Chapter 21 Possible functions of transmitter-controlled plateau potentials in α motoneurones

1989 ◽  
pp. 257-267 ◽  
Author(s):  
T. Eken ◽  
H. Hultborn ◽  
O. Kiehn
Keyword(s):  
Plateau Potentials

Slow active potentials and bursting motor patterns in pyloric network of the lobster, Panulirus interruptus

1982 ◽  
Vol 48 (4) ◽  
pp. 914-937 ◽  
Author(s):  
D. F. Russell ◽  
D. K. Hartline
Keyword(s):  
Motor Pattern ◽  
Membrane Properties ◽  
Plateau Potentials ◽  
Motor Patterns ◽  
Potential Oscillations ◽  
Panulirus Interruptus ◽  
Pyloric Network ◽  
Current Pulses ◽  
Voltage Dependent ◽  
High Level

1. Neurons in the central pattern generator for the "pyloric" motor rhythm of the lobster stomatogastric ganglion were investigated for the possible involvement of regenerative membrane properties in their membrane-potential oscillations and bursting output patterns. 2. Evidence was found that each class of pyloric-system neurons can possess a capability for generating prolonged regenerative depolarizations by a voltage-dependent membrane mechanism. Such responses have been termed plateau potentials. 3. Several tests were applied to determine whether a given cell possessed a plateau capability. First among these was the ability to trigger all-or-none bursts of nerve impulses by brief depolarizing current pulses and to terminate bursts in an all-or-none fashion with brief hyperpolarizing current pulses. Tests were made under conditions of a high level of activity in the pyloric generator, often in conjunction with the use of hyperpolarizing offsets to the cell under test to suppress ongoing bursting. 4. For each class, the network of synaptic interconnections among the pyloric-system neurons was shown to not be the cause of the regenerative responses observed. 5. Plateau potentials are viewed as a driving force for axon spiking during bursts and as interacting with the synaptic network in the formation of the pyloric motor pattern.

scholarly journals Contribution of extrasynaptic N -methyl- d -aspartate and adenosine A1 receptors in the generation of dendritic glutamate-mediated plateau potentials

2015 ◽  
Vol 370 (1672) ◽  
pp. 20140193 ◽  
Author(s):  
Katerina D. Oikonomou ◽  
Mandakini B. Singh ◽  
Matthew T. Rich ◽  
Shaina M. Short ◽  
Srdjan D. Antic
Keyword(s):  
Pyramidal Neurons ◽  
Calcium Influx ◽  
Glutamate Uptake ◽  
Plateau Potentials ◽  
Adenosine A1 Receptors ◽  
Basal Dendrites ◽  
Adenosine A1 ◽  
Dendritic Spikes ◽  
Neuronal Output

Thin basal dendrites can strongly influence neuronal output via generation of dendritic spikes. It was recently postulated that glial processes actively support dendritic spikes by either ceasing glutamate uptake or by actively releasing glutamate and adenosine triphosphate (ATP). We used calcium imaging to study the role of NR2C/D-containing N -methyl- d -aspartate (NMDA) receptors and adenosine A1 receptors in the generation of dendritic NMDA spikes and plateau potentials in basal dendrites of layer 5 pyramidal neurons in the mouse prefrontal cortex. We found that NR2C/D glutamate receptor subunits contribute to the amplitude of synaptically evoked NMDA spikes. Dendritic calcium signals associated with glutamate-evoked dendritic plateau potentials were significantly shortened upon application of the NR2C/D receptor antagonist PPDA, suggesting that NR2C/D receptors prolong the duration of calcium influx during dendritic spiking. In contrast to NR2C/D receptors, adenosine A1 receptors act to abbreviate dendritic and somatic signals via the activation of dendritic K + current. This current is characterized as a slow-activating outward-rectifying voltage- and adenosine-gated current, insensitive to 4-aminopyridine but sensitive to TEA. Our data support the hypothesis that the release of glutamate and ATP from neurons or glia contribute to initiation, maintenance and termination of local dendritic glutamate-mediated regenerative potentials.

