scholarly journals Locally Balanced Dendritic Integration by Short-Term Synaptic Plasticity and Active Dendritic Conductances

2009 ◽  
Vol 102 (6) ◽  
pp. 3234-3250 ◽  
Author(s):  
Vladislav Volman ◽  
Herbert Levine ◽  
Eshel Ben-Jacob ◽  
Terrence J. Sejnowski
Keyword(s):  
Pyramidal Neurons ◽  
Place Cells ◽  
Synaptic Inhibition ◽  
Dendritic Branch ◽  
Short Term ◽  
Testable Prediction ◽  
Hippocampal Ca1 ◽  
Output Spike ◽  
High Degree

The high degree of variability observed in spike trains and membrane potentials of pyramidal neurons in vivo is thought to be a consequence of a balance between excitatory and inhibitory inputs, which depends on the dynamics of the network. We simulated synaptic currents and ion channels in a reconstructed hippocampal CA1 pyramidal cell and show here that a local balance can be achieved on a dendritic branch with a different mechanism, based on presynaptic depression of quantal release interacting with active dendritic conductances. This mechanism, which does not require synaptic inhibition, allows each dendritic branch to remain sensitive to correlated synaptic inputs, induces a high degree of variability in the output spike train, and can be combined with other balance mechanisms based on network dynamics. This hypothesis makes a testable prediction for the cause of the observed variability in the firing of hippocampal place cells.

Hippocampus Retains the Periodicity of Gamma Stimulation In Vivo

2002 ◽  
Vol 88 (5) ◽  
pp. 2349-2354 ◽  
Author(s):  
J. E. Mikkonen ◽  
T. Grönfors ◽  
J. J. Chrobak ◽  
M. Penttonen
Keyword(s):  
Information Acquisition ◽  
Pyramidal Cells ◽  
Gamma Oscillations ◽  
Short Term ◽  
Ca1 Pyramidal Cells ◽  
State Dependent ◽  
Hippocampal Ca1 ◽  
Oscillatory Rhythms ◽  
The Brain

Several behavioral state dependent oscillatory rhythms have been identified in the brain. Of these neuronal rhythms, gamma (20–70 Hz) oscillations are prominent in the activated brain and are associated with various behavioral functions ranging from sensory binding to memory. Hippocampal gamma oscillations represent a widely studied band of frequencies co-occurring with information acquisition. However, induction of specific gamma frequencies within the hippocampal neuronal network has not been satisfactorily established. Using both in vivo intracellular and extracellular recordings from anesthetized rats, we show that hippocampal CA1 pyramidal cells can discharge at frequencies determined by the preceding gamma stimulation, provided that the gamma is introduced in theta cycles, as occurs in vivo. The dynamic short-term alterations in the oscillatory discharge described in this paper may serve as a coding mechanism in cortical neuronal networks.

An ultrasound-guided procedure to administer a label of DNA synthesis into fetal sheep

1999 ◽  
Vol 11 (5) ◽  
pp. 303 ◽  
Author(s):  
Paul L. Greenwood ◽  
Ramona M. Slepetis ◽  
Alan W. Bell ◽  
John W. Hermanson
Keyword(s):  
Bolus Dose ◽  
S Phase ◽  
Fetal Weight ◽  
Ultrasound Guided ◽  
Short Term ◽  
Fetal Sheep ◽  
Novel Technique ◽  
Cellular Events ◽  
High Degree

A novel technique was developed to deliver a bolus dose of a DNA label into the peritoneal cavity of fetal sheep at 85–130 days gestation. Use of markers to identify the site of injection in fetuses from litters up to quadruplets, and immunohistochemistry to detect the DNA label, 5-bromo-2¢-deoxyuridine (BrdU), confirmed the procedure was successful in 85% of cases. Duration of the procedure was (mean SD) 44 16 min, and recovery from anaesthesia was rapid and uneventful in all cases. Fetal weight was estimated with a high degree of accuracy (residual standard deviation (RSD) = 297 g and r 2 = 0.93, P<0.001) and the dose of label administered (110 33 mg BrdU/kg fetal weight) was adequate in all cases. BrdU detected in fetal nuclei following injection into amniotic fluid highlights the need for positive identification of the injection site in timed, short-term studies, and suggests potential to further develop the technique to investigate cellular events in fetal sheep younger than 85 days of gestation. The results demonstrate that the procedure can be used to determine in vivo whether or not nuclei have entered the S-phase of the cell cycle.

