Arecoline Induces Theta Rhythm, Reduces Pyramidal Cell Excitability and Moderately Impairs LTP In Vivo

1988 ◽  
pp. 155-158 ◽  
Author(s):  
H. R. Olpe ◽  
H. Jutzeler ◽  
E. Kueng ◽  
P. Campiche ◽  
K. Klebs ◽  
...  
Keyword(s):  
Pyramidal Cell ◽  
Theta Rhythm ◽  
Cell Excitability

scholarly journals Linking minimal and detailed models of CA1 microcircuits reveals how theta rhythms emerge and how their frequencies are controlled

2020 ◽  
Author(s):  
Alexandra P Chatzikalymniou ◽  
Melisa Gumus ◽  
Anton R Lunyov ◽  
Scott Rich ◽  
Jeremie Lefebvre ◽  
...  
Keyword(s):  
Pyramidal Cell ◽  
Theta Rhythm ◽  
Computational Models ◽  
Pyramidal Cells ◽  
Cell Types ◽  
Minimal Models ◽  
Detailed Model ◽  
Theta Frequency ◽  
Hippocampal Theta

AbstractThe wide variety of cell types and their inherent biophysical complexities pose a challenge to our understanding of oscillatory activities produced by cellular-based computational models. This challenge stems from the high-dimensional and multi-parametric nature of these systems. To overcome this issue, we implement systematic comparisons of minimal and detailed models of CA1 microcircuits that generate intra-hippocampal theta rhythms (3-12 Hz). We leverage insights from minimal models to guide detailed model explorations and obtain a cellular perspective of theta generation. Our findings distinguish the pyramidal cells as the theta rhythm initiators and reveal that their activity is regularized by the inhibitory cell populations, supporting an ‘inhibition-based tuning’ mechanism. We find a strong correlation between the pyramidal cell input current and the resulting LFP theta frequency, establishing that the intrinsic pyramidal cell properties underpin network frequency characteristics. This work provides a cellular-based foundation from which in vivo theta activities can be explored.

The effect of propofol on ca1 pyramidal cell excitability and gabaa-mediated inhibition in the rat hippocampal slice

Life Sciences ◽  
1996 ◽  
Vol 58 (26) ◽  
pp. 2397-2407 ◽  
Author(s):  
T.E. Albertson ◽  
W.F. Walby ◽  
L.G. Stark ◽  
R.M. Joy
Keyword(s):  
Pyramidal Cell ◽  
Hippocampal Slice ◽  
Cell Excitability

scholarly journals Sub-optimal Discontinuous Current-Clamp switching rates lead to deceptive mouse neuronal firing

2020 ◽  
Author(s):  
Marin Manuel
Keyword(s):  
Membrane Potential ◽  
Neuronal Firing ◽  
Intracellular Recordings ◽  
Optimal Switching ◽  
Switching Rate ◽  
Current Clamp ◽  
Care Needs ◽  
Cell Potential ◽  
Cell Excitability

AbstractIntracellular recordings using sharp microelectrodes often rely on a technique called Discontinuous Current-Clamp to accurately record the membrane potential while injecting current through the same microelectrode. It is well known that a poor choice of DCC switching rate can lead to under-or over-estimation of the cell potential, however, its effect on the cell firing is rarely discussed. Here, we show that sub-optimal switching rates lead to an overestimation of cell excitability. We performed intracellular recordings of mouse spinal motoneurons and recorded their firing in response to pulses and ramps of current in Bridge and DCC mode at various switching rates. We demonstrate that using an incorrect (too low) DCC frequency leads not only to an underestimation of the input resistance, but also, paradoxically, to an artificial overestimation of the firing of these cells: neurons fire at lower current, and at higher frequencies than at higher DCC rates, or than the same neuron recorded in Bridge mode. These effects are dependent on the membrane time constant of the recorded cell, and special care needs to be taken in large cells with very short time constants. Our work highlights the importance of choosing an appropriate DCC switching rate to obtain not only accurate membrane potential readings but also an accurate representation of the firing of the cell.Significance StatementDiscontinuous Current-Clamp is a technique often used during intracellular recordings in vivo. However, incorrect usage of this technique can lead to incorrect interpretations. Poor choice of the DCC switching rate can lead to under- or over-estimation of the cell potential. In addition, we show here that sub-optimal switching rates lead to an overestimation of the cell excitability.

