Increased Excitatory Synaptic Activity and Local Connectivity of Hippocampal CA1 Pyramidal Cells in Rats With Kainate-Induced Epilepsy

2004 ◽  
Vol 92 (3) ◽  
pp. 1366-1373 ◽  
Author(s):  
Li-Rong Shao ◽  
F. Edward Dudek
Keyword(s):  
Pyramidal Neurons ◽  
Flash Photolysis ◽  
Pyramidal Cells ◽  
Mean Amplitude ◽  
Synaptic Activity ◽  
Control Group ◽  
Ca1 Pyramidal Cells ◽  
Hippocampal Ca1 ◽  
Caged Glutamate ◽  
Ca1 Area

Formation of local excitatory circuits may contribute to epileptogenesis. We tested the hypothesis that epileptogenesis is associated with increased recurrent excitation in the hippocampal CA1 area of rats with kainate-induced epilepsy. Whole cell recordings were obtained during focal flash photolysis of caged glutamate, which served as a focal excitant to activate local pyramidal cells and to study possible connections between neurons. Kainate-treated rats with spontaneous seizures were studied months after status epilepticus and were compared with saline-injected control rats. Experiments were done in isolated CA1 minislices and in bicuculline to block GABAA receptors. Spontaneous excitatory postsynaptic currents (sEPSCs) were present in 42% of the CA1 pyramidal cells from controls and 62% from kainate-treated rats. The frequency of sEPSCs in the kainate group was significantly higher than that in the control group, but mean amplitude was not different. Flash photolysis of caged glutamate on the somatodendritic area of CA1 pyramidal neurons caused a burst of action potentials. Local excitatory connections between CA1 pyramidal cells were found in 4 of 48 neurons (8%) in slices from control animals, but in significantly more neurons (12 of 37; 32%) from rats with kainate-induced epilepsy exhibited interconnections ( P < 0.001). Photoactivation of glutamate on recorded CA1 pyramidal cells in the kainate group sometimes caused afterdischarges, but not in controls. The kainate-treated rats with pyramidal cells that responded to photostimulaltion with repetitive EPSCs appeared to have experienced more severe seizures. These data provide new electrophysiological evidence for the formation of recurrent excitatory circuits in the CA1 area of rats with kainate-induced epilepsy.

Electrophysiological Evidence Using Focal Flash Photolysis of Caged Glutamate That CA1 Pyramidal Cells Receive Excitatory Synaptic Input From the Subiculum

2005 ◽  
Vol 93 (5) ◽  
pp. 3007-3011 ◽  
Author(s):  
Li-Rong Shao ◽  
F. Edward Dudek
Keyword(s):  
Synaptic Input ◽  
Flash Photolysis ◽  
Pyramidal Cells ◽  
Adult Rat ◽  
Ca1 Pyramidal Cells ◽  
Electrophysiological Evidence ◽  
Excitatory Synaptic Input ◽  
Cell Recording ◽  
Caged Glutamate ◽  
Ca1 Area

The hippocampus sends efferent fibers to the subiculum, which projects to the entorinal cortex. Previous studies suggest that the hippocampal CA1 area may receive a projection back from the subiculum. This hypothesis was tested using whole cell recording from CA1 pyramidal cells while subicular neurons were selectively stimulated with focal flash photolysis of caged glutamate, which avoids stimulation of fibers of passage. Control experiments showed that focal flash stimulations caused direct glutamate-mediated depolarizations and bursts of action potentials in the recorded CA1 pyramidal cells, but only when the stimulation targeted the somatodendritic regions of a neuron, not the axons. To block GABAA-mediated inhibition and isolate local excitatory circuits, bicuculline was applied to minislices containing only the isolated CA1 area and the subiculum. Of 24 CA1 pyramidal cells, 25% (6 of 24) consistently generated repetitive excitatory postsynaptic currents (EPSCs) in response to flash stimulation in the subiculum. The responsive neurons were located 200–500 μm from the distal end of CA1 and 400–1,100 μm from the stimulation sites in subiculum, suggesting excitatory synaptic projections from the subicular neurons to CA1 pyramidal cells. This study provides new electrophysiological evidence that CA1 pyramidal cells receive excitatory synaptic input from the subiculum. Thus a reciprocal excitatory synaptic circuit connects the subiculum and the CA1 area in the normal adult rat.

scholarly journals Kaempferol promotes memory retention and density of hippocampal CA1 neurons in intra-cerebroventricular STZ-induced experimental AD model in Wistar rats

Biologija ◽  
2016 ◽  
Vol 62 (3) ◽  
Author(s):  
Niloufar Darbandi ◽  
Matin Ramezani ◽  
Fariba Khodagholi ◽  
Mitra Noori
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Pyramidal Neurons ◽  
Neuronal Damage ◽  
Pyramidal Cells ◽  
Control Group ◽  
Memory Retention ◽  
Hippocampal Ca1 ◽  
Learning Test ◽  
Ca1 Area

