scholarly journals Characterization of Na+-Activated K+ Currents in Larval Lamprey Spinal Cord Neurons

2007 ◽  
Vol 97 (5) ◽  
pp. 3484-3493 ◽  
Author(s):  
Dietmar Hess ◽  
Evanthia Nanou ◽  
Abdeljabbar El Manira
Keyword(s):  
Spinal Cord ◽  
Action Potential ◽  
Feedback Mechanism ◽  
Neuronal Firing ◽  
Repetitive Firing ◽  
Spinal Cord Neurons ◽  
Negative Feedback Mechanism ◽  
Synaptic Interactions ◽  
Action Potential Waveform

Potassium channels play an important role in controlling neuronal firing and synaptic interactions. Na+-activated K+ ( KNa) channels have been shown to exist in neurons in different regions of the CNS, but their physiological function has been difficult to assess. In this study, we have examined if neurons in the spinal cord possess KNa currents. We used whole cell recordings from isolated spinal cord neurons in lamprey. These neurons display two different KNa currents. The first was transient and activated by the Na+ influx during the action potentials, and it was abolished when Na+ channels were blocked by tetrodotoxin. The second KNa current was sustained and persisted in tetrodotoxin. Both KNa currents were abolished when Na+ was substituted with choline or N-methyl-d-glucamine, indicating that they are indeed dependent on Na+ influx into neurons. When Na+ was substituted with Li+, the amplitude of the inward current was unchanged, whereas the transient KNa current was reduced but not abolished. This suggests that the transient KNa current is partially activated by Li+. These two KNa currents have different roles in controlling the action potential waveform. The transient KNa appears to act as a negative feedback mechanism sensing the Na+ influx underlying the action potential and may thus be critical for setting the amplitude and duration of the action potential. The sustained KNa current has a slow kinetic of activation and may underlie the slow Ca2+-independent afterhyperpolarization mediated by repetitive firing in lamprey spinal cord neurons.

High Safety Factor for Action Potential Conduction Along Axons But Not Dendrites of Cultured Hippocampal and Cortical Neurons

1998 ◽  
Vol 80 (4) ◽  
pp. 2089-2101 ◽  
Author(s):  
Paul J. Mackenzie ◽  
Timothy H. Murphy
Keyword(s):  
Action Potential ◽  
Safety Factor ◽  
Cortical Neurons ◽  
Neuronal Firing ◽  
Repetitive Firing ◽  
Current Clamp ◽  
Similar Reduction ◽  
Axonal Conduction ◽  
Cultured Cortical Neurons ◽  
20 Nm

Mackenzie, Paul J. and Timothy H. Murphy. High safety factor for action potential conduction along axons but not dendrites of cultured hippocampal and cortical neurons. J. Neurophysiol. 80: 2089–2101, 1998. By using a combination of Ca2+ imaging and current-clamp recording, we previously reported that action potential (AP) conduction is reliably observed from the soma to axonal terminals in cultured cortical neurons. To extend these studies, we evaluated Ca2+ influx evoked by Na+ APs as a marker of AP conduction under conditions that are expected to lower the conduction safety factor to explore mechanisms of axonal and dendritic excitability. As expected, reducing the extracellular Na+ concentration from 150 to ∼60 mM decreased the amplitude of APs recorded in the soma but surprisingly did not influence axonal conduction, as monitored by measuring Ca2+ transients. Furthermore, reliable axonal conduction was observed in dilute (20 nM) tetrodotoxin (TTX), despite a similar reduction in AP amplitude. In contrast, the Ca2+ transient measured along dendrites was markedly reduced in low Na+, although still mediated by TTX-sensitive Na+ channels. Dendritic action-potential evoked Ca2+ transients were also markedly reduced in 20 nM TTX. These data provide further evidence that strongly excitable axons are functionally compartmentalized from weakly excitable dendrites. We conclude that modulation of Na+ currents or membrane potential by neurotransmitters or repetitive firing is more likely to influence neuronal firing before AP generation than the propagation of signals to axonal terminals. In contrast, the relatively low safety factor for back-propagating APs in dendrites would suggest a stronger effect of Na+ current modulation.

scholarly journals A computational model for how the fast afterhyperpolarization paradoxically increases gain in regularly firing neurons

