Faculty Opinions recommendation of Gamma oscillatory firing reveals distinct populations of pyramidal cells in the CA1 region of the hippocampus.

2008 ◽  
Author(s):  
Kathleen Rockland
Keyword(s):  
Pyramidal Cells ◽  
Ca1 Region

scholarly journals Location of Sialoglycoconjugates Containing the Siaα2–3Gal and Siaα2–6Gal Groups in the Rat Hippocampus and the Effect of Aging on Their Expression

2001 ◽  
Vol 49 (10) ◽  
pp. 1311-1319 ◽  
Author(s):  
Yuji Sato ◽  
Yoshihiro Akimoto ◽  
Hayato Kawakami ◽  
Hiroshi Hirano ◽  
Tamao Endo
Keyword(s):  
Electron Microscopy ◽  
Plasma Membranes ◽  
Pyramidal Cells ◽  
Staining Intensity ◽  
Rat Hippocampus ◽  
Maackia Amurensis ◽  
Ca1 Region ◽  
Old Rats ◽  
Maackia Amurensis Lectin ◽  
Stratum Lacunosum Moleculare

The histochemical distribution of sialoglycoconjugates in the CA1 region in the hippocampus formation of 9-week-old rats and 30-month-old rats was examined using electron microscopy in combination with two lectins, Maackia amurensis lectin, specific for Siaα2–3Gal, and Sambucus sieboldiana agglutinin, specific for Siaα2–6Gal. Each lectin stained the plasma membranes of pyramidal cells, indicating that the Siaα2–3Gal and Siaα2–6Gal groups were expressed on their plasma membranes. These lectins also bound to synapses in the stratum lacunosum moleculare. The staining intensity of the lectins in the synapses in these layers was downregulated in the 30-month-old rats. These results indicated that both the Siaα2–3Gal and Siaα2–6Gal groups are expressed on these synapses and that the expression of these sialyl linkages decreases in the aged brain.

scholarly journals Pycnogenol® Supplementation Attenuates Memory Deficits and Protects Hippocampal CA1 Pyramidal Neurons via Antioxidative Role in a Gerbil Model of Transient Forebrain Ischemia

Nutrients ◽  
2020 ◽  
Vol 12 (8) ◽  
pp. 2477
Author(s):  
Bora Kim ◽  
Tae-Kyeong Lee ◽  
Cheol Woo Park ◽  
Dae Won Kim ◽  
Ji Hyeon Ahn ◽  
...  
Keyword(s):  
Pyramidal Neurons ◽  
Neuroprotective Effect ◽  
Ischemic Injury ◽  
Pyramidal Cells ◽  
Acid Oxidation ◽  
Forebrain Ischemia ◽  
Transient Forebrain Ischemia ◽  
Ca1 Region ◽  
Pine Tree ◽  
Before And After

Pycnogenol® (an extract of the bark of French maritime pine tree) is used for dietary supplement and known to have excellent antioxidative efficacy. However, there are few reports on neuroprotective effect of Pycnogenol® supplementation and its mechanisms against ischemic injury following transient forebrain ischemia (TFI) in gerbils. Now, we examined neuroprotective effect and its mechanisms of Pycnogenol® in the gerbils with 5-min TFI, which evokes a significant death (loss) of pyramidal cells located in the cornu ammonis (CA1) region of gerbil hippocampus from 4–5 days post-TFI. Gerbils were pretreated with 30, 40, and 50 mg/kg of Pycnogenol® once a day for 7 days before TFI surgery. Treatment with 50 mg/kg, not 30 or 40 mg/kg, of Pycnogenol® potently protected learning and memory, as well as CA1 pyramidal cells, from ischemic injury. Treatment with 50 mg/kg Pycnogenol® significantly enhanced immunoreactivity of antioxidant enzymes (superoxide dismutases and catalase) in the pyramidal cells before and after TFI induction. Furthermore, the treatment significantly reduced the generation of superoxide anion, ribonucleic acid oxidation and lipid peroxidation in the pyramidal cells. Moreover, interestingly, its neuroprotective effect was abolished by administration of sodium azide (a potent inhibitor of SODs and catalase activities). Taken together, current results clearly indicate that Pycnogenol® supplementation can prevent neurons from ischemic stroke through its potent antioxidative role.

