Electrotonic profiles of interneurons in stratum pyramidale of the CA1 region of rat hippocampus

1994 ◽  
Vol 71 (5) ◽  
pp. 1948-1958 ◽  
Author(s):  
D. Thurbon ◽  
A. Field ◽  
S. Redman
Keyword(s):  
Current Pulse ◽  
Time Course ◽  
Pyramidal Neurons ◽  
Regional Distribution ◽  
Total Surface Area ◽  
Pulse Response ◽  
Axon Collateral ◽  
Ca1 Region ◽  
Stratum Pyramidale ◽  
Specific Membrane

1. Whole-cell recordings have been made from interneurons located in stratum pyramidale in the CA1 region of the hippocampus. The responses of these interneurons to brief current pulses were recorded; the neurons were filled with biocytin and their morphology was reconstructed. 2. The interneurons were identified as basket cells on the basis of the regional distribution of their axon collateral network and their location in stratum pyramidale. 3. A compartmental model of the reconstructed neuron was made, and the specific membrane resistivity (Rm), specific cytoplasmic resistivity (Ri), and somatic shunt leakage resistance (Rs) determined by adjusting these parameters until an optimal fit was obtained between the compartmental model's current pulse response and the recorded current pulse response of the neuron. 4. This procedure was successful for six neurons, giving Rm from 7 to 66 k omega cm2, Ri from 52 to 484 omega cm, and Rs from 84 M omega to infinity. The specific membrane capacitance was assumed to be 1 microF/cm2. The electrotonic length of the apical dendrites was 1.06 +/- 0.4, and for the basal dendrites it was 0.51 +/- 0.26 (mean +/- SD). 5. Although the total surface area of the interneurons and the physical length of their dendrites was much smaller than for CA1 pyramidal neurons, their electrotonic profiles were similar. Neurons with small physical profiles cannot be assumed to be more electrotonically compact than larger neurons, especially if the dendrites of the smaller neurons have a proportional reduction in diameter. 6. Two neurons did not require a somatic leakage conductance in their electrical representation. This suggests that when a somatic leakage conductance is required, it is an artifact resulting from electrode damage, rather than a requirement caused by a lower resistivity of the somatic membrane compared with the dendritic membrane. 7. Simulations of synaptic currents evoked in the dendrites of these interneurons while the soma is voltage clamped indicate large errors will occur in the time course measurements and amplitude of these currents. Also the ratio of N-methyl-D-aspartate:alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (NMDA:AMPA) currents at these synapses calculated from currents recorded at the soma will be in error because of the differential attenuation of the faster AMPA currents compared with the NMDA currents.

Activity-Dependent [Ca2+]i Changes in Guinea Pig Vagal Motoneurons: Relationship to the Slow Afterhyperpolarization

1997 ◽  
Vol 78 (2) ◽  
pp. 825-834 ◽  
Author(s):  
Nechama Lasser-Ross ◽  
William N. Ross ◽  
Yosef Yarom
Keyword(s):  
Guinea Pig ◽  
Time Constant ◽  
Recovery Time ◽  
Time Course ◽  
Pyramidal Neurons ◽  
Cell Types ◽  
Time To Peak ◽  
Ca1 Region ◽  
Activity Dependent ◽  
Calcium Green

Lasser-Ross, Nechama, William N. Ross, and Yosef Yarom. Activity-dependent [Ca2+]i changes in guinea pig vagal motoneurons: relationship to the slow afterhyperpolarization. J. Neurophysiol. 78: 825–834, 1997. Vagal motoneurons in slices from the guinea-pig brain stem were injected with the fluorescent [Ca2+]i indicators fura-2, furaptra, or Calcium Green-1. Spike-induced fluorescence changes were measured in the soma and dendrites and simultaneously the long-lasting afterhyperpolarization was recorded with a sharp microelectrode in the soma. Na+ spikes or Ca2+ spikes increased [Ca2+]i (measured as a change in indicator fluorescence) in all locations in the soma and dendrites. Each spike in a train of action potentials caused a step increase in fluorescence of about equal amplitude when nonsaturating indicators were used. Peak changes at all locations occurred at the time of the last action potential. Transients measured with low concentrations of Calcium Green-1 or furaptra had a recovery time constant of ∼500–1,500 ms in the cell body. The recovery time course was faster in the dendrites than in the soma. The norepinephrine-sensitive, slow afterhyperpolarization (sAHP) had a time to peak of ∼800 ms and a recovery time constant of 2–5 s, much longer than the recovery time course of the fluorescence changes. Some of these experiments were repeated on pyramidal neurons from the CA1 region of the rat hippocampus with similar results. In both cell types, the data suggest that the time course of neither the rising phase nor the falling phase of the sAHP, nor the underlying conductance, directly reflects the time course of the [Ca2+]i change. The mechanism connecting the parameters remains unclear. One possibility is that an additional second messenger system is involved.