2018 ◽  
Vol 119 (4) ◽  
pp. 1506-1520 ◽  
Author(s):  
David B. Jaffe ◽  
Robert Brenner
Keyword(s):  
Action Potential ◽  
Computational Model ◽  
Interspike Interval ◽  
Computational Study ◽  
Stimulus Frequency ◽  
Bk Channels ◽  
Neuronal Firing ◽  
Inward Current ◽  
Action Potential Waveform ◽  
Potential Waveform

The gain of a neuron, the number and frequency of action potentials triggered in response to a given amount of depolarizing injection, is an important behavior underlying a neuron’s function. Variations in action potential waveform can influence neuronal discharges by the differential activation of voltage- and ion-gated channels long after the end of a spike. One component of the action potential waveform, the afterhyperpolarization (AHP), is generally considered an inhibitory mechanism for limiting firing rates. In dentate gyrus granule cells (DGCs) expressing fast-gated BK channels, large fast AHPs (fAHP) are paradoxically associated with increased gain. In this article, we describe a mechanism for this behavior using a computational model. Hyperpolarization provided by the fAHP enhances activation of a dendritic inward current (a T-type Ca2+ channel is suggested) that, in turn, boosts rebound depolarization at the soma. The model suggests that the fAHP may both reduce Ca2+ channel inactivation and, counterintuitively, enhance its activation. The magnitude of the rebound depolarization, in turn, determines the activation of a subsequent, slower inward current (a persistent Na+ current is suggested) limiting the interspike interval. Simulations also show that the effect of AHP on gain is also effective for physiologically relevant stimulation; varying AHP amplitude affects interspike interval across a range of “noisy” stimulus frequency and amplitudes. The mechanism proposed suggests that small fAHPs in DGCs may contribute to their limited excitability. NEW & NOTEWORTHY The afterhyperpolarization (AHP) is canonically viewed as a major factor underlying the refractory period, serving to limit neuronal firing rate. We recently reported that enhancing the amplitude of the fast AHP (fAHP) in a relatively slowly firing neuron (vs. fast spiking neurons) expressing fast-gated BK channels augments neuronal excitability. In this computational study, we present a novel, quantitative hypothesis for how varying the amplitude of the fAHP can, paradoxically, influence a subsequent spike tens of milliseconds later.

scholarly journals Identification of Sodium Channel Isoforms That Mediate Action Potential Firing in Lamina I/II Spinal Cord Neurons

2011 ◽  
Vol 7 ◽  
pp. 1744-8069-7-67 ◽  
Author(s):  
Michael E Hildebrand ◽  
Janette Mezeyova ◽  
Paula L Smith ◽  
Michael W Salter ◽  
Elizabeth Tringham ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Action Potential ◽  
Sodium Channel ◽  
Action Potential Firing ◽  
Spinal Cord Neurons ◽  
Lamina I ◽  
Potential Firing

Neurophysiological characterization of the anterolateral spinal cord neurons contributing to pain perception in man

Pain ◽  
1975 ◽  
Vol 1 (1) ◽  
pp. 51-58 ◽  
Author(s):  
David J. Mayer ◽  
Donald D. Price ◽  
Donald P. Becker
Keyword(s):  
Spinal Cord ◽  
Pain Perception ◽  
Spinal Cord Neurons

Characterization of benzodiazepine receptors in primary cultures of fetal mouse brain and spinal cord neurons

1980 ◽  
Vol 190 (2) ◽  
pp. 485-491 ◽  
Author(s):  
Ann Huang ◽  
Jeffery L. Barker ◽  
Steven M. Paul ◽  
Victoria Moncada ◽  
Phil Skolnick
Keyword(s):  
Spinal Cord ◽  
Mouse Brain ◽  
Benzodiazepine Receptors ◽  
Primary Cultures ◽  
Spinal Cord Neurons ◽  
Fetal Mouse ◽  
Brain And Spinal Cord

Effects of 5-hydroxytryptamine on the afterhyperpolarization, spike frequency regulation, and oscillatory membrane properties in lamprey spinal cord neurons

1989 ◽  
Vol 61 (4) ◽  
pp. 759-768 ◽  
Author(s):  
P. Wallen ◽  
J. T. Buchanan ◽  
S. Grillner ◽  
R. H. Hill ◽  
J. Christenson ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Action Potential ◽  
Late Phase ◽  
Calcium Entry ◽  
Spike Frequency ◽  
Frequency Regulation ◽  
Spinal Cord Neurons ◽  
Cyclic Monophosphate ◽  
Calcium Dependent ◽  
Dorsal Cells

