scholarly journals Survival of dentate hilar mossy cells after pilocarpine-induced seizures and their synchronized burst discharges with area CA3 pyramidal cells

Neuroscience ◽  
2001 ◽  
Vol 104 (3) ◽  
pp. 741-759 ◽  
Author(s):  
H.E Scharfman ◽  
K.L Smith ◽  
J.H Goodman ◽  
A.L Sollas
Keyword(s):  
Pyramidal Cells ◽  
Mossy Cells ◽  
Ca3 Pyramidal Cells ◽  
Area Ca3

Evidence from simultaneous intracellular recordings in rat hippocampal slices that area CA3 pyramidal cells innervate dentate hilar mossy cells

1994 ◽  
Vol 72 (5) ◽  
pp. 2167-2180 ◽  
Author(s):  
H. E. Scharfman
Keyword(s):  
Pyramidal Cell ◽  
Action Potentials ◽  
Granule Cells ◽  
Hippocampal Slices ◽  
Pyramidal Cells ◽  
Probability Of Failure ◽  
Mossy Cells ◽  
Mossy Cell ◽  
Ca3 Pyramidal Cells ◽  
Area Ca3

1. Simultaneous intracellular recordings of area CA3 pyramidal cells and dentate hilar “mossy” cells were made in rat hippocampal slices to test the hypothesis that area CA3 pyramidal cells excite mossy cells monosynaptically. Mossy cells and pyramidal cells were differentiated by location and electrophysiological characteristics. When cells were impaled near the border of area CA3 and the hilus, their identity was confirmed morphologically after injection of the marker Neurobiotin. 2. Evidence for monosynaptic excitation of a mossy cell by a pyramidal cell was obtained in 7 of 481 (1.4%) paired recordings. In these cases, a pyramidal cell action potential was followed immediately by a 0.40 to 6.75 (mean, 2.26) mV depolarization in the simultaneously recorded mossy cell (mossy cell membrane potentials, -60 to -70 mV). Given that pyramidal cells used an excitatory amino acid as a neurotransmitter (Cotman and Nadler 1987; Ottersen and Storm-Mathisen 1987) and recordings were made in the presence of the GABAA receptor antagonist bicuculline (25 microM), it is likely that the depolarizations were unitary excitatory postsynaptic potentials (EPSPs). 3. Unitary EPSPs of mossy cells were prone to apparent “failure.” The probability of failure was extremely high (up to 0.72; mean = 0.48) if the effects of all presynaptic action potentials were examined, including action potentials triggered inadvertently during other spontaneous EPSPs of the mossy cell. Probability of failure was relatively low (as low as 0; mean = 0.24) if action potentials that occurred during spontaneous activity of the mossy cell were excluded. These data suggest that unitary EPSPs produced by pyramidal cells are strongly affected by concurrent synaptic inputs to the mossy cell. 4. Unitary EPSPs were not clearly affected by manipulation of the mossy cell's membrane potential. This is consistent with the recent report that area CA3 pyramidal cells innervate distal dendrites of mossy cells (Kunkel et al. 1993). Such a distal location also may contribute to the high incidence of apparent failures. 5. Characteristics of unitary EPSPs generated by pyramidal cells were compared with the properties of the unitary EPSPs produced by granule cells. In two slices, pyramidal cell and granule cell inputs to the same mossy cell were compared. In other slices, inputs to different mossy cells were compared. In all experiments, unitary EPSPs produced by granule cells were larger in amplitude but similar in time course to unitary EPSPs produced by pyramidal cells. Probability of failure was lower and paired-pulse facilitation more common among EPSPs triggered by granule cells.(ABSTRACT TRUNCATED AT 400 WORDS)

scholarly journals Dentate Gyrus Mossy Cells Share a Role in Pattern Separation with Dentate Granule Cells and Proximal CA3 Pyramidal Cells

2019 ◽  
Vol 39 (48) ◽  
pp. 9570-9584 ◽  
Author(s):  
Douglas GoodSmith ◽  
Heekyung Lee ◽  
Joshua P. Neunuebel ◽  
Hongjun Song ◽  
James J. Knierim
Keyword(s):  
Dentate Gyrus ◽  
Granule Cells ◽  
Pyramidal Cells ◽  
Pattern Separation ◽  
Dentate Granule Cells ◽  
Mossy Cells ◽  
Ca3 Pyramidal Cells

Amplification of Perforant-Path EPSPs in CA3 Pyramidal Cells by LVA Calcium and Sodium Channels

1998 ◽  
Vol 80 (3) ◽  
pp. 1558-1561 ◽  
Author(s):  
Nathaniel N. Urban ◽  
Darrell A. Henze ◽  
German Barrionuevo
Keyword(s):  
Sodium Channels ◽  
Entorhinal Cortex ◽  
Low Voltage ◽  
Pyramidal Cells ◽  
Perforant Path ◽  
Monosynaptic Connection ◽  
Voltage Dependent ◽  
Hippocampal Area ◽  
Ca3 Pyramidal Cells ◽  
Area Ca3

Urban, Nathaniel N., Darrell A. Henze, and German Barrionuevo. Amplification of perforant-path EPSPs in CA3 pyramidal cells by LVA calcium and sodium channels. J. Neurophysiol. 80: 1558–1561, 1998. The perforant path forms a monosynaptic connection between the cells of layer II of the entorhinal cortex and the pyramidal cells in hippocampal area CA3. Although this projection is prominent anatomically, very little is known about the physiological properties of this input. The distal location of these synapses suggests that somatically recorded perforant-path excitatory postsynaptic potentials (EPSPs) may be influenced by the activation of voltage-dependent channels in CA3 cells. We observed that perforant-path EPSPs are reduced (by ∼25%) by blockade of postsynaptic low-voltage–activated calcium and sodium channels, indicating that perforant-path EPSPs are amplified by the activation of these channels. These data suggest that the perforant path may represent an important and highly modifiable direct connection between the entorhinal cortex and area CA3.