scholarly journals Increased Calbindin D28k Expression via Long-Term Alternate-Day Fasting Does Not Protect against Ischemia-Reperfusion Injury: A Focus on Delayed Neuronal Death, Gliosis and Immunoglobulin G Leakage

2021 ◽  
Vol 22 (2) ◽  
pp. 644
Author(s):  
Hyejin Sim ◽  
Tae-Kyeong Lee ◽  
Yeon Ho Yoo ◽  
Ji Hyeon Ahn ◽  
Dae Won Kim ◽  
...  
Keyword(s):  
Immunoglobulin G ◽  
Pyramidal Neurons ◽  
Short Term Memory ◽  
Forebrain Ischemia ◽  
Short Term ◽  
Term Memory ◽  
Transient Forebrain Ischemia ◽  
Ca1 Pyramidal Neurons ◽  
Ca1 Region ◽  
Calbindin D28k

Calbindin-D28k (CB), a calcium-binding protein, mediates diverse neuronal functions. In this study, adult gerbils were fed a normal diet (ND) or exposed to intermittent fasting (IF) for three months, and were randomly assigned to sham or ischemia operated groups. Ischemic injury was induced by transient forebrain ischemia for 5 min. Short-term memory was examined via passive avoidance test. CB expression was investigated in the Cornu Ammonis 1 (CA1) region of the hippocampus via western blot analysis and immunohistochemistry. Finally, histological analysis was used to assess neuroprotection and gliosis (microgliosis and astrogliosis) in the CA1 region. Short-term memory did not vary significantly between ischemic gerbils with IF and those exposed to ND. CB expression was increased significantly in the CA1 pyramidal neurons of ischemic gerbils with IF compared with that of gerbils fed ND. However, the CB expression was significantly decreased in ischemic gerbils with IF, similarly to that of ischemic gerbils exposed to ND. The CA1 pyramidal neurons were not protected from ischemic injury in both groups, and gliosis (astrogliosis and microgliosis) was gradually increased with time after ischemia. In addition, immunoglobulin G was leaked into the CA1 parenchyma from blood vessels and gradually increased with time after ischemic insult in both groups. Taken together, our study suggests that IF for three months increases CB expression in hippocampal CA1 pyramidal neurons; however, the CA1 pyramidal neurons are not protected from transient forebrain ischemia. This failure in neuroprotection may be attributed to disruption of the blood–brain barrier, which triggers gliosis after ischemic insults.

scholarly journals High levels of 27-hydroxycholesterol results in synaptic plasticity alterations in the hippocampus

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Raul Loera-Valencia ◽  
Erika Vazquez-Juarez ◽  
Alberto Muñoz ◽  
Gorka Gerenu ◽  
Marta Gómez-Galán ◽  
...  
Keyword(s):  
Pyramidal Neurons ◽  
Memory Function ◽  
Long Term Potentiation ◽  
Synaptic Function ◽  
Cholesterol Homeostasis ◽  
Stratum Radiatum ◽  
Actin Binding ◽  
Ca1 Region ◽  
Hippocampal Ca1 Region ◽  
Term Potentiation

AbstractAlterations in brain cholesterol homeostasis in midlife are correlated with a higher risk of developing Alzheimer’s disease (AD). However, global cholesterol-lowering therapies have yielded mixed results when it comes to slowing down or preventing cognitive decline in AD. We used the transgenic mouse model Cyp27Tg, with systemically high levels of 27-hydroxycholesterol (27-OH) to examine long-term potentiation (LTP) in the hippocampal CA1 region, combined with dendritic spine reconstruction of CA1 pyramidal neurons to detect morphological and functional synaptic alterations induced by 27-OH high levels. Our results show that elevated 27-OH levels lead to enhanced LTP in the Schaffer collateral-CA1 synapses. This increase is correlated with abnormally large dendritic spines in the stratum radiatum. Using immunohistochemistry for synaptopodin (actin-binding protein involved in the recruitment of the spine apparatus), we found a significantly higher density of synaptopodin-positive puncta in CA1 in Cyp27Tg mice. We hypothesize that high 27-OH levels alter synaptic potentiation and could lead to dysfunction of fine-tuned processing of information in hippocampal circuits resulting in cognitive impairment. We suggest that these alterations could be detrimental for synaptic function and cognition later in life, representing a potential mechanism by which hypercholesterolemia could lead to alterations in memory function in neurodegenerative diseases.

