scholarly journals Analytical solution of linearized equations of the Morris-Lecar neuron model at large constant stimulation

2019 ◽  
Author(s):  
A.V. Paraskevov ◽  
T.S. Zemskova
Keyword(s):  
Neuron Model ◽  
Neuronal Excitability ◽  
Finite Interval ◽  
Spike Generation ◽  
Linearized Equations ◽  
Spike Amplitude ◽  
Model Equations ◽  
Applicability Boundary ◽  
Upper Boundary ◽  
Stimulation Of

AbstractThe classical biophysical Morris-Lecar model of neuronal excitability predicts that upon stimulation of the neuron with a sufficiently large constant depolarizing current there exists a finite interval of the current values where periodic spike generation occurs. Above the upper boundary of this interval there is a four-stage damping of the spike amplitude: 1) minor primary damping, which reflects a typical transient to stationary state, 2) plateau of nearly undamped periodic oscillations, 3) strong damping, and 4) reaching a constant stationary asymptotic value Vst of the neuron potential. We have linearized the Morris-Lecar model equations at the vicinity of Vst and have shown that the linearized equations can be reduced to a standard equation for exponentially damped harmonic oscillations. Importantly, all coefficients of this equation can be explicitly expressed through parameters of the original Morris-Lecar model, enabling direct comparison (i.e. without any fitting) of the numerical and analytical solutions for the neuron potential dynamics at later stages of the spike amplitude damping. This allows to explore quantitatively the applicability boundary of linear stability analysis that implies exponential damping.

scholarly journals Stimulation of neuronal KATP channels by cGMP-dependent protein kinase: involvement of ROS and 5-hydroxydecanoate-sensitive factors in signal transduction

2010 ◽  
Vol 298 (4) ◽  
pp. C875-C892 ◽  
Author(s):  
Yongping Chai ◽  
Yu-Fung Lin
Keyword(s):  
Protein Kinase ◽  
Signaling Pathway ◽  
Neuronal Excitability ◽  
Single Channel ◽  
Katp Channels ◽  
Membrane Excitability ◽  
Dependent Protein Kinase ◽  
Cgmp Dependent Protein Kinase ◽  
Dependent Protein ◽  
Stimulation Of

The ATP-sensitive potassium (KATP) channel couples intracellular metabolic state to membrane excitability. Recently, we demonstrated that neuronal KATP channels are functionally enhanced by activation of a nitric oxide (NO)/cGMP/cGMP-dependent protein kinase (PKG) signaling cascade. In this study, we further investigated the intracellular mechanism underlying PKG stimulation of neuronal KATP channels. By performing single-channel recordings in transfected HEK293 and neuroblastoma SH-SY5Y cells, we found that the increase of Kir6.2/SUR1 (i.e., the neuronal-type KATP) channel currents by PKG activation in cell-attached patches was diminished by 5-hydroxydecanoate (5-HD), an inhibitor of the putative mitochondrial KATP channel; N-(2-mercaptopropionyl)glycine, a reactive oxygen species (ROS) scavenger, and catalase, a hydrogen peroxide (H2O2)-decomposing enzyme. These reagents also ablated NO-induced KATP channel stimulation and prevented the shifts in the single-channel open- and closed-time distributions resulting from PKG activation and NO induction. Bath application of H2O2 reproduced PKG stimulation of Kir6.2/SUR1 but did not activate tetrameric Kir6.2LRKR368/369/370/371AAAA channels. Moreover, neither the PKG activator nor exogenous H2O2 was able to enhance the function of KATP channels in the presence of Ca2+ chelators and calmodulin antagonists, whereas the stimulatory effect of H2O2 was unaffected by 5-HD. Altogether, in this report we provide novel evidence that activation of PKG stimulates neuronal KATP channels by modulating intrinsic channel gating via a 5-HD-sensitive factor(s)/ROS/Ca2+/calmodulin signaling pathway that requires the presence of the SUR1 subunit. This signaling pathway may contribute to neuroprotection against ischemic injury and regulation of neuronal excitability and neurotransmitter release by modulating the function of neuronal KATP channels.

Brain-derived neurotrophic factor stimulation of T-type Ca2+ channels in sensory neurons contributes to increased peripheral pain sensitivity

2019 ◽  
Vol 12 (600) ◽  
pp. eaaw2300 ◽  
Author(s):  
Hua Wang ◽  
Yuan Wei ◽  
Yichen Pu ◽  
Dongsheng Jiang ◽  
Xinghong Jiang ◽  
...  
Keyword(s):  
Protein Kinase ◽  
Sensory Neurons ◽  
Neurotrophic Factor ◽  
Pain Sensitivity ◽  
Neuronal Excitability ◽  
Brain Derived Neurotrophic Factor ◽  
Mitogen Activated Protein Kinase ◽  
Mechanical Stimuli ◽  
Action Potential Firing ◽  
Stimulation Of

