Chamberlin ◽  
R. D. Traub ◽  
R. Dingledine
Keyword(s):  
Hippocampal Neurons ◽  
Pyramidal Neurons ◽  
Hippocampal Slices ◽  
Pyramidal Cells ◽  
Burst Firing ◽  
Interictal Spikes ◽  
High Potassium ◽  
Synaptic Excitation ◽  
Ca3 Neurons

1. Spontaneous discharges that resemble interictal spikes arise in area CA3 b/c of rat hippocampal slices bathed in 8.5 mM [K+]o. Excitatory postsynaptic potentials (EPSPs) also appear at irregular intervals in these cells. The role of local synaptic excitation in burst initiation was examined with intracellular and extracellular recordings from CA3 pyramidal neurons. 2. Most (70%) EPSPs were small (less than 2 mV in amplitude), suggesting that they were the product of quantal release or were evoked by a single presynaptic action potential in another cell. It is unlikely that most EPSPs were evoked by a presynaptic burst of action potentials. Indeed, intrinsic burst firing was not prominent in CA3 b/c pyramidal cells perfused in 8.5 mM [K+]o. 3. The likelihood of occurrence and the amplitude of EPSPs were higher in the 50-ms interval just before the onset of each burst than during a similar interval 250 ms before the burst. This likely reflects increased firing probability of CA3 neurons as they emerge from the afterhyperpolarization (AHP) and conductance shunt associated with the previous burst. 4. Perfusion with 2 microM 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX), a potent quisqualate receptor antagonist, decreased the frequency of EPSPs in CA3 b/c neurons from 3.6 +/- 0.9 to 0.9 +/- 0.3 (SE) Hz. Likewise, CNQX reversibly reduced the amplitude of evoked EPSPs in CA3 b/c cells. 5. Spontaneous burst firing in 8.5 mM [K+]o was abolished in 11 of 31 slices perfused with 2 microM CNQX.(ABSTRACT TRUNCATED AT 250 WORDS)

Permanent Reduction of Seizure Threshold in Post-Ischemic CA3 Pyramidal Neurons

2000 ◽  
Vol 83 (4) ◽  
pp. 2040-2046 ◽  
Author(s):  
Patrice Congar ◽  
Jean-Luc Gaïarsa ◽  
Théodora Popovici ◽  
Yezekiel Ben-Ari ◽  
Valérie Crépel
Keyword(s):  
Pyramidal Neurons ◽  
Hippocampal Slices ◽  
Pyramidal Cells ◽  
Input Resistance ◽  
Seizure Threshold ◽  
Resting Membrane Potential ◽  
Epileptic Syndromes ◽  
Ca3 Pyramidal Neurons ◽  
Ca3 Pyramidal Cells ◽  
Firing Properties

The effects of ischemia were examined on CA3 pyramidal neurons recorded in hippocampal slices 2–4 mo after a global forebrain insult. With intracellular recordings, CA3 post-ischemic neurons had a more depolarized resting membrane potential but no change of the input resistance, spike threshold and amplitude, fast and slow afterhyperpolarization (AHP) or ADP, and firing properties in response to depolarizing pulses. With both field and whole-cell recordings, synaptic responses were similar in control and post-ischemic neurons. Although there were no spontaneous network-driven discharges, the post-ischemic synaptic network had a smaller threshold to generate evoked and spontaneous synchronized burst discharges. Thus lower concentrations of convulsive agents (kainate, high K+) triggered all-or-none network-driven synaptic events in post-ischemic neurons more readily than in control ones. Also, paired-pulse protocol generates, in post-ischemics but not controls, synchronized field burst discharges when interpulse intervals ranged from 60 to 100 ms. In conclusion, 2–4 mo after the insult, the post-ischemic CA3 pyramidal cells are permanently depolarized and have a reduced threshold to generate synchronized bursts. This may explain some neuropathological and behavioral consequences of ischemia as epileptic syndromes observed several months to several years after the ischemic insult.