Deciphering how interneuron specific 3 cells control oriens lacunosum-moleculare cells to contribute to circuit function

2021 ◽  
Author(s):  
Alexandre Guet-McCreight ◽  
Frances K Skinner
Keyword(s):  
Pyramidal Cell ◽  
Inhibitory Interneuron ◽  
Cell Type ◽  
Cell Recruitment ◽  
External Modulation ◽  
Theta Frequency ◽  
Cell Firing ◽  
Circuit Function

The wide diversity of inhibitory cells across the brain makes them suitable to contribute to network dynamics in specialized fashions. However, the contributions of a particular inhibitory cell type in a behaving animal are challenging to untangle as one needs to both record cellular activities and identify the cell type being recorded. Thus, using computational modeling and theory to predict and hypothesize cell-specific contributions is desirable. Here, we examine potential contributions of interneuron-specific 3 (I-S3) cells - an inhibitory interneuron found in CA1 hippocampus that only targets other inhibitory interneurons - during simulated theta rhythms. We use previously developed multi-compartment models of oriens lacunosum-moleculare (OLM) cells, the main target of I-S3 cells, and explore how I-S3 cell inputs during in vitro and in vivo scenarios contribute to theta. We find that I-S3 cells suppress OLM cell spiking, rather than engender its spiking via post-inhibitory rebound mechanisms, and contribute to theta frequency spike resonance during simulated in vivo scenarios. To elicit recruitment similar to in vitro experiments, inclusion of disinhibited pyramidal cell inputs is necessary, implying that I-S3 cell firing broadens the window for pyramidal cell disinhibition. Using in vivo virtual networks, we show that I-S3 cells contribute to a sharpening of OLM cell recruitment at theta frequencies. Further, shifting the timing of I-S3 cell spiking due to external modulation shifts the timing of the OLM cell firing and thus disinhibitory windows. We propose a specialized contribution of I-S3 cells to create temporally precise coordination of modulation pathways.

scholarly journals Inhibition of N-type calcium channels in cardiac sympathetic neurons attenuates ventricular arrhythmogenesis in heart failure

2020 ◽  
Author(s):  
Dongze Zhang ◽  
Huiyin Tu ◽  
Chaojun Wang ◽  
Liang Cao ◽  
Wenfeng Hu ◽  
...  
Keyword(s):  
Heart Failure ◽  
Coronary Artery ◽  
Ventricular Arrhythmias ◽  
Sympathetic Neurons ◽  
Coronary Artery Ligation ◽  
Channel Blockers ◽  
Artery Ligation ◽  
Cell Excitability ◽  
Ventricular Arrhythmogenesis

Abstract Aims Cardiac sympathetic overactivation is an important trigger of ventricular arrhythmias in patients with chronic heart failure (CHF). Our previous study demonstrated that N-type calcium (Cav2.2) currents in cardiac sympathetic post-ganglionic (CSP) neurons were increased in CHF. This study investigated the contribution of Cav2.2 channels in cardiac sympathetic overactivation and ventricular arrhythmogenesis in CHF. Methods and results Rat CHF was induced by surgical ligation of the left coronary artery. Lentiviral Cav2.2-α shRNA or scrambled shRNA was transfected in vivo into stellate ganglia (SG) in CHF rats. Final experiments were performed at 14 weeks after coronary artery ligation. Real-time polymerase chain reaction and western blot data showed that in vivo transfection of Cav2.2-α shRNA reduced the expression of Cav2.2-α mRNA and protein in the SG in CHF rats. Cav2.2-α shRNA also reduced Cav2.2 currents and cell excitability of CSP neurons and attenuated cardiac sympathetic nerve activities (CSNA) in CHF rats. The power spectral analysis of heart rate variability (HRV) further revealed that transfection of Cav2.2-α shRNA in the SG normalized CHF-caused cardiac sympathetic overactivation in conscious rats. Twenty-four-hour continuous telemetry electrocardiogram recording revealed that this Cav2.2-α shRNA not only decreased incidence and duration of ventricular tachycardia/ventricular fibrillation but also improved CHF-induced heterogeneity of ventricular electrical activity in conscious CHF rats. Cav2.2-α shRNA also decreased susceptibility to ventricular arrhythmias in anaesthetized CHF rats. However, Cav2.2-α shRNA failed to improve CHF-induced cardiac contractile dysfunction. Scrambled shRNA did not affect Cav2.2 currents and cell excitability of CSP neurons, CSNA, HRV, and ventricular arrhythmogenesis in CHF rats. Conclusions Overactivation of Cav2.2 channels in CSP neurons contributes to cardiac sympathetic hyperactivation and ventricular arrhythmogenesis in CHF. This suggests that discovering purely selective and potent small-molecule Cav2.2 channel blockers could be a potential therapeutic strategy to decrease fatal ventricular arrhythmias in CHF.

scholarly journals Enhanced LTP of population spikes in the dentate gyrus of mice haploinsufficient for neurobeachin

2020 ◽  
Vol 10 (1) ◽  
Author(s):  
Julia Muellerleile ◽  
Aline Blistein ◽  
Astrid Rohlmann ◽  
Frederieke Scheiwe ◽  
Markus Missler ◽  
...  
Keyword(s):  
Dentate Gyrus ◽  
Granule Cell ◽  
Field Potential ◽  
Synaptic Function ◽  
Spatial Learning And Memory ◽  
Neurotransmitter Receptor ◽  
Cell Excitability ◽  
Neuronal Protein ◽  
Electrophysiological Recordings

