scholarly journals Signal Propagation in Oblique Dendrites of CA1 Pyramidal Cells

2005 ◽  
Vol 94 (6) ◽  
pp. 4145-4155 ◽  
Author(s):  
Michele Migliore ◽  
Michele Ferrante ◽  
Giorgio A. Ascoli
Keyword(s):  
Pyramidal Neurons ◽  
Back Propagation ◽  
Three Dimensional ◽  
Pyramidal Cells ◽  
Signal Propagation ◽  
Morphological Properties ◽  
Ca1 Neurons ◽  
Electrophysiological Properties ◽  
Ca1 Pyramidal Cells ◽  
Dendritic Spikes

The electrophysiological properties of the oblique branches of CA1 pyramidal neurons are largely unknown and very difficult to investigate experimentally. These relatively thin dendrites make up the majority of the apical tree surface area and constitute the main target of Schaffer collateral axons from CA3. Their electrogenic properties might have an important role in defining the computational functions of CA1 neurons. It is thus important to determine if and to what extent the back- and forward propagation of action potentials (AP) in these dendrites could be modulated by local properties such as morphology or active conductances. In the first detailed study of signal propagation in the full extent of CA1 oblique dendrites, we used 27 reconstructed three-dimensional morphologies and different distributions of the A-type K+ conductance ( KA), to investigate their electrophysiological properties by computational modeling. We found that the local KA distribution had a major role in modulating action potential back propagation, whereas the forward propagation of dendritic spikes originating in the obliques was mainly affected by local morphological properties. In both cases, signal processing in any given oblique was effectively independent of the rest of the neuron and, by and large, of the distance from the soma. Moreover, the density of KA in oblique dendrites affected spike conduction in the main shaft. Thus the anatomical variability of CA1 pyramidal cells and their local distribution of voltage-gated channels may suit a powerful functional compartmentalization of the apical tree.

scholarly journals A new reduced-morphology model for CA1 pyramidal cells and its validation and comparison with other models using HippoUnit

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Matus Tomko ◽  
Lubica Benuskova ◽  
Peter Jedlicka
Keyword(s):  
Pyramidal Cell ◽  
Pyramidal Neurons ◽  
Standardized Test ◽  
Dendritic Tree ◽  
Pyramidal Cells ◽  
Computational Time ◽  
Ca1 Neurons ◽  
Ca1 Pyramidal Cells ◽  
Morphology Model ◽  
Complex Models

AbstractModeling long-term neuronal dynamics may require running long-lasting simulations. Such simulations are computationally expensive, and therefore it is advantageous to use simplified models that sufficiently reproduce the real neuronal properties. Reducing the complexity of the neuronal dendritic tree is one option. Therefore, we have developed a new reduced-morphology model of the rat CA1 pyramidal cell which retains major dendritic branch classes. To validate our model with experimental data, we used HippoUnit, a recently established standardized test suite for CA1 pyramidal cell models. The HippoUnit allowed us to systematically evaluate the somatic and dendritic properties of the model and compare them to models publicly available in the ModelDB database. Our model reproduced (1) somatic spiking properties, (2) somatic depolarization block, (3) EPSP attenuation, (4) action potential backpropagation, and (5) synaptic integration at oblique dendrites of CA1 neurons. The overall performance of the model in these tests achieved higher biological accuracy compared to other tested models. We conclude that, due to its realistic biophysics and low morphological complexity, our model captures key physiological features of CA1 pyramidal neurons and shortens computational time, respectively. Thus, the validated reduced-morphology model can be used for computationally demanding simulations as a substitute for more complex models.

Cluster Analysis–Based Physiological Classification and Morphological Properties of Inhibitory Neurons in Layers 2–3 of Monkey Dorsolateral Prefrontal Cortex

2005 ◽  
Vol 94 (5) ◽  
pp. 3009-3022 ◽  
Author(s):  
Leonid S. Krimer ◽  
Aleksey V. Zaitsev ◽  
Gabriela Czanner ◽  
Sven Kröner ◽  
Guillermo González-Burgos ◽  
...  
Keyword(s):  
Cluster Analysis ◽  
Prefrontal Cortex ◽  
Dorsolateral Prefrontal Cortex ◽  
Pyramidal Cells ◽  
Inhibitory Neurons ◽  
Morphological Properties ◽  
Electrophysiological Properties ◽  
Dorsolateral Prefrontal ◽  
Fast Spiking ◽  
Monkey Prefrontal Cortex