Although brain-derived neurotrophic factor (BDNF) is implicated in the nociceptive signaling of peripheral sensory neurons, the underlying mechanisms remain largely unknown. Here, we elucidated the effects of BDNF on the neuronal excitability of trigeminal ganglion (TG) neurons and the pain sensitivity of rats mediated by T-type Ca2+ channels. BDNF reversibly and dose-dependently enhanced T-type channel currents through the activation of tropomyosin receptor kinase B (TrkB). Antagonism of phosphatidylinositol 3-kinase (PI3K) but not of its downstream target, the kinase AKT, abolished the BDNF-induced T-type channel response. BDNF application activated p38 mitogen-activated protein kinase (MAPK), and this effect was prevented by inhibition of PI3K but not of protein kinase A (PKA). Antagonism of either PI3K or p38 MAPK prevented the BDNF-induced stimulation of PKA activity, whereas PKA inhibition blocked the BDNF-mediated increase in T-type currents. BDNF increased the rate of action potential firing in TG neurons and enhanced the pain sensitivity of rats to mechanical stimuli. Moreover, inhibition of TrkB signaling abolished the increased mechanical sensitivity in a rat model of chronic inflammatory pain, and this effect was attenuated by either T-type channel blockade or knockdown of the channel Cav3.2. Together, our findings indicate that BDNF enhances T-type currents through the stimulation of TrkB coupled to PI3K-p38-PKA signaling, thereby inducing neuronal hyperexcitability of TG neurons and pain hypersensitivity in rats.

scholarly journals Chaotic States Induced By Resetting Process In Izhikevich Neuron Model

2015 ◽  
Vol 5 (2) ◽  
pp. 109-119 ◽  
Author(s):  
Sou Nobukawa ◽  
Haruhiko Nishimura ◽  
Teruya Yamanishi ◽  
Jian-Qin Liu
Keyword(s):  
Neuron Model ◽  
Large Range ◽  
Neuron Models ◽  
Spike Generation ◽  
Izhikevich Neuron Model ◽  
State Dependent ◽  
Spiking Neuron Models ◽  
Generation Mechanisms ◽  
Spike Patterns ◽  
Transition Scheme

Abstract Several hybrid neuron models, which combine continuous spike-generation mechanisms and discontinuous resetting process after spiking, have been proposed as a simple transition scheme for membrane potential between spike and hyperpolarization. As one of the hybrid spiking neuron models, Izhikevich neuron model can reproduce major spike patterns observed in the cerebral cortex only by tuning a few parameters and also exhibit chaotic states in specific conditions. However, there are a few studies concerning the chaotic states over a large range of parameters due to the difficulty of dealing with the state dependent jump on the resetting process in this model. In this study, we examine the dependence of the system behavior on the resetting parameters by using Lyapunov exponent with saltation matrix and Poincaré section methods, and classify the routes to chaos.

scholarly journals Identification of Linear and Nonlinear Sensory Processing Circuits from Spiking Neuron Data

2018 ◽  
Vol 30 (3) ◽  
pp. 670-707 ◽  
Author(s):  
Dorian Florescu ◽  
Daniel Coca
Keyword(s):  
Sensory Processing ◽  
Neuron Model ◽  
Linear Filter ◽  
Spiking Neuron ◽  
Neuron Models ◽  
Integrate And Fire ◽  
Spiking Neuron Model ◽  
In Series ◽  
Linear And Nonlinear ◽  
Model Equations

Inferring mathematical models of sensory processing systems directly from input-output observations, while making the fewest assumptions about the model equations and the types of measurements available, is still a major issue in computational neuroscience. This letter introduces two new approaches for identifying sensory circuit models consisting of linear and nonlinear filters in series with spiking neuron models, based only on the sampled analog input to the filter and the recorded spike train output of the spiking neuron. For an ideal integrate-and-fire neuron model, the first algorithm can identify the spiking neuron parameters as well as the structure and parameters of an arbitrary nonlinear filter connected to it. The second algorithm can identify the parameters of the more general leaky integrate-and-fire spiking neuron model, as well as the parameters of an arbitrary linear filter connected to it. Numerical studies involving simulated and real experimental recordings are used to demonstrate the applicability and evaluate the performance of the proposed algorithms.

scholarly journals Cytosolic inositol 1,4,5-trisphosphate dynamics during intracellular calcium oscillations in living cells

2006 ◽  
Vol 173 (5) ◽  
pp. 755-765 ◽  
Author(s):  
Toru Matsu-ura ◽  
Takayuki Michikawa ◽  
Takafumi Inoue ◽  
Atsushi Miyawaki ◽  
Manabu Yoshida ◽  
...  
Keyword(s):  
Metabotropic Glutamate Receptor ◽  
Living Cells ◽  
Calcium Oscillations ◽  
Spike Generation ◽  
Metabotropic Glutamate ◽  
Endogenous Histamine ◽  
Rate Of Increase ◽  
Constant Rate ◽  
Inositol 1,4,5 Trisphosphate ◽  
Stimulation Of