Postsynaptic Induction and Presynaptic Expression of Group 1 mGluR-Dependent LTD in the Hippocampal CA1 Region

2002 ◽  
Vol 87 (3) ◽  
pp. 1395-1403 ◽  
Author(s):  
Ayako M. Watabe ◽  
Holly J. Carlisle ◽  
Thomas J. O'Dell
Keyword(s):  
Synaptic Transmission ◽  
Transmitter Release ◽  
Metabotropic Glutamate Receptors ◽  
Calcium Influx ◽  
Pyramidal Cells ◽  
Excitatory Synapses ◽  
Ca1 Pyramidal Cells ◽  
Ca1 Region ◽  
Group I ◽  
Sites Of Action

Activation of metabotropic glutamate receptors (mGluRs) with the group I mGluR selective agonist (R,S)-3,5-dihydroxyphenylglycine (DHPG) induces a long-term depression (LTD) of excitatory synaptic transmission in the CA1 region of the hippocampus. Here we investigated the potential roles of pre- and postsynaptic processes in the DHPG-induced LTD at excitatory synapses onto hippocampal pyramidal cells in the mouse hippocampus. Activation of mGluRs with DHPG, but not ACPD, induced LTD at both Schaffer collateral/commissural fiber synapses onto CA1 pyramidal cells and at associational/commissural fiber synapses onto CA3 pyramidal cells. DHPG-induced LTD was blocked when the G-protein inhibitor guanosine-5′- O-(2-thiodiphosphate) was selectively delivered into postsynaptic CA1 pyramidal cells via an intracellular recording electrode, suggesting that DHPG depresses synaptic transmission through a postsynaptic, GTP-dependent signaling pathway. The effects of DHPG were also strongly modulated, however, by experimental manipulations that altered presynaptic calcium influx. In these experiments, we found that elevating extracellular Ca2+ concentrations ([Ca2+]o) to 6 mM almost completely blocked the effects of DHPG, whereas lowering [Ca2+]o to 1 mM significantly enhanced the ability of DHPG to depress synaptic transmission. Enhancing Ca2+ influx by prolonging action potential duration with bath applications of the K+ channel blocker 4-aminopyridine (4-AP) also strongly reduced the effects of DHPG in the presence of normal [Ca2+]o (2 mM). Although these findings indicate that alterations in Ca2+-dependent signaling processes strongly regulate the effects of DHPG on synaptic transmission, they do not distinguish between potential pre- versus postsynaptic sites of action. We found, however, that while inhibiting both pre- and postsynaptic K+ channels with bath-applied 4-AP blocked the effects of DHPG; inhibition of postsynaptic K+channels alone with intracellular Cs+ and TEA had no effect on the ability of DHPG to inhibit synaptic transmission. This suggests that presynaptic changes in transmitter release contribute to the depression of synaptic transmission by DHPG. Consistent with this, DHPG induced a persistent depression of both AMPA and N-methyl-d-aspartate receptor-mediated components of excitatory postsynaptic currents in voltage-clamped pyramidal cells. Together our results suggest that activation of postsynaptic mGluRs suppresses transmission at excitatory synapses onto CA1 pyramidal cells through presynaptic effects on transmitter release.

Cell-Specific Alterations in Synaptic Properties of Hippocampal CA1 Interneurons After Kainate Treatment

1998 ◽  
Vol 80 (6) ◽  
pp. 2836-2847 ◽  
Author(s):  
F. Morin ◽  
C. Beaulieu ◽  
J.-C. Lacaille
Keyword(s):  
Time Constant ◽  
Decay Time ◽  
Pyramidal Cells ◽  
Stratum Radiatum ◽  
Inhibitory Interneurons ◽  
Cell Type ◽  
Postsynaptic Currents ◽  
Ca1 Region ◽  
Hippocampal Ca1 ◽  
Stratum Lacunosum Moleculare