Spontaneous and stimulation-induced synchronized burst afterdischarges in the isolated CA1 of kainate-treated rats

1996 ◽  
Vol 76 (4) ◽  
pp. 2231-2239 ◽  
Author(s):  
C. L. Meier ◽  
F. E. Dudek
Keyword(s):  
Hippocampal Slices ◽  
Pyramidal Cells ◽  
Stratum Radiatum ◽  
Maximal Response ◽  
Gamma Aminobutyric Acid ◽  
Population Spikes ◽  
Ca3 Pyramidal Cells ◽  
Ca1 Area ◽  
Hilar Neurons ◽  
Area Ca3

1. Kainate treatment preferentially kills dentate hilar neurons and CA3 pyramidal cells and ultimately leads to a chronic epileptic state. Bicuculline-induced epileptiform bursts were studied to test the hypothesis that multiple kainate injections and consequent status epilepticus would lead-after weeks to months of recovery-to prolonged synchronous afterdischarges in the isolated CA1 area of rat hippocampal slices, as would be expected if new recurrent excitatory circuits had formed. 2. Synaptic responses evoked in CA1 pyramidal cells of rats injected subcutaneously with kainate (10 hourly injections, 5 mg/kg each) 24-316 days before the slice experiment were compared with responses in slices from untreated and saline-injected controls. The maximal response to stratum radiatum stimulation in normal solution consisted of two to eight population spikes. 3. When gamma-aminobutyric acid-A receptor-mediated inhibition was reduced with bicuculline, synchronized burst afterdischarges after the initial stimulation-evoked burst, similar to the type of activity described in area CA3 under conditions where inhibition is impaired, occurred in 23% of slices. 4. The prolonged synchronized burst afterdischarges in the isolated CA1 area of kainate-treated rats were associated with large excitatory postsynaptic potentials (EPSPs). These prolonged bursts were not graded with the stimulus intensity; rather, they were triggered in an all-or-none manner, even though there was some variability across bursts. The bursts of population spikes also were correlated with subthreshold EPSPs. 5. Slices that had synchronized burst afterdischarges had significantly more damage in area CA3 than slices without afterdischarges. 6. The data indicate that kainate-induced damage in CA3 can lead to prolonged synchronous afterdischarges, even after CA1 is surgically isolated from the CA3 area. Because the repetitive bursts during the prolonged and synchronous afterdischarges were associated with large EPSPs, these data suggest that kainate-induced damage to CA3 and subsequent degeneration of synaptic terminals in the CA1 area causes the formation of new recurrent excitatory circuits that could be involved in the development of chronic epilepsy.

scholarly journals Sex differences in hippocampal area CA3 pyramidal cells

2016 ◽  
Vol 95 (1-2) ◽  
pp. 563-575 ◽  
Author(s):  
Helen E. Scharfman ◽  
Neil J. MacLusky
Keyword(s):  
Sex Differences ◽  
Pyramidal Cells ◽  
Hippocampal Area ◽  
Ca3 Pyramidal Cells ◽  
Area Ca3

Origin of the Apparent Asynchronous Activity of Hippocampal Mossy Fibers

1997 ◽  
Vol 78 (1) ◽  
pp. 24-30 ◽  
Author(s):  
Darrell A. Henze ◽  
Nathaniel N. Urban ◽  
German Barrionuevo
Keyword(s):  
Mossy Fiber ◽  
Molecular Layer ◽  
Mossy Fibers ◽  
Pyramidal Cells ◽  
Antidromic Activation ◽  
Stratum Lucidum ◽  
Hippocampal Area ◽  
Ca3 Pyramidal Cells ◽  
Area Ca3

Henze, Darrell A., Nathaniel N. Urban, and German Barrionuevo. Origin of the apparent asynchronous activity of hippocampal mossy fibers. J. Neurophysiol. 78: 24–30, 1997. Fiber volleys (FVs) from the stratum lucidum of rat hippocampal area CA3 were recorded extracellularly from in vitro slices in the presence of 10 mM kynurenic acid. In agreement with previous work, bulk stimulation of the dentate gyrus (DG) near the hilar border leads to an asynchronous FV. Transection of the stratum lucidum between the DG stimulation site and the CA3 recording site reduced or eliminated the early components of the asynchronous FV, indicating that they are of mossy fiber (MF) origin. In contrast, moving the stimulating electrode away from the hilus toward the hippocampal fissure reduced or eliminated the late components of the FV. Subsequently, we found that bulk stimulation on the DG/hilar border induces an antidromic population spike in CA3 pyramidal cells. Finally, the MFs and associational collaterals have differentconduction velocities (0.51 and 0.37 m/s, respectively; temperature =33°C). From these data, we conclude that the late components of the asynchronous FV are due to antidromic activation of CA3 collaterals that have been shown to be present in the DG and hilus. A corollary of these findings is that bulk stimulation on the DG/hilar border can lead to at least two different monosynaptic inputs to CA3 pyramidal cells: the MFs and the antidromically activated associational collaterals. We suggest that when MF synaptic responses are being evoked with the use of bulk stimulation, stimulating electrodes should be placed in the outer molecular layer of the DG to prevent the activation of hilar-projecting associational collaterals. This procedure should be added to the previously proposed criteria for preventing polysynaptic contamination of the intracellularly recorded evoked MF synaptic response.

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