1. Local application of 5-hydroxytryptamine (5-HT) in the area in which a dense 5-HT plexus is located in the lamprey spinal cord leads to a marked depression of the late phase of the afterhyperpolarization (AHP) following the action potential. This effect was observed in motoneurons, premotor interneurons, and giant interneurons, whereas no effect was observed in the sensory dorsal cells and edge cells. 2. The late 5-HT sensitive phase of the AHP was increased in amplitude when calcium entry was enhanced during the prolongation of action potentials caused by tetraethylammonium (TEA). Conversely, a blockade of Ca2+ entry by manganese reduced the AHP amplitude, suggesting that a calcium-dependent current, most likely carried by potassium, underlies the late phase of the AHP in these cells, as is the case in many other types of neurons. 3. The late phase of the AHP could be depressed by 5-HT although no effects were exerted on either the resting input resistance or on the shape of the action potential in 54% of the cells. The membrane conductance increase associated with the late phase of the AHP was markedly attenuated by 5-HT application. 4. In voltage-clamp experiments, Na+ currents and most K+ currents were blocked by tetrodotoxin (TTX) and TEA, respectively. Under these conditions, voltage steps elicited a slow outward current, most likely representing a Ca2+-activated K+ current, which was depressed by 5-HT application. 5. 5-HT does not appear to reduce AHP amplitude by blocking the calcium entry occurring during the action potential. No evidence was obtained for an involvement of second messengers such as adenosine-3':5'-cyclic monophosphate (cAMP), guanosine-3':5'-cyclic monophosphate (cGMP), diacyglycerol, or arachidonic acid. The effect of 5-HT on the late AHP may be due to a direct action on the calcium-dependent potassium channels or on the intracellular handling of Ca2+ ions. 6. The amplitude reduction of the AHP has a profound influence on the spike frequency regulation of any given cell; the frequency of spikes evoked by a given excitatory stimulus is therefore markedly increased by application of 5-HT. 5-HT thus increases the "gain" of the input-output relation of interneurons and motoneurons responsible for generating the locomotor rhythm. In addition, 5-HT causes a prolongation of the depolarized plateau of the N-methyl-D-aspartate (NMDA) receptor-induced membrane potential oscillations, as expected from the 5-HT-induced effects on the Ca2+-activated K+ channels that contribute to the repolarization.

scholarly journals Kv3 channels contribute to the excitability of sub-populations of spinal cord neurons in lamina VII

2021 ◽  
Author(s):  
Pierce Mullen ◽  
Nadia Pilati ◽  
Charles H Large ◽  
Jim Deuchars ◽  
Susan A Deuchars
Keyword(s):  
Spinal Cord ◽  
Firing Frequency ◽  
Neuronal Firing ◽  
Recurrent Inhibition ◽  
Inhibitory Neurons ◽  
Spinal Cord Neurons ◽  
Lumbosacral Spinal Cord ◽  
Whole Cell Patch Clamp ◽  
Neuronal Types ◽  
Fast Firing

Autonomic parasympathetic preganglionic neurons (PGN) drive contraction of the bladder during micturition but remain quiescent during bladder filling. This quiescence is postulated to be due to recurrent inhibition of PGN by fast-firing adjoining interneurons. Here, we defined four distinct neuronal types within lamina VII of the lumbosacral spinal cord, where PGN are situated, by combining whole cell patch clamp recordings with k-means clustering of a range of electrophysiological parameters. Additional morphological analysis separated these neuronal classes into parasympathetic preganglionic populations (PGN) and a fast firing interneuronal population. Kv3 channels are voltage-gated potassium channels (Kv) that allow fast and precise firing of neurons. We found that blockade of Kv3 channels by tetraethylammonium (TEA) reduced neuronal firing frequency and isolated high-voltage-activated Kv currents in the fast-firing population but had no effect in PGN populations. Furthermore, Kv3 blockade potentiated the local and descending inhibitory inputs to PGN indicating that Kv3-expressing inhibitory neurons are synaptically connected to PGN. Taken together, our data reveal that Kv3 channels are crucial for fast and regulated neuronal output of a defined population that may be involved in intrinsic spinal bladder circuits that underpin recurrent inhibition of PGN.

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