Background. Alzheimer’s disease (AD) is a progressive degenerative disease which causes memory disorders, decreases cognitive functions and abilities, and results in behavioural changes. Some studies have indicated that the flavonoids are able to cross the blood–brain barrier and have a positive effect on the reduction of neuronal damage disorders in the brain such as Alzheimer’s disease. Materials and Methods. ICV administration of streptozotocin (3 mg/kg) was done on the first and the third day of the surgery and the animals’ memory was evaluated through passive avoidance tasks. Animals were divided into five groups: Salin-Salin, STZ-Salin, and STZ- different kaempferol doses (5, 7/5, 10 mg/kg). All animals received different doses of kaempferol or saline for 3 weeks starting one day before the surgery. Later, they were put into a learning test. After the memory test, the animals were killed and their brains were fixed with Paraformaldehyde 4%, and tissue processing was done. Finally, density of intact neurons in the CA1 area of the hippocampus in the brains of all groups was investigated. Results. The ICV injections of STZ significantly reduced memory retention and intact pyramidal cells compared to the control group. The kaempferol improved the effects of STZ. Conclusion. Our findings show that kaempferol can optimize cognitive deficits caused by injections of STZ and also has some useful impacts on hippocampal CA1 pyramidal neurons.

scholarly journals Effect of Curcumin and N-Acetylcysteine on Brain Histology and Inflammatory Factors (MMP-2, 9 and TNF-α) in Rats Exposed to Arsenic

2018 ◽  
Vol 24 (4) ◽  
pp. 264-272 ◽  
Author(s):  
Mostafa Fallah ◽  
Najmeh Moghble ◽  
Iraj Javadi ◽  
Hossein Bahadoran ◽  
Alireza Shahriary
Keyword(s):  
Single Dose ◽  
Gelatin Zymography ◽  
White Matter Lesions ◽  
Pyramidal Cells ◽  
Inflammatory Factors ◽  
Ca1 Pyramidal Cells ◽  
Hippocampal Ca1 ◽  
Tnf Α ◽  
Ca1 Area ◽  
Factor Α

Background: Arsenic is a toxic element that widely widespread in environment. Inflammation is now considered as one of the major mechanisms implicated in arsenic poisoning. Curcumin (Cur) and N-acetylcysteine (NAC) are potential antioxidants that protect cells against inflammation. This study aimed to compare the protective effect of Cur and NAC on brain histology and inflammatory factors, including matrix metalloproteinases-2, -9 (MMP-2, 9) and tumor necrosis factor-α (TNF-α) in rats exposed to single dose of arsenic. Methods: Rats were exposed to single dose of arsenic (20mg/kg, by gavage) for 30 days and then treated with 300mg/kg NAC (by gavage) and 100mg/kg Cur (by gavage), individually. Serum level of TNF-α was measured using specific ELISA kits. MMP2 and MMP9 contents were measured using Gelatin Zymography method. Brain samples were collected for histopathological and morphological examinations. Results: Arsenic treatment induced white matter lesions and cellular damages at hippocampal CA1 area of the brain. The number of hippocampal CA1 pyramidal cells was significantly declined in arsenic exposed rats (p<0.05). Treatment with NAC and Cur improved these abnormalities. The mean levels of MMP2, MMP9 and TNF-α inflammatory biomarkers were slightly declined after treatment with NAC and Cur (p>0.05). Conclusion: NAC and Cur play an important role in protecting the hippocampal CA1 cells injury induced by arsenic.

scholarly journals Differential Structure of Hippocampal CA1 Pyramidal Neurons in the Human and Mouse

2019 ◽  
Author(s):  
Ruth Benavides-Piccione ◽  
Mamen Regalado-Reyes ◽  
Isabel Fernaud-Espinosa ◽  
Asta Kastanauskaite ◽  
Silvia Tapia-González ◽  
...  
Keyword(s):  
Pyramidal Neurons ◽  
Pyramidal Cells ◽  
Homologous Region ◽  
Ca1 Pyramidal Cells ◽  
Ca1 Region ◽  
Hippocampal Ca1 ◽  
Structural Differences ◽  
Species Specific ◽  
Human And Mouse ◽  
Shed Light

Abstract Pyramidal neurons are the most common cell type and are considered the main output neuron in most mammalian forebrain structures. In terms of function, differences in the structure of the dendrites of these neurons appear to be crucial in determining how neurons integrate information. To further shed light on the structure of the human pyramidal neurons we investigated the geometry of pyramidal cells in the human and mouse CA1 region—one of the most evolutionary conserved archicortical regions, which is critically involved in the formation, consolidation, and retrieval of memory. We aimed to assess to what extent neurons corresponding to a homologous region in different species have parallel morphologies. Over 100 intracellularly injected and 3D-reconstructed cells across both species revealed that dendritic and axonal morphologies of human cells are not only larger but also have structural differences, when compared to mouse. The results show that human CA1 pyramidal cells are not a stretched version of mouse CA1 cells. These results indicate that there are some morphological parameters of the pyramidal cells that are conserved, whereas others are species-specific.