We developed genetically encoded fluorescent inositol 1,4,5-trisphosphate (IP3) sensors that do not severely interfere with intracellular Ca2+ dynamics and used them to monitor the spatiotemporal dynamics of both cytosolic IP3 and Ca2+ in single HeLa cells after stimulation of exogenously expressed metabotropic glutamate receptor 5a or endogenous histamine receptors. IP3 started to increase at a relatively constant rate before the pacemaker Ca2+ rise, and the subsequent abrupt Ca2+ rise was not accompanied by any acceleration in the rate of increase in IP3. Cytosolic [IP3] did not return to its basal level during the intervals between Ca2+ spikes, and IP3 gradually accumulated in the cytosol with a little or no fluctuations during cytosolic Ca2+ oscillations. These results indicate that the Ca2+-induced regenerative IP3 production is not a driving force of the upstroke of Ca2+ spikes and that the apparent IP3 sensitivity for Ca2+ spike generation progressively decreases during Ca2+ oscillations.

scholarly journals A dialogue between glia and neurons in the retina: modulation of neuronal excitability

2004 ◽  
Vol 1 (3) ◽  
pp. 245-252 ◽  
Author(s):  
ERIC A. NEWMAN
Keyword(s):  
Synaptic Transmission ◽  
Glial Cells ◽  
Neuronal Excitability ◽  
Ganglion Cells ◽  
Brain Slices ◽  
Müller Cells ◽  
Muller Cells ◽  
Signaling Mechanisms ◽  
Bidirectional Signaling ◽  
Stimulation Of

Bidirectional signaling between neurons and glial cells has been demonstrated in brain slices and is believed to mediate glial modulation of synaptic transmission in the CNS. Our laboratory has characterized similar neuron–glia signaling in the mammalian retina. We find that light-evoked neuronal activity elicits Ca2+ increases in Müller cells, which are specialized retinal glial cells. Neuron to glia signaling is likely mediated by the release of ATP from neurons and is potentiated by adenosine. Glia to neuron signaling has also been observed and is mediated by several mechanisms. Stimulation of glial cells can result in either facilitation or depression of synaptic transmission. Release of D-serine from Müller cells might also potentiate NMDA receptor transmission. Müller cells directly inhibit ganglion cells by releasing ATP, which, following hydrolysis to adenosine, activates neuronal A1 receptors. The existence of bidirectional signaling mechanisms indicates that glial cells participate in information processing in the retina.

scholarly journals Ps in the (Channel) Pod Are Not Alike …

2007 ◽  
Vol 7 (5) ◽  
pp. 136-137
Author(s):  
Yoav Noam ◽  
Tallie Z. Baram
Keyword(s):  
Neuronal Activity ◽  
Hippocampal Neurons ◽  
Neuronal Excitability ◽  
Phosphorylation Sites ◽  
Voltage Dependent ◽  
Activity Dependent ◽  
Stimulation Of ◽  
Cultured Hippocampal Neurons

Bidirectional Activity-Dependent Regulation of Neuronal Ion Channel Phosphorylation. Misonou H, Menegola M, Mohapatra DP, Guy LK, Park KS, Trimmer JS. J Neurosci 2006;26(52):13505–13514. Activity-dependent dephosphorylation of neuronal Kv2.1 channels yields hyperpolarizing shifts in their voltage-dependent activation and homoeostatic suppression of neuronal excitability. We recently identified 16 phosphorylation sites that modulate Kv2.1 function. Here, we show that in mammalian neurons, compared with other regulated sites, such as serine (S)563, phosphorylation at S603 is supersensitive to calcineurin-mediated dephosphorylation in response to kainate-induced seizures in vivo, and brief glutamate stimulation of cultured hippocampal neurons. In vitro calcineurin digestion shows that supersensitivity of S603 dephosphorylation is an inherent property of Kv2.1. Conversely, suppression of neuronal activity by anesthetic in vivo causes hyperphosphorylation at S603 but not S563. Distinct regulation of individual phosphorylation sites allows for graded and bidirectional homeostatic regulation of Kv2.1 function. S603 phosphorylation represents a sensitive bidirectional biosensor of neuronal activity.

Solution Methods for a New Class of Simple Model Neurons

2007 ◽  
Vol 19 (12) ◽  
pp. 3216-3225 ◽  
Author(s):  
Mark D. Humphries ◽  
Kevin Gurney
Keyword(s):  
Simple Model ◽  
Neuron Model ◽  
Solution Method ◽  
Cortical Cell ◽  
Spike Generation ◽  
Firing Patterns ◽  
New Class ◽  
Efficient Simulation ◽  
Different Types ◽  
Solution Methods

Izhikevich (2003) proposed a new canonical neuron model of spike generation. The model was surprisingly simple yet able to accurately replicate the firing patterns of different types of cortical cell. Here, we derive a solution method that allows efficient simulation of the model.

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