In primates, little is known about intrinsic electrophysiological properties of neocortical neurons and their morphological correlates. To classify inhibitory cells (interneurons) in layers 2–3 of monkey dorsolateral prefrontal cortex we used whole cell voltage recordings and intracellular labeling in slice preparation with subsequent morphological reconstructions. Regular spiking pyramidal cells have been also included in the sample. Neurons were successfully segregated into three physiological clusters: regular-, intermediate-, and fast-spiking cells using cluster analysis as a multivariate exploratory technique. When morphological types of neurons were mapped on the physiological clusters, the cluster of regular spiking cells contained all pyramidal cells, whereas the intermediate- and fast-spiking clusters consisted exclusively of interneurons. The cluster of fast-spiking cells contained all of the chandelier cells and the majority of local, medium, and wide arbor (basket) interneurons. The cluster of intermediate spiking cells predominantly consisted of cells with the morphology of neurogliaform or vertically oriented (double-bouquet) interneurons. Thus a quantitative approach enabled us to demonstrate that intrinsic electrophysiological properties of neurons in the monkey prefrontal cortex define distinct cell types, which also display distinct morphologies.

Transient Suppression of GABAA-Receptor–Mediated IPSPs After Epileptiform Burst Discharges in CA1 Pyramidal Cells

1998 ◽  
Vol 79 (2) ◽  
pp. 659-669 ◽  
Author(s):  
F.E.N. Le Beau ◽  
B. E. Alger
Keyword(s):  
G Proteins ◽  
Pyramidal Neurons ◽  
Membrane Conductance ◽  
Pyramidal Cells ◽  
Postsynaptic Membrane ◽  
Burst Discharge ◽  
Ca1 Pyramidal Cells ◽  
Acid Bath ◽  
Bath Application ◽  
Intracellular Ca

Le Beau, F.E.N. and B. E. Alger. Transient suppression ofGABAA-receptor–mediated IPSPs after epileptiform burst discharges in CA1 pyramidal cells. J. Neurophysiol. 79: 659–669, 1998. Epileptiform burst discharges were elicited in CA1 hippocampal pyramidal cells in the slice preparation by perfusion with Mg2+-free saline. Intracellular recordings revealed paroxysmal depolarization shifts (PDSs) that either occurred spontaneously or were evoked by stimulation of Schaffer collaterals. These bursts involved activation of N-methyl-d-aspartate receptors because burst discharges were reduced or abolished by dl-2-amino-5-phosphonovaleric acid. Bath application of carbachol caused an increase in spontaneous activity that was predominantly due to γ-aminobutyric acid-A-receptor–mediated spontaneous inhibitory postsynaptic potentials (sIPSPs). A marked reduction in sIPSPs (31%) was observed after each epileptiform burst discharge, which subsequently recovered to preburst levels after ∼4–20 s. This sIPSP suppression was not associated with any change in postsynaptic membrane conductance. A suppression of sIPSPs also was seen after burst discharges evoked by brief (100–200 ms) depolarizing current pulses. N-ethylmaleimide, which blocks pertussis-toxin–sensitive G proteins, significantly reduced the suppression of sIPSPs seen after a burst response. When increases in intracellular Ca2+ were buffered by intracellular injection of ethylene glycol bis(β-aminoethyl)ether- N,N,N′,N′-tetraacetic acid, the sIPSP suppression seen after a single spontaneous or evoked burst discharge was abolished. Although we cannot exclude other Ca2+-dependent mechanisms, this suppression of sIPSPs shared many of the characteristics of depolarization-induced suppression of inhibition (DSI) in that it involved activation of G proteins and was dependent on increases in intracellular calcium. These findings suggest that a DSI-like process may be activated by the endogenous burst firing of CA1 pyramidal neurons.

scholarly journals PRMT7 deficiency causes dysregulation of the HCN channels in the CA1 pyramidal cells and impairment of social behaviors

2020 ◽  
Vol 52 (4) ◽  
pp. 604-614
Author(s):  
Seul-Yi Lee ◽  
Tuan Anh Vuong ◽  
Hyun-Kyung So ◽  
Hyun-Ji Kim ◽  
Yoo Bin Kim ◽  
...  
Keyword(s):  
Pyramidal Cells ◽  
Neuropsychiatric Disorders ◽  
Autism Spectrum ◽  
Resting Potential ◽  
Hcn Channels ◽  
Hcn Channel ◽  
Ca1 Neurons ◽  
Protein Levels ◽  
Ca1 Pyramidal Cells ◽  
Ca1 Region