Morin, F., C. Beaulieu, and J.-C. Lacaille. Cell-specific alterations in synaptic properties of hippocampal CA1 interneurons after kainate treatment. J. Neurophysiol. 80: 2836–2847, 1998. Hippocampal sclerosis and hyperexcitability are neuropathological features of human temporal lobe epilepsy that are reproduced in the kainic acid (KA) model of epilepsy in rats. To assess directly the role of inhibitory interneurons in the KA model, the membrane and synaptic properties of interneurons located in 1) stratum oriens near the alveus (O/A) and 2) at the border of stratum radiatum and stratum lacunosum-moleculare (LM), as well as those of pyramidal cells, were examined with whole cell recordings in slices of control and KA-lesioned rats. In current-clamp recordings, intrinsic cell properties such as action potential amplitude and duration, amplitude of fast and medium duration afterhyperpolarizations, membrane time constant, and input resistance were generally unchanged in all cell types after KA treatment. In voltage-clamp recordings, the amplitude and conductance of pharmacologically isolated excitatory postsynaptic currents (EPSCs) were significantly reduced in LM interneurons of KA-treated animals but were not significantly changed in O/A and pyramidal cells. The rise time of EPSCs was not significantly changed in any cell type after KA treatment. In contrast, the decay time constant of EPSCs was significantly faster in O/A interneurons of KA-treated rats but was unchanged in LM and pyramidal cells. The amplitude and conductance of pharmacologically isolated γ-aminobutyric acid-A (GABAA) inhibitory postsynaptic currents (IPSCs) were not significantly changed in any cell type of KA-treated rats. The rise time and decay time constant of GABAA IPSCs were significantly faster in pyramidal cells of KA-treated rats but were not significantly changed in O/A and LM interneurons. These results suggest that complex alterations in synaptic currents occur in specific subpopulations of inhibitory interneurons in the CA1 region after KA lesions. A reduction of evoked excitatory drive onto inhibitory cells located at the border of stratum radiatum and stratum lacunosum-moleculare may contribute to disinhibition and polysynaptic epileptiform activity in the CA1 region. Compensatory changes, involving excitatory synaptic transmission on other interneuron subtypes and inhibitory synaptic transmission on pyramidal cells, may also take place and contribute to the residual, functional monosynaptic inhibition observed in principal cells after KA treatment.

Spatial representations of self and other in the hippocampus

Science ◽  
2018 ◽  
Vol 359 (6372) ◽  
pp. 213-218 ◽  
Author(s):  
Teruko Danjo ◽  
Taro Toyoizumi ◽  
Shigeyoshi Fujisawa
Keyword(s):  
Receptive Fields ◽  
Pyramidal Cells ◽  
Spatial Location ◽  
The Self ◽  
The Other ◽  
Spatial Representations ◽  
Self And Other ◽  
Ca1 Pyramidal Cells ◽  
Ca1 Region ◽  
Reward Information

An animal’s awareness of its location in space depends on the activity of place cells in the hippocampus. How the brain encodes the spatial position of others has not yet been identified. We investigated neuronal representations of other animals’ locations in the dorsal CA1 region of the hippocampus with an observational T-maze task in which one rat was required to observe another rat’s trajectory to successfully retrieve a reward. Information reflecting the spatial location of both the self and the other was jointly and discretely encoded by CA1 pyramidal cells in the observer rat. A subset of CA1 pyramidal cells exhibited spatial receptive fields that were identical for the self and the other. These findings demonstrate that hippocampal spatial representations include dimensions for both self and nonself.

scholarly journals Simulations of Learning, Memory, and Forgetting Processes with Model of CA1 Region of the Hippocampus

Complexity ◽  
2018 ◽  
Vol 2018 ◽  
pp. 1-13 ◽  
Author(s):  
Dariusz Świetlik
Keyword(s):  
Hardware Implementation ◽  
Pyramidal Cells ◽  
Coincidence Detection ◽  
High Rate ◽  
Synaptic Potentiation ◽  
Postsynaptic Potentials ◽  
Ca1 Region ◽  
Analog Memory ◽  
External Stimuli

The aim of this paper is to present a computational model of the CA1 region of the hippocampus, whose properties include (a) attenuation of receptors for external stimuli, (b) delay and decay of postsynaptic potentials, (c) modification of internal weights due to propagation of postsynaptic potentials through the dendrite, and (d) modification of weights for the analog memory of each input due to a pattern of long-term synaptic potentiation (LTP) with regard to its decay. The computer simulations showed that CA1 model performs efficient LTP induction and high rate of sub-millisecond coincidence detection. We also discuss a possibility of hardware implementation of pyramidal cells of CA1 region of the hippocampus.

