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.

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.

Interneurons in Area CA1 Stratum Radiatum and Stratum Oriens Remain Functionally Connected to Excitatory Synaptic Input in Chronically Epileptic Animals

1997 ◽  
Vol 78 (3) ◽  
pp. 1504-1515 ◽  
Author(s):  
D. A. Rempe ◽  
E. H. Bertram ◽  
J. M. Williamson ◽  
E. W. Lothman
Keyword(s):  
Temporal Lobe Epilepsy ◽  
Temporal Lobe ◽  
Synaptic Input ◽  
Pyramidal Cells ◽  
Stratum Radiatum ◽  
Ca1 Pyramidal Cells ◽  
Control Tissue ◽  
Stratum Oriens ◽  
Area Ca1 ◽  
Excitatory Synaptic Input

Rempe, D. A., E. H. Bertram, J. M. Williamson, and E. W. Lothman. Interneurons in area CA1 stratum radiatum and stratum oriens remain functionally connected to excitatory synaptic input in chronically epileptic animals. J. Neurophysiol. 78: 1504–1515, 1997. Past work has demonstrated a reduction of stimulus-evoked inhibitory input to hippocampal CA1 pyramidal cells in chronic models of temporal lobe epilepsy (TLE). It has been postulated that this reduction in inhibition results from impaired excitation of inhibitory interneurons. In this report, we evaluate the connectivity of area CA1 interneurons to their excitatory afferents in hippocampal-parahippocampal slices obtained from a rat model of chronic TLE. Rats were made chronically epileptic by a period of continuous electrical stimulation of the hippocampus, which establishes an acute condition of self-sustained limbic status epilepticus (SSLSE). This period of SSLSE is followed by a development of chronic recurrent spontaneous limbic seizures that are associated with chronic neuropathological changes reminiscent of those encountered in human TLE. Under visual control, whole cell patch-clamp recordings of interneurons and pyramidal cells were obtained in area CA1 of slices taken from adult, chronically epileptic post-SSLSE rats. Neurons were activated by means of electrodes positioned in stratum radiatum. Intrinsic membrane properties, including resting membrane potential, action potential (AP) threshold, AP half-height width, and membrane impedance, were unchanged in interneurons from chronically epileptic (post-SSLSE) tissue compared with control tissue. Single stimuli delivered to stratum radiatum evoked depolarizing excitatory postsynaptic potentials and APs in interneurons, whereas paired-pulse stimulation evoked facilitation of the postsynaptic current (PSC) in both control and post-SSLSE tissue. No differences between interneurons in control versus post-SSLSE tissue could be found with respect to the mean stimulus intensity or mean stimulus duration needed to evoke an AP. A multiple linear regression analysis over a range of stimulus intensities demonstrated that a greater number of APs could be evoked in interneurons in post-SSLSE tissue compared with control tissue. Spontaneous PSCs were observed in area CA1 interneurons in both control and post-SSLSE tissue and were markedly attenuated by glutamatergic antagonists. In conclusion, our data suggest that stimulus-evoked and spontaneous excitatory synaptic input to area CA1 interneurons remains functional in an animal model of chronic temporal lobe epilepsy. These findings suggest, therefore, that the apparent decrease of polysynaptic inhibitory PSPs in CA1 pyramidal cells in epileptic tissue is not due to a deficit in excitatory transmission from Schaffer collaterals to interneurons in stratum radiatum and straum oriens.

Network Interactions Mediated by New Excitatory Connections Between CA1 Pyramidal Cells in Rats With Kainate-Induced Epilepsy

2002 ◽  
Vol 87 (3) ◽  
pp. 1655-1658 ◽  
Author(s):  
Bret N. Smith ◽  
F. Edward Dudek
Keyword(s):  
Status Epilepticus ◽  
Action Potentials ◽  
Cell Layer ◽  
Hippocampal Slices ◽  
Pyramidal Cells ◽  
Ca1 Pyramidal Cells ◽  
Axon Sprouting ◽  
Synaptic Interactions ◽  
Network Bursts ◽  
Ca1 Area

Axon sprouting and synaptic reorganization in the hippocampus are associated with the development of seizures in temporal lobe epilepsy. Synaptic interactions among CA1 pyramidal cells were examined in fragments of hippocampal slices containing only the CA1 area from saline- and kainate-treated rats. Glutamate microapplication to the pyramidal cell layer increased excitatory postsynaptic current (EPSC) frequency, but only in rats with kainate-induced epilepsy. In bicuculline, action potentials evoked in single pyramidal cells increased the frequency of network bursts only in slices from rats with kainate-induced epilepsy. These data further support the hypothesis that excitatory connections between CA1 pyramidal cells increase after kainate-induced status epilepticus.

scholarly journals Does a Unique Type of CA3 Pyramidal Cell in Primates Bypass the Dentate Gate?