Cumulative Effects of Glutamate Microstimulation on Ca2+ Responses of CA1 Hippocampal Pyramidal Neurons in Slice

2000 ◽  
Vol 83 (1) ◽  
pp. 90-98 ◽  
Author(s):  
John A. Connor ◽  
Robert J. Cormier
Keyword(s):  
Time Course ◽  
Pyramidal Neurons ◽  
Stratum Radiatum ◽  
Neuron Death ◽  
Hippocampal Pyramidal Neurons ◽  
Ca1 Neurons ◽  
Hippocampal Ca1 ◽  
High Resolution Images ◽  
Stimulation Of

Glutamate stimulation of hippocampal CA1 neurons in slice was delivered via iontophoresis from a microelectrode. Five pulses (∼5 μA, 10 s duration, repeated at 1 min intervals) were applied with the electrode tip positioned in the stratum radiatum near the dendrites of a neuron filled with the Ca2+ indicator fura-2. A single stimulus set produced Ca2+ elevations that ranged from several hundred nM to several μM and that, in all but a few neurons, recovered within 1 min of stimulus termination. Subsequent identical stimulation produced Ca2+ elevations that outlasted the local glutamate elevations by several minutes as judged by response recoveries in neighboring cells or in other parts of the same neuron. These long responses ultimately recovered but persisted for up to 10 min and were most prominent in the mid and distal dendrites. Recovery was not observed for responses that spread to the soma. The elevated Ca2+ levels were accompanied by membrane depolarization but did not appear to depend on the depolarization. High-resolution images demonstrated responsive areas that involved only a few μm of dendrite. Our results confirm the previous general findings from isolated and cell culture neurons that glutamate stimulation, if carried beyond a certain range, results in long-lasting Ca2+ elevation. The response characterized here in mature in situ neurons was significantly different in terms of time course and reversibility. We suggest that the extended Ca2+ elevations might serve not only as a trigger for delayed neuron death but, where more spatially restricted, as a signal for local remodeling in dendrites.

scholarly journals Signal Propagation in Oblique Dendrites of CA1 Pyramidal Cells

2005 ◽  
Vol 94 (6) ◽  
pp. 4145-4155 ◽  
Author(s):  
Michele Migliore ◽  
Michele Ferrante ◽  
Giorgio A. Ascoli
Keyword(s):  
Pyramidal Neurons ◽  
Back Propagation ◽  
Three Dimensional ◽  
Pyramidal Cells ◽  
Signal Propagation ◽  
Morphological Properties ◽  
Ca1 Neurons ◽  
Electrophysiological Properties ◽  
Ca1 Pyramidal Cells ◽  
Dendritic Spikes

The electrophysiological properties of the oblique branches of CA1 pyramidal neurons are largely unknown and very difficult to investigate experimentally. These relatively thin dendrites make up the majority of the apical tree surface area and constitute the main target of Schaffer collateral axons from CA3. Their electrogenic properties might have an important role in defining the computational functions of CA1 neurons. It is thus important to determine if and to what extent the back- and forward propagation of action potentials (AP) in these dendrites could be modulated by local properties such as morphology or active conductances. In the first detailed study of signal propagation in the full extent of CA1 oblique dendrites, we used 27 reconstructed three-dimensional morphologies and different distributions of the A-type K+ conductance ( KA), to investigate their electrophysiological properties by computational modeling. We found that the local KA distribution had a major role in modulating action potential back propagation, whereas the forward propagation of dendritic spikes originating in the obliques was mainly affected by local morphological properties. In both cases, signal processing in any given oblique was effectively independent of the rest of the neuron and, by and large, of the distance from the soma. Moreover, the density of KA in oblique dendrites affected spike conduction in the main shaft. Thus the anatomical variability of CA1 pyramidal cells and their local distribution of voltage-gated channels may suit a powerful functional compartmentalization of the apical tree.

scholarly journals Photolysis of Postsynaptic Caged Ca2+ Can Potentiate and Depress Mossy Fiber Synaptic Responses in Rat Hippocampal CA3 Pyramidal Neurons

2004 ◽  
Vol 91 (4) ◽  
pp. 1596-1607 ◽  
Author(s):  
Jun Wang ◽  
Mark F. Yeckel ◽  
Daniel Johnston ◽  
Robert S. Zucker
Keyword(s):  
Tyrosine Kinases ◽  
Pyramidal Neurons ◽  
Mossy Fiber ◽  
Long Term Potentiation ◽  
Ca1 Neurons ◽  
Term Potentiation ◽  
Hippocampal Ca3 ◽  
Ca3 Pyramidal Neurons ◽  
Cell Somata