Compartmental Model of Vertebrate Motoneurons for Ca2+-Dependent Spiking and Plateau Potentials Under Pharmacological Treatment

1997 ◽  
Vol 78 (6) ◽  
pp. 3371-3385 ◽  
Author(s):  
Victoria Booth ◽  
John Rinzel ◽  
Ole Kiehn
Keyword(s):  
Ion Channel ◽  
Compartmental Model ◽  
Ionic Currents ◽  
Channel Blockers ◽  
Spinal Motoneurons ◽  
Plateau Potentials ◽  
Firing Patterns ◽  
Calcium Dependent ◽  
Ion Channel Blockers ◽  
Experimental Effect

Booth, Victoria, John Rinzel, and Ole Kiehn. Compartmental model of vertebrate motoneurons for Ca2+-dependent spiking and plateau potentials under pharmacological treatment. J. Neurophysiol. 78: 3371–3385, 1997. In contrast to the limited response properties observed under normal experimental conditions, spinal motoneurons generate complex firing patterns, such as Ca2+-dependent regenerative spiking and plateaus, in the presence of certain neurotransmitters and ion-channel blockers. We have developed a quantitative motoneuron model, based on turtle motoneuron data, toinvestigate the roles of specific ionic currents and the effects of their soma and dendritic distribution in generating these complex firing patterns. In addition, the model is used to explore the effects of multiple ion channel blockers and neurotransmitters that are known to modulate motoneuron firing patterns. To represent the distribution of ionic currents across the soma and dendrites, the model contains two compartments. The soma compartment, representing the soma and proximal dendrites, contains Hodgkin-Huxley-like sodium ( I Na) and delayed rectifier K+ ( I K−dr) currents, an N-like Ca2+ current ( I Ca−N), and a calcium-dependent K+ current [ I K(Ca)]. The dendritic compartment, representing the lumped distal dendrites, contains, in addition to I Ca−N and I K(Ca) as in the soma, a persistent L-like calcium current ( I Ca−L). We determined kinetic parameters for I Na, I K−dr, I Ca−N, and I K(Ca) in order to reproduce normal action-potential firing observed in turtle spinal motoneurons, including fast and slow afterhyperpolarizations (AHPs) and a linear steady-state frequency-current relation. With this parameter set as default, a sequence of pharmacological manipulations were systematically simulated. A small reduction of I K−dr [mimicking the experimental effect of tetraethylammonium (TEA) in low concentration] enhanced the slow AHP and caused calcium spiking (mediated by I Ca−N) when I Na was blocked. Firing patterns observed experimentally in high TEA [and tetrodotoxin (TTX)], namely calcium spikes riding on a calcium plateau, were reproduced only when both I K−dr and I K(Ca) were reduced. Dendritic plateau potentials, mediated by I Ca−L, were reliably unmasked when I K(Ca) was reduced, mimicking the experimental effect of the bee venom apamin. The effect of 5-HT, which experimentally induces the ability to generate calcium-dependent plateau potentials but not calcium spiking, was reproduced in the model by reducing I K(Ca) alone. The plateau threshold current level, however, was reduced substantially if a simultaneous increase in I Ca−L was simulated, suggesting that serotonin (5-HT) induces plateau potentials by regulating more than one conductance. The onset of the plateau potential showed significant delays in response to near-threshold, depolarizing current steps. In addition, the delay times were sensitive to the current step amplitude. The delay and its sensitivity were explained by examining the model's behavior near the threshold for plateau onset. This modeling study thus accurately accounts for the basic firing behavior of vertebrate motoneurons as well as a range of complex firing patterns invoked by ion-channel blockers and 5-HT. In addition, our computational results support the hypothesis that the electroresponsiveness of motoneurons depends on a nonuniform distribution of ionic conductances, and they predict modulatory effects of 5-HT and properties of plateau activation that have yet to be tested experimentally.