Systemic CI-966, a new γ-aminobutyric acid uptake blocker, enhances γ-aminobutyric acid action in CA1 pyramidal layer in situ

1990 ◽  
Vol 68 (9) ◽  
pp. 1194-1199 ◽  
Author(s):  
U. Ebert ◽  
K. Krnjević
Keyword(s):  
Aminobutyric Acid ◽  
Gaba Uptake ◽  
Acid Uptake ◽  
Sprague Dawley ◽  
Nipecotic Acid ◽  
Ca1 Region ◽  
Stratum Pyramidale ◽  
Sprague Dawley Rats ◽  
Pyramidal Layer ◽  
Urethane Anaesthesia

A new potent, blood–brain barrier permeable γ-aminobutyric acid (GABA) uptake blocker, 1-[2-[bis[4-(trifluoromethyl)-phenyl]methoxy]ethyl]-1,2,5,6-tetrahydro-3-pyridinecarboxylic acid (CI-966) was administered systemically by i.p. injection (5 mg/kg) in Sprague–Dawley rats under urethane anaesthesia. Twenty to thirty minutes after injection there was a highly variable, but overall significant, enhancement of the inhibition of hippocampal population spikes by GABA applied by microiontophoresis in the CA1 region. Like the effect of nipecotic acid (applied locally by iontophoresis), the potentiation by CI-966 was clearest when GABA was applied in or near the stratum pyramidale where its action normally is weakest and shows the most pronounced fading. This change in GABA potency is most simply explained by a reduction in GABA uptake.Key words: GABA, muscimol, nipecotic acid, GABA-uptake blocker, epilepsy.

scholarly journals Lack of change in CA1 dendritic spine density or clustering in rats following training on a radial-arm maze task

2020 ◽  
Vol 5 ◽  
pp. 68
Author(s):  
Emma Craig ◽  
Christopher M. Dillingham ◽  
Michal M. Milczarek ◽  
Heather M. Phillips ◽  
Moira Davies ◽  
...  
Keyword(s):  
Dendritic Spines ◽  
Pyramidal Neurons ◽  
Memory Load ◽  
Spatial Location ◽  
Memory Formation ◽  
Spatial Task ◽  
Radial Arm Maze ◽  
Nearest Neighbour ◽  
Spine Density ◽  
Ca1 Region

Background: Neuronal plasticity is thought to underlie learning and memory formation. The density of dendritic spines in the CA1 region of the hippocampus has been repeatedly linked to mnemonic processes. Both the number and spatial location of the spines, in terms of proximity to nearest neighbour, have been implicated in memory formation. To examine how spatial training impacts synaptic structure in the hippocampus, Lister-Hooded rats were trained on a hippocampal-dependent spatial task in the radial-arm maze.  Methods: One group of rats were trained on a hippocampal-dependent spatial task in the radial arm maze. Two further control groups were included: a yoked group which received the same sensorimotor stimulation in the radial-maze but without a memory load, and home-cage controls. At the end of behavioural training, the brains underwent Golgi staining. Spines on CA1 pyramidal neuron dendrites were imaged and quantitatively assessed to provide measures of density and distance from nearest neighbour.  Results: There was no difference across behavioural groups either in terms of spine density or in the clustering of dendritic spines. Conclusions: Spatial learning is not always accompanied by changes in either the density or clustering of dendritic spines on the basal arbour of CA1 pyramidal neurons when assessed using Golgi imaging.

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.

Protein Kinase A Mediates the Modulation of the Slow Ca2+-Dependent K+ Current,I sAHP, by the Neuropeptides CRF, VIP, and CGRP in Hippocampal Pyramidal Neurons

2000 ◽  
Vol 83 (4) ◽  
pp. 2071-2079 ◽  
Author(s):  
Trude Haug ◽  
Johan F. Storm
Keyword(s):  
Protein Kinase ◽  
Time Course ◽  
Pyramidal Neurons ◽  
Hippocampal Slices ◽  
Cell Voltage ◽  
Dependent Protein Kinase ◽  
Hippocampal Pyramidal Neurons ◽  
Camp Dependent Protein Kinase ◽  
Dependent Protein ◽  
Camp Cascade