2005 ◽  
Vol 94 (1) ◽  
pp. 896-900 ◽  
Author(s):  
Paul S. Buckmaster
Keyword(s):  
Dentate Gyrus ◽  
Entorhinal Cortex ◽  
Synaptic Input ◽  
Granule Cells ◽  
Molecular Layer ◽  
Pyramidal Cells ◽  
Dendritic Morphology ◽  
Dentate Granule Cells ◽  
Excitatory Synaptic Input ◽  
Ca3 Pyramidal Cells

The predominant excitatory synaptic input to the hippocampus arises from entorhinal cortical axons that synapse with dentate granule cells, which in turn synapse with CA3 pyramidal cells.Thus two highly excitable brain areas—the entorhinal cortex and the CA3 field—are separated by dentate granule cells, which have been proposed to function as a gate or filter. However, unlike rats, primates have “dentate” CA3 pyramidal cells with an apical dendrite that extends into the molecular layer of the dentate gyrus, where they could receive strong, monosynaptic, excitatory synaptic input from the entorhinal cortex. To test this possibility, the dentate gyrus molecular layer was stimulated while intracellular recordings were obtained from CA3 pyramidal cells in hippocampal slices from neurologically normal macaque monkeys. Stimulus intensity of the outer molecular layer of the dentate gyrus was standardized by the threshold intensity for evoking a dentate gyrus field potential population spike. Recorded proximal CA3 pyramidal cells were labeled with biocytin, processed with diaminobenzidine for visualization, and classified according to their dendritic morphology. In response to stimulation of the dentate gyrus molecular layer, action potential thresholds were similar in proximal CA3 pyramidal cells with different dendritic morphologies. These findings do not support the hypothesis that dentate CA3 pyramidal cells receive stronger synaptic input from the entorhinal cortex than do other proximal CA3 pyramidal cells.

Cannabinoid receptor activation in CA1 pyramidal cells in adult rat hippocampus

2000 ◽  
Vol 863 (1-2) ◽  
pp. 120-131 ◽  
Author(s):  
M.Todd Kirby ◽  
Robert E Hampson ◽  
Sam A Deadwyler
Keyword(s):  
Cannabinoid Receptor ◽  
Pyramidal Cells ◽  
Receptor Activation ◽  
Rat Hippocampus ◽  
Adult Rat ◽  
Ca1 Pyramidal Cells

scholarly journals Tonic Control of Secretory Acid Sphingomyelinase Over Ventral Hippocampal Synaptic Transmission and Neuron Excitability

2021 ◽  
Vol 15 ◽  
Author(s):  
Chih-Hung Lin ◽  
Johannes Kornhuber ◽  
Fang Zheng ◽  
Christian Alzheimer
Keyword(s):  
Synaptic Transmission ◽  
Synaptic Input ◽  
Antidepressant Drugs ◽  
Field Potential ◽  
Pyramidal Cells ◽  
Acid Sphingomyelinase ◽  
Membrane Hyperpolarization ◽  
Cell Excitability ◽  
Ca1 Pyramidal Cells ◽  
Major Player

The acid sphingomyelinase (ASM) converts sphingomyelin into ceramide. Recent work has advanced the ASM/ceramide system as a major player in the pathogenesis of major depressive disorder (MDD). Indeed, ASM activity is enhanced in MDD patients and antidepressant drugs like fluoxetine act as functional inhibitors of ASM. Here, we employed the specific ASM inhibitor ARC39 to explore the acute effects of the enzyme on hippocampal synaptic transmission and cell excitability in adult mouse brain slice preparations. In both field potential and whole-cell recordings, ARC39 (1–3 μM) enhanced excitatory synaptic input onto ventral hippocampal CA1 pyramidal cells. The specificity of drug action was demonstrated by its lacking effect in slices from ASM knockout mice. In control condition, ARC39 strongly reduced firing in most CA1 pyramidal cells, together with membrane hyperpolarization. Such pronounced inhibitory action of ARC39 on soma excitability was largely reversed when GABAA receptors were blocked. The idea that ARC39 recruits GABAergic inhibition to dampen cell excitability was further reinforced by the drug’s ability to enhance the inhibitory synaptic drive onto pyramidal cells. In pyramidal cells that were pharmacologically isolated from synaptic input, the overall effect of ARC39 on cell firing was inhibitory, but some neurons displayed a biphasic response with a transient increase in firing, suggesting that ARC39 might alter intrinsic firing properties in a cell-specific fashion. Because ARC39 is charged at physiological pH and exerted all its effects within minutes of application, we propose that the neurophysiological actions reported here are due to the inhibition of secretory rather than lysosomal ASM. In summary, the ASM inhibitor ARC39 reveals a tonic control of the enzyme over ventral hippocampal excitability, which involves the intrinsic excitability of CA1 pyramidal cells as well as their excitatory and inhibitory synaptic inputs.

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.

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