Serotonin blocks the facilitatory action of muscarinic and nicotinic agents in the hippocampus in vivo

1989 ◽  
Vol 67 (1) ◽  
pp. 47-53 ◽  
Author(s):  
Y. Hong ◽  
K. Krnjević
Keyword(s):  
Inhibitory Action ◽  
Pyramidal Cells ◽  
Inhibitory Effect ◽  
Population Spike ◽  
Rat Hippocampus ◽  
Population Spikes ◽  
Ca1 Region ◽  
Facilitatory Action ◽  
Hippocampal Pyramidal Cells

The inhibitory effect of serotonin, released iontophoretically, on acetylcholine-induced facilitation of population spikes evoked by fimbria–commissural stimulation was studied in the CA1 region of rat hippocampus in vivo. After serotonin was applied for 2.6 ± 0.8 min, acetylcholine's action was inhibited in 39 cases out of 57 (68.4%), by 68.9 ± 23.1%, irrespective of whether serotonin alone increased or reduced the population spike. Spiperone, used as a 5-hydroxytryptamine1A (5-HT1A) antagonist, suppressed the inhibitory action of serotonin in 14 of 21 tests. Serotonin had similar effects on population spike facilitations induced by acetyl-β-methylcholine and dimethylphenylpiperazinium. Thus serotonin, probably acting on 5-HT1A receptors, blocks effectively but indiscriminately all cholinergic facilitations, whether mediated by nicotinic or muscarinic receptors.Key words: serotonin, cholinergic facilitation, hippocampal pyramidal cells, spiperone, muscarinic and nicotinic actions.

scholarly journals Ischemic Damage in Hippocampal CA1 is Dependent on Glutamate Release and Intact Innervation from CA3

1989 ◽  
Vol 9 (5) ◽  
pp. 629-639 ◽  
Author(s):  
H. Benveniste ◽  
M. B. Jørgensen ◽  
M. Sandberg ◽  
T. Christensen ◽  
H. Hagberg ◽  
...  
Keyword(s):  
Injection Site ◽  
Glutamate Release ◽  
Pyramidal Cells ◽  
Global Ischemia ◽  
Ischemic Damage ◽  
Ca1 Pyramidal Cells ◽  
Ca1 Region ◽  
Hippocampal Tissue ◽  
Hippocampal Ca1 ◽  
Transient Global Ischemia

The removal of glutamatergic afferents to CA1 by destruction of the CA3 region is known to protect CA1 pyramidal cells against 10 min of transient global ischemia. To investigate further the pathogenetic significance of glutamate, we measured the release of glutamate in intact and CA3-lesioned CA1 hippocampal tissue. In intact CA1 hippocampal tissue, glutamate increased sixfold during ischemia; in the CA3-lesioned CA1 region, however, glutamate only increased 1.4-fold during ischemia. To assess the neurotoxic potential of the ischemia-induced release of glutamate, we injected the same concentration of glutamate into the CA1 region as is released during ischemia in normal, CA3-lesioned, and ischemic CA1 tissue. We found that this particular concentration of glutamate was sufficient to destroy CA1 pyramids in the vicinity of the injection site in intact and CA3-lesioned CA1 tissue when administered during control (non-ischemic) conditions. In contrast, the same amount injected during ischemia in the CA3-lesioned CA1 region destroyed pyramidal cells in a widely distributed zone around the injection site in the CA1 region. It is concluded that the ischemia-induced damage of pyramidal cells in CA1 is dependent on glutamate release and intact innervation from CA3.

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