We have studied modulation of the slow Ca2+-activated K+current ( I sAHP) in CA1 hippocampal pyramidal neurons by three peptide transmitters: corticotropin releasing factor (CRF, also called corticotropin releasing hormone, CRH), vasoactive intestinal peptide (VIP), and calcitonin gene–related peptide (CGRP). These peptides are known to be expressed in interneurons. Using whole cell voltage clamp in hippocampal slices from young rats, in the presence of tetrodotoxin (TTX, 0.5 μM) and tetraethylammonium (TEA, 5 mM), I sAHP was measured after a brief depolarizing voltage step eliciting inward Ca2+ current. Each of the peptides CRF (100–250 nM), VIP (400 nM), and CGRP (1 μM) significantly reduced the amplitude of I sAHP. Thus the I sAHP amplitude was reduced to 22% by 100 nM CRF, to 17% by 250 nM CRF, to 22% by 400 nM VIP, and to 40% by 1 μM CGRP. We found no consistent concomitant changes in the Ca2+ current or in the time course of I sAHP for any of the three peptides, suggesting that the suppression of I sAHP was not secondary to a general suppression of Ca2+ channel activity. Because each of these peptides is known to activate the cyclic AMP (cAMP) cascade in various cell types, and I sAHP is known to be suppressed by cAMP via the cAMP-dependent protein kinase (PKA), we tested whether the effects on I sAHP by CRF, VIP, and CGRP are mediated by PKA. Intracellular application of the PKA-inhibitor Rp-cAMPS significantly reduced the suppression of I sAHP by CRF, VIP, and CGRP. Thus with 1 mM Rp-cAMPS in the recording pipette, the average suppression of I sAHP was reduced from 78 to 26% for 100 nM CRF, from 83 to 32% for 250 nM CRF, from 78 to 30% for 400 nM VIP, and from 60 to 7% for 1 μM CGRP. We conclude that CRF, VIP, and CGRP suppress the slow Ca2+-activated K+ current, I sAHP, in CA1 hippocampal pyramidal neurons by activating the cAMP-dependent protein kinase, PKA. Together with the monoamine transmitters norepinephrine, serotonin, histamine, and dopamine, these peptide transmitters all converge on the cAMP cascade modulating I sAHP.

scholarly journals Site Independence of EPSP Time Course Is Mediated by DendriticI h in Neocortical Pyramidal Neurons

2000 ◽  
Vol 83 (5) ◽  
pp. 3177-3182 ◽  
Author(s):  
Stephen R. Williams ◽  
Greg J. Stuart
Keyword(s):  
Sodium Channels ◽  
Temporal Summation ◽  
Time Course ◽  
Pyramidal Neurons ◽  
Apical Dendrite ◽  
Linear Increase ◽  
Nonuniform Distribution ◽  
Excitatory Synaptic Input ◽  
Pharmacological Blockade ◽  
Apical Dendrites

Neocortical layer 5 pyramidal neurons possess long apical dendrites that receive a significant portion of the neurons excitatory synaptic input. Passive neuronal models indicate that the time course of excitatory postsynaptic potentials (EPSPs) generated in the apical dendrite will be prolonged as they propagate toward the soma. EPSP propagation may, however, be influenced by the recruitment of dendritic voltage-activated channels. Here we investigate the properties and distribution of I h channels in the axon, soma, and apical dendrites of neocortical layer 5 pyramidal neurons, and their effect on EPSP time course. We find a linear increase (9 pA/100 μm) in the density of dendritic I hchannels with distance from soma. This nonuniform distribution of I h channels generates site independence of EPSP time course, such that the half-width at the soma of distally generated EPSPs (up to 435 μm from soma) was similar to somatically generated EPSPs. As a corollary, a normalization of temporal summation of EPSPs was observed. The site independence of somatic EPSP time course was found to collapse after pharmacological blockade of I h channels, revealing pronounced temporal summation of distally generated EPSPs, which could be further enhanced by TTX-sensitive sodium channels. These data indicate that an increasing density of apical dendritic I hchannels mitigates the influence of cable filtering on somatic EPSP time course and temporal summation in neocortical layer 5 pyramidal neurons.