scholarly journals Alterations of in vivo CA1 network activity in Dp(16)1Yey Down syndrome model mice

eLife ◽  
2018 ◽  
Vol 7 ◽  
Author(s):  
Matthieu Raveau ◽  
Denis Polygalov ◽  
Roman Boehringer ◽  
Kenji Amano ◽  
Kazuhiro Yamakawa ◽  
...  
Keyword(s):  
Down Syndrome ◽  
Pyramidal Neurons ◽  
Chromosome 21 ◽  
Network Activity ◽  
Inhibitory Neurons ◽  
Spatial Coding ◽  
Extra Copy ◽  
Hippocampal Ca1

Down syndrome, the leading genetic cause of intellectual disability, results from an extra-copy of chromosome 21. Mice engineered to model this aneuploidy exhibit Down syndrome-like memory deficits in spatial and contextual tasks. While abnormal neuronal function has been identified in these models, most studies have relied on in vitro measures. Here, using in vivo recording in the Dp(16)1Yey model, we find alterations in the organization of spiking of hippocampal CA1 pyramidal neurons, including deficits in the generation of complex spikes. These changes lead to poorer spatial coding during exploration and less coordinated activity during sharp-wave ripples, events involved in memory consolidation. Further, the density of CA1 inhibitory neurons expressing neuropeptide Y, a population key for the generation of pyramidal cell bursts, were significantly increased in Dp(16)1Yey mice. Our data refine the ‘over-suppression’ theory of Down syndrome pathophysiology and suggest specific neuronal subtypes involved in hippocampal dysfunction in these model mice.

scholarly journals Kv1.1 contributes to a rapid homeostatic plasticity of intrinsic excitability in CA1 pyramidal neurons in vivo

eLife ◽  
2019 ◽  
Vol 8 ◽  
Author(s):  
Peter James Morgan ◽  
Romain Bourboulou ◽  
Caroline Filippi ◽  
Julie Koenig-Gambini ◽  
Jérôme Epsztein
Keyword(s):  
Pyramidal Neurons ◽  
Place Cells ◽  
Homeostatic Plasticity ◽  
Intrinsic Excitability ◽  
Memory Interference ◽  
Ca1 Pyramidal Neurons ◽  
Whole Cell Patch Clamp ◽  
Activity Dependent

In area CA1 of the hippocampus, the selection of place cells to represent a new environment is biased towards neurons with higher excitability. However, different environments are represented by orthogonal cell ensembles, suggesting that regulatory mechanisms exist. Activity-dependent plasticity of intrinsic excitability, as observed in vitro, is an attractive candidate. Here, using whole-cell patch-clamp recordings of CA1 pyramidal neurons in anesthetized rats, we have examined how inducing theta-bursts of action potentials affects their intrinsic excitability over time. We observed a long-lasting, homeostatic depression of intrinsic excitability which commenced within minutes, and, in contrast to in vitro observations, was not mediated by dendritic Ih. Instead, it was attenuated by the Kv1.1 channel blocker dendrotoxin K, suggesting an axonal origin. Analysis of place cells’ out-of-field firing in mice navigating in virtual reality further revealed an experience-dependent reduction consistent with decreased excitability. We propose that this mechanism could reduce memory interference.