Modeling Hippocampal CA1 Gabaergic Synapses of Audiogenic Rats

2020 ◽  
Vol 30 (05) ◽  
pp. 2050022
Author(s):  
Rodrigo F. O. Pena ◽  
Cesar Celis Ceballos ◽  
Júnia Lara De Deus ◽  
Antonio Carlos Roque ◽  
Norberto Garcia-Cairasco ◽  
...  
Keyword(s):  
Computational Model ◽  
Pyramidal Neurons ◽  
Temporal Dynamics ◽  
Pyramidal Cells ◽  
Homogeneous Population ◽  
Ca1 Pyramidal Cells ◽  
Physiological Properties ◽  
Hippocampal Ca1 ◽  
Gabaergic Synapses ◽  
Ca1 Pyramidal Neuron

Wistar Audiogenic Rats (WARs) are genetically susceptible to sound-induced seizures that start in the brainstem and, in response to repetitive stimulation, spread to limbic areas, such as hippocampus. Analysis of the distribution of interevent intervals of GABAergic inhibitory postsynaptic currents (IPSCs) in CA1 pyramidal cells showed a monoexponential trend in Wistar rats, suggestive of a homogeneous population of synapses, but a biexponential trend in WARs. Based on this, we hypothesize that there are two populations of GABAergic synaptic release sites in CA1 pyramidal neurons from WARs. To address this hypothesis, we used a well-established neuronal computational model of a CA1 pyramidal neuron previously developed to replicate physiological properties of these cells. Our simulations replicated the biexponential trend only when we decreased the release frequency of synaptic currents by a factor of six in at least 40% of distal synapses. Our results suggest that almost half of the GABAergic synapses of WARs have a drastically reduced spontaneous release frequency. The computational model was able to reproduce the temporal dynamics of GABAergic inhibition that could underlie susceptibility to the spread of seizures.

Distribution of Slow AHP Channels on Hippocampal CA1 Pyramidal Neurons

2000 ◽  
Vol 83 (3) ◽  
pp. 1756-1759 ◽  
Author(s):  
John M. Bekkers
Keyword(s):  
Action Potentials ◽  
Pyramidal Neurons ◽  
Pyramidal Cells ◽  
Apical Dendrite ◽  
Ca1 Pyramidal Cells ◽  
Ca1 Pyramidal Neurons ◽  
Basal Dendrites ◽  
Hippocampal Ca1 ◽  
Cell Current ◽  
Whole Cell Current

This work was designed to localize the Ca2+-activated K+ channels underlying the slow afterhyperpolarization (sAHP) in hippocampal CA1 pyramidal cells. Cell-attached patches on the proximal 100 μm of the apical dendrite contained K+ channels, but not sAHP channels, activated by backpropagating action potentials. Amputation of the apical dendrite ∼30 μm from the soma, while simultaneously recording the sAHP whole cell current at the soma, depressed the sAHP amplitude by only ∼30% compared with control. Somatic cell-attached and nucleated patches did not contain sAHP current. Amputation of the axon ≥20 μm from the soma had little effect on the amplitude of the sAHP recorded in cortical pyramidal cells. By this process of elimination, it is suggested that sAHP channels may be concentrated in the basal dendrites of CA1 pyramids.

Intracellular QX-314 inhibits calcium currents in hippocampal CA1 pyramidal neurons

1996 ◽  
Vol 76 (3) ◽  
pp. 2120-2124 ◽  
Author(s):  
M. J. Talbot ◽  
R. J. Sayer
Keyword(s):  
Pyramidal Neurons ◽  
Pyramidal Cells ◽  
Calcium Currents ◽  
High Threshold ◽  
Chloride Salt ◽  
Ca1 Pyramidal Cells ◽  
Na Currents ◽  
Hippocampal Ca1 ◽  
And Control ◽  
In Cells

1. The effects of intracellular QX-314 on Ca2+ currents were examined in CA1 pyramidal cells acutely isolated from rat hippocampus. In neurons dialyzed with 10 mM QX-314 (bromide salt), the amplitude of the high-threshold Ca2+ current was on average 20% of that in control cells and the current-voltage relationships (I-Vs) were shifted in the positive voltage direction. 2. The positive shift in the I-Vs was due to the presence of intracellular Br-, because it was reproduced by 10 mM NaBr and was not present when the chloride salt of QX-314 was used. 3. Low-threshold (T-type) Ca2+ currents, at test voltages of -50 and -40 mV, were on average < 45% of control amplitude in cells containing 10 mM QX-314 (chloride salt) and < 10% of control amplitude in cells with 10 mM QX-314 (bromide salt). 4. In neurons dialyzed with 1 mM QX-314, high-threshold Ca2+ currents were still significantly different from control and Na+ currents were not completely blocked. 5. The proportions of high-threshold Ca2+ current blocked by omega-conotoxin GVIA, omega-agatoxin IVA, and nimodipine were similar in cells dialyzed with 10 mM QX-314 and control cells, indicating that the drug does not selectively inhibit any of the Ca2+ channel subtypes distinguished by these antagonists.

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