Abstract Deletion of the autism candidate molecule neurobeachin (Nbea), a large PH-BEACH-domain containing neuronal protein, has been shown to affect synaptic function by interfering with neurotransmitter receptor targeting and dendritic spine formation. Previous analysis of mice lacking one allele of the Nbea gene identified impaired spatial learning and memory in addition to altered autism-related behaviours. However, no functional data from living heterozygous Nbea mice (Nbea+/−) are available to corroborate the behavioural phenotype. Here, we explored the consequences of Nbea haploinsufficiency on excitation/inhibition balance and synaptic plasticity in the intact hippocampal dentate gyrus of Nbea+/− animals in vivo by electrophysiological recordings. Based on field potential recordings, we show that Nbea+/− mice display enhanced LTP of the granule cell population spike, but no differences in basal synaptic transmission, synapse numbers, short-term plasticity, or network inhibition. These data indicate that Nbea haploinsufficiency causes remarkably specific alterations to granule cell excitability in vivo, which may contribute to the behavioural abnormalities in Nbea+/− mice and to related symptoms in patients.

Identifying the Functional Role of Martinotti Cells in Cortical Sensory Processing

2009 ◽  
Vol 102 (1) ◽  
pp. 9-11 ◽  
Author(s):  
James C. H. Cottam
Keyword(s):  
Sensory Processing ◽  
Pyramidal Cell ◽  
Functional Significance ◽  
Functional Role ◽  
Neural Computation ◽  
Inhibitory Interneurons ◽  
Local Circuit ◽  
Processing Function

Inhibitory interneurons are highly diverse, although the functional significance of their diversity is not yet well understood. This presents a barrier to understanding neural computation at the local circuit level. This review focuses on a recent study by Murayama et al. who used a novel in vivo technique in neocortex to demonstrate a specific sensory processing function of dendritic-targeting Martinotti interneurons. The function of Martinotti cells arises from their interaction with layer 5 pyramidal cell dendrites.

scholarly journals Hearing Loss Alters Serotonergic Modulation of Intrinsic Excitability in Auditory Cortex

2010 ◽  
Vol 104 (5) ◽  
pp. 2693-2703 ◽  
Author(s):  
Deepti Rao ◽  
Gregory J. Basura ◽  
Joseph Roche ◽  
Scott Daniels ◽  
Jaime G. Mancilla ◽  
...  
Keyword(s):  
Hearing Loss ◽  
Auditory Cortex ◽  
Sensorineural Hearing Loss ◽  
Pyramidal Cell ◽  
Receptor Activation ◽  
Sensorineural Hearing ◽  
Receptor Expression ◽  
Intrinsic Excitability ◽  
Receptor Subtypes ◽  
Cell Excitability

Sensorineural hearing loss during early childhood alters auditory cortical evoked potentials in humans and profoundly changes auditory processing in hearing-impaired animals. Multiple mechanisms underlie the early postnatal establishment of cortical circuits, but one important set of developmental mechanisms relies on the neuromodulator serotonin (5-hydroxytryptamine [5-HT]). On the other hand, early sensory activity may also regulate the establishment of adultlike 5-HT receptor expression and function. We examined the role of 5-HT in auditory cortex by first investigating how 5-HT neurotransmission and 5-HT2 receptors influence the intrinsic excitability of layer II/III pyramidal neurons in brain slices of primary auditory cortex (A1). A brief application of 5-HT (50 μM) transiently and reversibly decreased firing rates, input resistance, and spike rate adaptation in normal postnatal day 12 (P12) to P21 rats. Compared with sham-operated animals, cochlear ablation increased excitability at P12–P21, but all the effects of 5-HT, except for the decrease in adaptation, were eliminated in both sham-operated and cochlear-ablated rats. At P30–P35, cochlear ablation did not increase intrinsic excitability compared with shams, but it did prevent a pronounced decrease in excitability that appeared 10 min after 5-HT application. We also tested whether the effects on excitability were mediated by 5-HT2 receptors. In the presence of the 5-HT2-receptor antagonist, ketanserin, 5-HT significantly decreased excitability compared with 5-HT or ketanserin alone in both sham-operated and cochlear-ablated P12–P21 rats. However, at P30–P35, ketanserin had no effect in sham-operated and only a modest effect cochlear-ablated animals. The 5-HT2-specific agonist 5-methoxy- N, N-dimethyltryptamine also had no effect at P12–P21. These results suggest that 5-HT likely regulates pyramidal cell excitability via multiple receptor subtypes with opposing effects. These data also show that early sensorineural hearing loss affects the ability of 5-HT receptor activation to modulate A1 pyramidal cell excitability.

scholarly journals The role of axonal Kv1 channels in CA3 pyramidal cell excitability

2017 ◽  
Vol 7 (1) ◽  
Author(s):  
Sylvain Rama ◽  
Mickael Zbili ◽  
Aurélie Fékété ◽  
Mónica Tapia ◽  
Maria José Benitez ◽  
...  
Keyword(s):  
Pyramidal Cell ◽  
Cell Excitability
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