Abstract WP329: The Role of miR-34b/c in Global Ischemic Stroke

Stroke ◽  
2020 ◽  
Vol 51 (Suppl_1) ◽  
Author(s):  
Hyae-Ran Byun ◽  
Morgan Porch ◽  
Fabrizio Pontarelli ◽  
Brenda L Court Vazquez ◽  
R.Suzanne Zukin ◽  
...  
Keyword(s):  
Ischemic Stroke ◽  
Cognitive Deficits ◽  
Neuronal Death ◽  
Target Genes ◽  
Pyramidal Neurons ◽  
Unmet Need ◽  
Global Ischemia ◽  
Hippocampal Ca1

Transient global ischemia arising as a consequence of cardiac arrest in humans causes selective, delayed death of hippocampal CA1 pyramidal neurons and cognitive impairment. Effective treatments to ameliorate the neurodegeneration and cognitive dysfunction associated with global ischemia are an unmet need. Emerging evidence points to a widespread role for microRNAs (miRNAs) as key modulators of target gene expression in neurons. Accordingly, dysregulation of miRNAs are implicated in the pathophysiology of neurodegenerative disease and neurological disorders. Our findings, derived via miRNA-seq, indicate that expression of a subset of microRNAs are altered in postischemic CA1 including miR-34b/c, miR-21, miR-331, miR-181 and miR-29. Ingenuity pathway analysis reveals that miR-34b/c is the leading miR candidate implicated in cell death and survival. A role for miR-34 in the pathogenesis of global ischemia is, as yet, unclear. Here we show ischemia induces p53-dependent activation of miR-34b/c and downregulation of its target genes Bcl-2 and Sirt1, which together promote neuronal death in selectively vulnerable hippocampal CA1 in vivo . Consistent with this, inhibition of miR-34b/c affords neuroprotection, rescues impaired synaptic plasticity and reduces memory deficits in global ischemia. These findings document a causal role for p53-dependent activation of miR-34b/c in neuronal death and identify a novel therapeutic target for amelioration of the neurodegeneration and cognitive deficits associated with ischemic stroke.

Modulatory effects of oligodendrocytes on the conduction velocity of action potentials along axons in the alveus of the rat hippocampal CA1 region

2007 ◽  
Vol 3 (4) ◽  
pp. 325-334 ◽  
Author(s):  
Yoshihiko Yamazaki ◽  
Yasukazu Hozumi ◽  
Kenya Kaneko ◽  
Toshimichi Sugihara ◽  
Satoshi Fujii ◽  
...  
Keyword(s):  
Electrical Stimulation ◽  
Nmda Receptors ◽  
Conduction Velocity ◽  
Action Potentials ◽  
Pyramidal Neurons ◽  
Ca1 Region ◽  
Hippocampal Ca1 Region ◽  
Hippocampal Ca1 ◽  
Inward Currents

AbstractLike neurons and astrocytes, oligodendrocytes have a variety of neurotransmitter receptors and ion channels. However, except for facilitating the rapid conduction of action potentials by forming myelin and buffering extracellular K+, little is known about the direct involvement of oligodendrocytes in neuronal activities. To investigate their physiological roles, we focused on oligodendrocytes in the alveus of the rat hippocampal CA1 region. These cells were found to respond to exogenously applied glutamate by depolarization through N-methyl-D-aspartate (NMDA) receptors and non-NMDA receptors. Electrical stimulation of the border between the alveus and stratum oriens evoked inward currents through several routes involving glutamate receptors and inward rectifier K+ channels. Moreover, electrical stimulation resembling in vivo activity evoked long-lasting depolarization. To examine the modulatory effects of oligodendrocytes on neuronal activities, we performed dual, whole-cell recording on CA1 pyramidal neurons and oligodendrocytes. Direct depolarization of oligodendrocytes shortened the latencies of action potentials evoked by antidromic stimulation. These results indicate that oligodendrocytes increase the conduction velocity of action potentials by a mechanism additional to saltatory conduction, and that they have active roles in information processing in the brain.

scholarly journals Dynamics of Cortical Dendritic Membrane Potential and Spikes in Freely Behaving Rats