Abstract HCN channels regulate excitability and rhythmicity in the hippocampal CA1 pyramidal cells. Perturbation in the HCN channel current (Ih) is associated with neuropsychiatric disorders, such as autism spectrum disorders. Recently, protein arginine methyltransferase 7 (PRMT7) was shown to be highly expressed in the hippocampus, including the CA1 region. However, the physiological function of PRMT7 in the CA1 neurons and the relationship to psychiatric disorders are unclear. Here we showed that PRMT7 knockout (KO) mice exhibit hyperactivity and deficits in social interaction. The firing frequency of the CA1 neurons in the PRMT7 KO mice was significantly higher than that in the wild-type (WT) mice. Compared with the WT CA1 neurons, the PRMT7 KO CA1 neurons showed a more hyperpolarized resting potential and a higher input resistance, which were occluded by the Ih-current inhibitor ZD7288; these findings were consistent with the decreased Ih and suggested the contribution of Ih-channel dysfunction to the PRMT7 KO phenotypes. The HCN1 protein level was decreased in the CA1 region of the PRMT7 KO mice in conjunction with a decrease in the expression of Shank3, which encodes a core scaffolding protein for HCN channel proteins. A brief application of the PRMT7 inhibitor DS437 did not reproduce the phenotype of the PRMT7 KO neurons, further indicating that PRMT7 regulates Ih by controlling the channel number rather than the open probability. Moreover, shRNA-mediated PRMT7 suppression reduced both the mRNA and protein levels of SHANK3, implying that PRMT7 deficiency might be responsible for the decrease in the HCN protein levels by altering Shank3 expression. These findings reveal a key role for PRMT7 in the regulation of HCN channel density in the CA1 pyramidal cells that may be amenable to pharmacological intervention for neuropsychiatric disorders.

scholarly journals Anatomical and Electrophysiological Comparison of CA1 Pyramidal Neurons of the Rat and Mouse

2009 ◽  
Vol 102 (4) ◽  
pp. 2288-2302 ◽  
Author(s):  
Brandy N. Routh ◽  
Daniel Johnston ◽  
Kristen Harris ◽  
Raymond A. Chitwood
Keyword(s):  
Pyramidal Neurons ◽  
Three Dimensional ◽  
Input Resistance ◽  
Genetically Engineered ◽  
Morphological Properties ◽  
Mouse Strains ◽  
Sprague Dawley ◽  
Maximal Conductance ◽  
Ca1 Pyramidal Neurons ◽  
Genetically Engineered Mice

The study of learning and memory at the single-neuron level has relied on the use of many animal models, most notably rodents. Although many physiological and anatomical studies have been carried out in rats, the advent of genetically engineered mice has necessitated the comparison of new results in mice to established results from rats. Here we compare fundamental physiological and morphological properties and create three-dimensional compartmental models of identified hippocampal CA1 pyramidal neurons of one strain of rat, Sprague–Dawley, and two strains of mice, C57BL/6 and 129/SvEv. We report several differences in neuronal physiology and anatomy among the three animal groups, the most notable being that neurons of the 129/SvEv mice, but not the C57BL/6 mice, have higher input resistance, lower dendritic surface area, and smaller spines than those of rats. A surprising species-specific difference in membrane resonance indicates that both mouse strains have lower levels of the hyperpolarization-activated nonspecific cation current Ih. Simulations suggest that differences in Ih kinetics rather than maximal conductance account for the lower resonance. Our findings indicate that comparisons of data obtained across strains or species will need to account for these and potentially other physiological and anatomical differences.

Propagating dendritic action potential mediates synaptic transmission in CA1 pyramidal cells in situ

1990 ◽  
Vol 64 (5) ◽  
pp. 1429-1441 ◽  
Author(s):  
O. Herreras
Keyword(s):  
Pyramidal Neurons ◽  
Current Source ◽  
Maximum Amplitude ◽  
Pyramidal Cells ◽  
Distal Portion ◽  
Ca1 Pyramidal Cells ◽  
Basal Dendrites ◽  
Voltage Dependent ◽  
Speed Of Propagation ◽  
Apical Dendrites