Transient voltage and calcium-dependent outward currents in hippocampal CA3 pyramidal neurons

1985 ◽  
Vol 53 (4) ◽  
pp. 1038-1058 ◽  
Author(s):  
K. L. Zbicz ◽  
F. F. Weight
Keyword(s):  
Time Course ◽  
Pyramidal Neurons ◽  
Sympathetic Neurons ◽  
Outward Current ◽  
Transient Current ◽  
Transient Outward Current ◽  
Molluscan Neurons ◽  
Voltage Sensitivity ◽  
Transient Currents ◽  
Fast Transient

Membrane currents activated by step changes in membrane potential were studied in hippocampal pyramidal neurons of region CA3 using the single microelectrode voltage-clamp technique. The transient outward current activated by depolarizing steps appeared to be composed of two transient currents that could be distinguished by differences in voltage sensitivity, time course, and pharmacological sensitivity. The more slowly decaying current was activated by voltage steps positive to -60 mV and declined exponentially with a time constant between 200 and 400 ms. This current inactivated as the holding potential was made more positive over the range of -75 to -45 mV and was 50% inactivated near -60 mV. The more slowly decaying transient current was selectively blocked by 0.5 mM 4-aminopyridine (4-AP) but not by 5-10 mM tetraethylammonium (TEA) or 2-5 mM Mn2+. The second transient current had a much faster time course than the 4-AP-sensitive current, having a duration of 5-20 ms. This very fast transient current was observed during potential steps positive to -45 mV. The fast transient current was inactivated when the holding potential was made positive to -45 mV. The amplitude of the fast transient current was greatly reduced by the application of 4 mM Mn2+ or Ca2+-free artificial cerebrospinal fluid (CSF). The fast transient current appeared to be unaffected by 0.5 mM 4-AP but was greatly reduced by 10 mM TEA. These results suggest that the transient outward current observed during depolarizing steps is composed of at least two distinct transient currents. The more slowly decaying current resembles the A-current originally described in molluscan neurons (9, 32, 42) in voltage sensitivity, time course, and pharmacological sensitivity. The faster transient current resembles a fast, Ca2+-dependent transient current previously observed in bull-frog sympathetic neurons (5, 27).

scholarly journals Neurodegeneration, Myelin Loss and Glial Response in the Three-Vessel Global Ischemia Model in Rat

2020 ◽  
Vol 21 (17) ◽  
pp. 6246
Author(s):  
Tatiana Anan’ina ◽  
Alena Kisel ◽  
Marina Kudabaeva ◽  
Galina Chernysheva ◽  
Vera Smolyakova ◽  
...  
Keyword(s):  
Pyramidal Neurons ◽  
Brain Slices ◽  
Global Cerebral Ischemia ◽  
Hippocampal Damage ◽  
Sham Operation ◽  
Ischemic Brain ◽  
Stratum Pyramidale ◽  
Male Wistar Rats ◽  
First Time ◽  
The Brain

(1) Background: Although myelin disruption is an integral part of ischemic brain injury, it is rarely the subject of research, particularly in animal models. This study assessed for the first time, myelin and oligodendrocyte loss in a three-vessel model of global cerebral ischemia (GCI), which causes hippocampal damage. In addition, we investigated the relationships between demyelination and changes in microglia and astrocytes, as well as oligodendrogenesis in the hippocampus; (2) Methods: Adult male Wistar rats (n = 15) underwent complete interruption of cerebral blood flow for 7 min by ligation of the major arteries supplying the brain or sham-operation. At 10 and 30 days after the surgery, brain slices were stained for neurodegeneration with Fluoro-Jade C and immunohistochemically to assess myelin content (MBP+ percentage of total area), oligodendrocyte (CNP+ cells) and neuronal (NeuN+ cells) loss, neuroinflammation (Iba1+ cells), astrogliosis (GFAP+ cells) and oligodendrogenesis (NG2+ cells); (3) Results: 10 days after GCI significant myelin and oligodendrocyte loss was found only in the stratum oriens and stratum pyramidale. By the 30th day, demyelination in these hippocampal layers intensified and affected the substratum radiatum. In addition to myelin damage, activation and an increase in the number of microglia and astrocytes in the corresponding layers, a loss of the CA1 pyramidal neurons, and neurodegeneration in the neocortex and thalamus was observed. At a 10-day time point, we observed rod-shaped microglia in the substratum radiatum. Parallel with ongoing myelin loss on the 30th day after ischemia, we found significant oligodendrogenesis in demyelinated hippocampal layers; (4) Conclusions: Our study showed that GCI-simulating cardiac arrest in humans—causes not only the loss of pyramidal neurons in the CA1 field, but also the myelin loss of adjacent layers of the hippocampus.

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