2016 ◽  
Author(s):  
Jason J. Moore ◽  
Pascal M. Ravassard ◽  
David Ho ◽  
Lavanya Acharya ◽  
Ashley L. Kees ◽  
...  
Keyword(s):  
Membrane Potential ◽  
Neural Coding ◽  
Pyramidal Neurons ◽  
Neural Computation ◽  
Limited Information ◽  
Neuronal Dendrites ◽  
Dendritic Membrane ◽  
Freely Behaving ◽  
High Degree

AbstractNeural activity in vivo is primarily measured using extracellular somatic spikes, which provide limited information about neural computation. Hence, it is necessary to record from neuronal dendrites, which generate dendritic action potentials (DAP) and profoundly influence neural computation and plasticity. We measured neocortical sub- and supra-threshold dendritic membrane potential (DMP) from putative distal-most dendrites using tetrodes in freely behaving rats over multiple days with a high degree of stability and sub-millisecond temporal resolution. DAP firing rates were several fold larger than somatic rates. DAP rates were modulated by subthreshold DMP fluctuations which were far larger than DAP amplitude, indicting hybrid, analog-digital coding in the dendrites. Parietal DAP and DMP exhibited egocentric spatial maps comparable to pyramidal neurons. These results have important implications for neural coding and plasticity.One Sentence SummaryMeasurement of cortical dendritic membrane potential for several days in freely behaving rats reveals disproportionate dendritic spiking and analog and digital coding.

Effects on Synaptic Inhibition in the Hippocampus Do Not Underlie the Amnestic and Convulsive Properties of the Nonimmobilizer 1,2-Dichlorohexafluorocyclobutane

2004 ◽  
Vol 101 (1) ◽  
pp. 66-74 ◽  
Author(s):  
Misha Perouansky ◽  
Robert A. Pearce
Keyword(s):  
Gabaa Receptor ◽  
Gabaa Receptors ◽  
Hippocampal Slices ◽  
Lipid Solubility ◽  
Synaptic Inhibition ◽  
Minimal Alveolar Concentration ◽  
Discernible Effect ◽  
Hippocampal Ca1 ◽  
Seizure Models

Background Although it does not suppress movement in response to noxious stimuli, the nonimmobilizer 1,2-dichlorohexafluorocyclobutane (F6, also known as 2N) does cause amnesia and seizures. These occur at 0.48 and 1.3 times, respectively, the concentrations that are predicted from its lipid solubility to cause immobility. The molecular and cellular basis of these effects is not known. The ionotropic gamma-aminobutyric acid type A (GABAA) receptor is modulated strongly by anesthetics, and it plays an important role in many seizure models. Also, the hippocampus is a structure central to the formation of memory and is susceptible to seizure generation. The authors therefore investigated the effect of F6 on GABAA receptor- mediated inhibition in hippocampal neurons. Methods Transverse hippocampal slices were prepared from young (12- to 21-day-old) Sprague-Dawley rats. Inhibitory postsynaptic currents were recorded from hippocampal CA1 pyramidal cells in the presence of ionotropic glutamate receptor antagonists. F6 was applied with the bath solution. The concentration of F6 achieved during the experiment at the location of synaptic inhibition was derived using a diffusion model. Results At tissue concentrations of up to 75 microm (approximately 5 x predicted minimal alveolar concentration), F6 had no discernible effect on either the amplitude or the kinetics of GABA-mediated synaptic currents. Isoflurane, by contrast, prolonged the decay time constant of these currents at 100 microm (approximately 0.3 x minimal alveolar concentration). Conclusions At concentrations that bracket the in vivo amnestic and seizure-inducing range, F6 has no discernible effect on fast synaptic GABAA receptors in hippocampal CA1 pyramidal neurons. Synaptic GABAA receptors sharply discriminate between volatile anesthetics and a prototype nonimmobilizer. Similar in vivo effects of anesthetics and nonimmobilizers may be mediated by different cellular mechanisms.

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