1. The events leading to the Schaffer collateral-induced discharge of CA1 pyramidal neurons were investigated in the hippocampus of anesthetized rats by current source-density (CSD) analysis. 2. The earliest evoked currents detected shortly after a stimulus were a sink in the zone where synapses are known to be located (300-350 microns ventral to the somatic layer) flanked by two smaller sources in the distal portion of the apical dendrites and in the somatic layer. This synaptic sink (SyS) extended over 75-100 microns; it lasted for 15-20 ms, and it reached its maximum amplitude some milliseconds after the population spike (PS) and remained in the same location. Stimuli submaximal and supramaximal for evoking a PS yielded the same pattern of current distribution for the SyS. Presynaptic fiber volleys were not detected in these recordings. 3. During the rising phase of the SyS a second sink appeared in a more proximal portion of the apical dendrites. This late dendritic sink (LS) extended over 50-75 microns and was centered 100-150 microns ventral to the somatic layer. This proximal dendritic sink was of amplitude comparable with the SyS; it outlasted the latter and was not necessarily followed by a somatic PS. The LS was extinguished with the appearance of a PS, whereas the SyS persisted regardless of the presence of a PS. 4. After maximal stimuli the LS grew until it exceeded a threshold amplitude, and then, it started to move somatopetally as a continuously propagating sink (PrS). The average speed of propagation was approximately 0.2 m/s. In 0.5-0.7 ms the PrS reached the cell-body layer displacing the passive source that moved into the basal dendrites. The PrS then became the intensive sink corresponding to the main (negative) phase of the somatic PS. This was followed by the development of an active source in the soma layer, probably corresponding to the repolarization phase of the PS. 5. From these observations it appears that the LS and PrS are active dendritic responses. It may be inferred that, shortly after the synaptic currents enter the dendrites, depolarization of adjacent membranes causes the opening of low-threshold, voltage-dependent, slowly inactivating channels that generate the LS. If the depolarization resulting from the LS current is intense enough, another population of channels open that are also voltage-dependent but of higher threshold and faster inactivation.(ABSTRACT TRUNCATED AT 400 WORDS)

scholarly journals Electrophysiological properties of genetically identified subtypes of layer 5 neocortical pyramidal neurons: Ca2+ dependence and differential modulation by norepinephrine

2015 ◽  
Vol 113 (7) ◽  
pp. 2014-2032 ◽  
Author(s):  
Dongxu Guan ◽  
William E. Armstrong ◽  
Robert C. Foehring
Keyword(s):  
Pyramidal Neurons ◽  
Fluorescent Protein ◽  
Brain Slices ◽  
Pyramidal Cells ◽  
Field Size ◽  
Repetitive Firing ◽  
Differential Modulation ◽  
Electrophysiological Properties ◽  
Laminar Distribution ◽  
Neocortical Pyramidal Neurons

We studied neocortical pyramidal neurons from two lines of bacterial artificial chromosome mice ( etv1 and glt; Gene Expression Nervous System Atlas: GENSAT project), each of which expresses enhanced green fluorescent protein (EGFP) in a different subpopulation of layer 5 pyramidal neurons. In barrel cortex, etv1 and glt pyramidal cells were previously reported to differ in terms of their laminar distribution, morphology, thalamic inputs, cellular targets, and receptive field size. In this study, we measured the laminar distribution of etv1 and glt cells. On average, glt cells were located more deeply; however, the distributions of etv1 and glt cells extensively overlap in layer 5. To test whether these two cell types differed in electrophysiological properties that influence firing behavior, we prepared acute brain slices from 2–4-wk-old mice, where EGFP-positive cells in somatosensory cortex were identified under epifluorescence and then studied using whole cell current- or voltage-clamp recordings. We studied the details of action potential parameters and repetitive firing, characterized by the larger slow afterhyperpolarizations (AHPs) in etv1 neurons and larger medium AHPs (mAHPS) in glt cells, and compared currents underlying the mAHP and slow AHP (sAHP) in etv1 and glt neurons. Etv1 cells exhibited lower d V/d t for spike polarization and repolarization and reduced direct current (DC) gain (lower f- I slope) for repetitive firing than glt cells. Most importantly, we found that 1) differences in the expression of Ca2+-dependent K+ conductances (small-conductance calcium-activated potassium channels and sAHP channels) determine major functional differences between etv1 and glt cells, and 2) there is differential modulation of etv1 and glt neurons by norepinephrine.