Recent Evidence for Plateau Potentials in Human Motoneurones

2002 ◽  
pp. 227-235 ◽  
Author(s):  
David F. Collins ◽  
Monica Gorassini ◽  
David Bennett ◽  
David Burke ◽  
Simon C. Gandevia
Keyword(s):  
Plateau Potentials

scholarly journals Event-based pattern detection in active dendrites

2019 ◽  
Author(s):  
Johannes Leugering ◽  
Pascal Nieters ◽  
Gordon Pipa
Keyword(s):  
Single Neuron ◽  
Logic Gate ◽  
Dendritic Tree ◽  
Dendritic Morphology ◽  
Neuron Models ◽  
Plateau Potentials ◽  
Computational Function ◽  
Movement Trajectories ◽  
Timing Variability ◽  
Long Timescales

AbstractMany behavioural tasks require an animal to integrate information on a slow timescale that can exceed hundreds of milliseconds. How this is realized by neurons with membrane time constants on the order of tens of milliseconds or less remains an open question. We show, how the interaction of two kinds of events within the dendritic tree, excitatory postsynaptic potentials and locally generated dendritic plateau potentials, can allow a single neuron to detect specific sequences of spiking input on such slow timescales. Our conceptual model reveals, how the morphology of a neuron’s dendritic tree determines its computational function, which can range from a simple logic gate to the gradual integration of evidence to the detection of complex spatio-temporal spike-sequences on long timescales. As an example, we illustrate in a simulated navigation task how this mechanism can even allow individual neurons to reliably detect specific movement trajectories with high tolerance for timing variability. We relate our results to conclusive findings in neurobiology and discuss implications for both experimental and theoretical neuroscience.Author SummaryThe recognition of patterns that span multiple timescales is a critical function of the brain. This is a conceptual challenge for all neuron models that rely on the passive integration of synaptic inputs and are therefore limited to the rigid millisecond timescale of post-synaptic currents. However, detailed biological measurements recently revealed that single neurons actively generate localized plateau potentials within the dendritic tree that can last hundreds of milliseconds. Here, we investigate single-neuron computation in a model that adheres to these findings but is intentionally simple. Our analysis reveals how plateaus act as memory traces, and their interaction as defined by the dendritic morphology of a neuron gives rise to complex non-linear computation. We demonstrate how this mechanism enables individual neurons to solve difficult, behaviorally relevant tasks that are commonly studied on the network-level, such as the detection of variable input sequences or the integration of evidence on long timescales. We also characterize computation in our model using rate-based analysis tools, demonstrate why our proposed mechanism of dendritic computation cannot be detected under this analysis and suggest an alternative based on plateau timings. The interaction of plateau events in dendritic trees is, according to our argument, an elementary principle of neural computation which implies the need for a fundamental change of perspective on the computational function of neurons.

A Time-Dependent Excitability change in the soma of an identified Insect Motoneurone

1992 ◽  
Vol 162 (1) ◽  
pp. 251-263
Author(s):  
JULES C. HANCOX ◽  
ROBERT M. PITMAN
Keyword(s):  
Cell Body ◽  
Action Potentials ◽  
Periplaneta Americana ◽  
Channel Blocker ◽  
Time Dependent ◽  
Sodium Channel Blocker ◽  
Plateau Potentials ◽  
Excitability Change ◽  
Membrane Oscillations

Long-term, current-clamp recordings were made from the cell body of the fast coxal depressor motoneurone (Df) of the third thoracic ganglion of the cockroach Periplaneta americana. In freshly dissected preparations the response to shortduration, suprathreshold, depolarising current pulses was a graded series of damped membrane oscillations similar to those reported previously in this neurone. The response to current injection changed, however, with increasing time after setting up the preparation: cells developed the ability to exhibit all-ornone action potentials. Their amplitude, however, was usually insufficient to overshoot 0 m V. Our observations suggest that the enhancement in excitability is dependent on time following dissection rather than on time following impalement. Recordings taken from neurone somata mechanically divided from their processes indicated that the time-dependent changes in excitability were not attributable to changes in synaptic input to the neurone and, moreover, that the cell body was involved in action potential genesis. The action potentials were resistant to treatment with the sodium channel blocker tetrodotoxin (up to 10−5 mol l−1), but were reversibly abolished when preparations were bathed in saline containing cadmium ions (1 mmol l−1) or manganese ions (20 or 40 mmol l−1) and, therefore, the inward current underlying these events was largely, if not entirely, carried by calcium ions. These time-dependent action potentials can co-exist with plateau potentials. In neurones giving both plateau potentials and time-dependent action potentials, plateau potentials can drive action potentials in bursts.

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