The induction of mossy fiber-CA3 long-term potentiation (LTP) and depression (LTD) has been variously described as being dependent on either pre- or postsynaptic factors. Some of the postsynaptic factors for LTP induction include ephrin-B receptor tyrosine kinases and a rise in postsynaptic Ca2+ ([Ca2+]i). Ca2+ is also believed to be involved in the induction of the various forms of LTD at this synapse. We used photolysis of caged Ca2+ compounds to test whether a postsynaptic rise in [Ca2+]i is sufficient to induce changes in synaptic transmission at mossy fiber synapses onto rat hippocampal CA3 pyramidal neurons. We were able to elevate postsynaptic [Ca2+]i to approximately 1 μm for a few seconds in pyramidal cell somata and dendrites. We estimate that CA3 pyramidal neurons have approximately fivefold greater endogenous Ca2+ buffer capacity than CA1 neurons, limiting the rise in [Ca2+]i achievable by photolysis. This [Ca2+]i rise induced either a potentiation or a depression at mossy fiber synapses in different preparations. Neither the potentiation nor the depression was accompanied by consistent changes in paired-pulse facilitation, suggesting that these forms of plasticity may be distinct from synaptically induced LTP and LTD at this synapse. Our results are consistent with a postsynaptic locus for the induction of at least some forms of synaptic plasticity at mossy fiber synapses.

scholarly journals Hilar Somatostatin Neurons are More Vulnerable to an Ischemic Insult Than CA1 Pyramidal Neurons

1993 ◽  
Vol 13 (2) ◽  
pp. 229-234 ◽  
Author(s):  
Tomohiro Matsuyama ◽  
Masato Tsuchiyama ◽  
Hitoshi Nakamura ◽  
Masayasu Matsumoto ◽  
Minoru Sugita
Keyword(s):  
Pyramidal Neurons ◽  
Significant Loss ◽  
Ischemic Tolerance ◽  
Synaptic Connections ◽  
Ischemic Insult ◽  
Ca1 Neurons ◽  
Ca1 Pyramidal Neurons ◽  
In Situ Hybridization Histochemistry ◽  
Somatostatin Neurons

The effects of a very short ischemic insult on hilar somatostatin (SS) neurons were investigated in the gerbil hippocampus by means of immunocytochemistry and in situ hybridization histochemistry. A selective and significant loss of 40% of hilar SS neurons took place after 1 day, and a 60% loss after 7 days following 2 min of ischemia, while no SS neurons were lost during recirculation after 1 min of ischemia. Repeated 2-min periods of ischemia, which induced ischemic tolerance by vulnerable CA1 neurons, caused almost complete loss of hilar SS neurons. This study clearly demonstrates that hilar SS neurons are more vulnerable to ischemic insult than CA1 pyramidal neurons. Ischemic tolerance may be induced during the progressive loss of SS neurons in the hilus by changes in their synaptic connections to CA1 pyramidal neurons.

Apamin-Sensitive Conductance Mediates the K+ Current Response During Chemical Ischemia in CA3 Pyramidal Cells

1999 ◽  
Vol 82 (6) ◽  
pp. 2876-2882 ◽  
Author(s):  
Mitsuo Tanabe ◽  
Masahiro Mori ◽  
Beat H. Gähwiler ◽  
Urs Gerber
Keyword(s):  
Pyramidal Neurons ◽  
Outward Current ◽  
Pyramidal Cells ◽  
Current Response ◽  
Kinase C ◽  
Hippocampal Ca3 ◽  
Organotypic Slice Cultures ◽  
K Current ◽  
Ca3 Pyramidal Neurons ◽  
Ca3 Pyramidal Cells

Pyramidal cells typically respond to ischemia with initial transient hyperpolarization, which may represent a neuroprotective response. To identify the conductance underlying this hyperpolarization in CA3 pyramidal neurons of rat hippocampal organotypic slice cultures, recordings were obtained using the single-electrode voltage-clamp technique. Brief chemical ischemia (2 mM 2-deoxyglucose and 3 mM NaN3, for 4 min) induced a response mediated by an increase in K+ conductance. This current was blocked by intracellular application of the Ca2+ chelator, bis-( o-aminophenoxy)- N,N,N′,N′-tetraacetic acid (BAPTA), reduced with low external [Ca2+], and inhibited by a selective L-type Ca2+ channel inhibitor, isradipine, consistent with the activation of a Ca2+-dependent K+ conductance. Experiments with charybdotoxin (10 nM) and tetraethylammonium (TEA; 1 mM), or with the protein kinase C activator, phorbol 12,13-diacetate (PDAc; 3 μM), ruled out an involvement of a large conductance–type or an apamin-insensitive small conductance, respectively. In the presence of apamin (1 μM), however, the outward current was significantly reduced. These results demonstrate that in rat hippocampal CA3 pyramidal neurons an apamin-sensitive Ca2+-dependent K+ conductance is activated in response to brief ischemia generating a pronounced outward current.

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