Physiological and Morphological Characterization of Local Interneurons in the Drosophila Antennal Lobe

2010 ◽  
Vol 104 (2) ◽  
pp. 1007-1019 ◽  
Author(s):  
Yoichi Seki ◽  
Jürgen Rybak ◽  
Dieter Wicher ◽  
Silke Sachse ◽  
Bill S. Hansson
Keyword(s):  
Antennal Lobe ◽  
Neural Circuit ◽  
Three Dimensional ◽  
Morphological Characterization ◽  
Morphological Properties ◽  
Electrophysiological Properties ◽  
Local Interneurons ◽  
Enhancer Trap Line ◽  
Almost All

The Drosophila antennal lobe (AL) has become an excellent model for studying early olfactory processing mechanisms. Local interneurons (LNs) connect a large number of glomeruli and are ideally positioned to increase computational capabilities of odor information processing in the AL. Although the neural circuit of the Drosophila AL has been intensively studied at both the input and the output level, the internal circuit is not yet well understood. An unambiguous characterization of LNs is essential to remedy this lack of knowledge. We used whole cell patch-clamp recordings and characterized four classes of LNs in detail using electrophysiological and morphological properties at the single neuron level. Each class of LN displayed unique characteristics in intrinsic electrophysiological properties, showing differences in firing patterns, degree of spike adaptation, and amplitude of spike afterhyperpolarization. Notably, one class of LNs had characteristic burst firing properties, whereas the others were tonically active. Morphologically, neurons from three classes innervated almost all glomeruli, while LNs from one class innervated a specific subpopulation of glomeruli. Three-dimensional reconstruction analyses revealed general characteristics of LN morphology and further differences in dendritic density and distribution within specific glomeruli between the different classes of LNs. Additionally, we found that LNs labeled by a specific enhancer trap line (GAL4-Krasavietz), which had previously been reported as cholinergic LNs, were mostly GABAergic. The current study provides a systematic characterization of olfactory LNs in Drosophila and demonstrates that a variety of inhibitory LNs, characterized by class-specific electrophysiological and morphological properties, construct the neural circuit of the AL.

scholarly journals Disinhibitory and neuromodulatory regulation of hippocampal synaptic plasticity

2020 ◽  
Author(s):  
Inês Guerreiro ◽  
Zhenglin Gu ◽  
Jerrel L. Yakel ◽  
Boris S. Gutkin
Keyword(s):  
Synaptic Plasticity ◽  
Pyramidal Neurons ◽  
Pyramidal Cells ◽  
General Mechanism ◽  
Excitatory Synapses ◽  
Ca1 Pyramidal Cells ◽  
Ca1 Pyramidal Neurons ◽  
Hippocampal Synaptic Plasticity ◽  
Local Circuitry ◽  
Feedforward Inhibition

AbstractHippocampal synaptic plasticity, particularly in the Schaffer collateral (SC) to CA1 pyramidal excitatory transmission, is considered as the cellular mechanism underlying learning. The CA1 pyramidal neurons are embedded in an intricate local circuitry that contains a variety of interneurons. The roles these interneurons play in the regulation of the excitatory synaptic plasticity remains largely understudied. Our recent experiments showed that repeated cholinergic activation of α7 nACh receptors expressed in oriens-lacunosum-moleculare (OLMα2) interneurons could induce LTP in SC-CA1 synapses, likely through disinhibition by inhibiting stratum radiatum (s.r.) interneurons that provide feedforward inhibition onto CA1 pyramidal neurons, revealing a potential mechanism for local interneurons to regulate SC-CA1 synaptic plasticity. Here, we pair in vitro studies with biophysically-based modeling to uncover the mechanisms through which cholinergic-activated GABAergic interneurons can disinhibit CA1 pyramidal cells, and how repeated disinhibition modulates hippocampal plasticity at the excitatory synapses. We found that α7 nAChR activation increases OLM activity. OLM neurons, in turn inhibit the fast-spiking interneurons that provide feedforward inhibition onto CA1 pyramidal neurons. This disinhibition, paired with tightly timed SC stimulation, can induce potentiation at the excitatory synapses of CA1 pyramidal neurons. Our work further describes the pairing of disinhibition with SC stimulation as a general mechanism for the induction of hippocampal synaptic plasticity.Disinhibition of the excitatory synapses, paired with SC stimulation, leads to increased NMDAR activation and intracellular calcium concentration sufficient to upregulate AMPAR permeability and potentiate the synapse. Repeated paired disinhibition of the excitatory synapse leads to larger and longer lasting increases of the AMPAR permeability. Our study thus provides a novel mechanism for inhibitory interneurons to directly modify glutamatergic synaptic plasticity. In particular, we show how cholinergic action on OLM interneurons can down-regulate the GABAergic signaling onto CA1 pyramidal cells, and how this shapes local plasticity rules. We identify paired disinhibition with SC stimulation as a general mechanism for the induction of hippocampal synaptic plasticity.

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