scholarly journals Altered Chloride Homeostasis Decreases the Action Potential Threshold and Increases Hyperexcitability in Hippocampal Neurons

eNeuro ◽  
2017 ◽  
Vol 4 (6) ◽  
pp. ENEURO.0172-17.2017 ◽  
Author(s):  
Andreas T. Sørensen ◽  
Marco Ledri ◽  
Miriam Melis ◽  
Litsa Nikitidou Ledri ◽  
My Andersson ◽  
...  
Keyword(s):  
Action Potential ◽  
Hippocampal Neurons ◽  
Chloride Homeostasis ◽  
Action Potential Threshold ◽  
Potential Threshold

scholarly journals Calcium stores regulate excitability in cultured rat hippocampal neurons

2018 ◽  
Vol 120 (5) ◽  
pp. 2694-2705 ◽  
Author(s):  
Menahem Segal
Keyword(s):  
Action Potential ◽  
Hippocampal Neurons ◽  
Extracellular Calcium ◽  
Calcium Stores ◽  
Sk Channels ◽  
Central Neurons ◽  
Action Potential Threshold ◽  
Potential Threshold ◽  
Small Conductance ◽  
Cultured Hippocampal Neurons

Extracellular calcium ions support synaptic activity but also reduce excitability of central neurons. In the present study, the effect of calcium on excitability was explored in cultured hippocampal neurons. CaCl2 injected by pressure in the vicinity of a neuron that is bathed only in MgCl2 as the main divalent cation caused a depolarizing shift in action potential threshold and a reduction in excitability. This effect was not seen if the intracellular milieu consisted of Cs+ instead of K-gluconate as the main cation or when it contained ruthenium red, which blocks release of calcium from stores. The suppression of excitability by calcium was mimicked by caffeine, and calcium store antagonists cyclopiazonic acid or thapsigargin blocked this action. Neurons taken from synaptopodin-knockout mice show significantly reduced efficacy of calcium modulation of action potential threshold. Likewise, in Orai1 knockdown cells, calcium is less effective in modulating excitability of neurons. Activation of small-conductance K (SK) channels increased action potential threshold akin to that produced by calcium ions, whereas blockade of SK channels but not big K channels reduced the threshold for action potential discharge. These results indicate that calcium released from stores may suppress excitability of central neurons. NEW & NOTEWORTHY Extracellular calcium reduces excitability of cultured hippocampal neurons. This effect is mediated by calcium-gated potassium currents, possibly small-conductance K channels. Release of calcium from internal stores mimics the effect of extracellular calcium. It is proposed that calcium stores modulate excitability of central neurons.

scholarly journals Calcium-induced calcium release activates spontaneous miniature outward currents in newt medullary reticular formation neurons

2018 ◽  
Vol 120 (6) ◽  
pp. 3140-3154 ◽  
Author(s):  
Daniel B. Yaeger ◽  
Emma J. Coddington
Keyword(s):  
Action Potential ◽  
Reticular Formation ◽  
Calcium Release ◽  
Motor Behavior ◽  
Brain Slices ◽  
Medullary Reticular Formation ◽  
Outward Currents ◽  
Decay Times ◽  
Action Potential Threshold ◽  
Potential Threshold

Neurons in the medullary reticular formation are involved in the control of postural and locomotor behaviors in all vertebrates. Reticulospinal neurons in this brain region provide one of the major descending projections to the spinal cord. Although neurons in the newt medullary reticular formation have been extensively studied using in vivo extracellular recordings, little is known of their intrinsic biophysical properties or of the underlying circuitry of this region. Using whole cell patch-clamp recordings in brain slices containing the rostromedial reticular formation from adult male newts, we observed spontaneous miniature outward currents (SMOCs) in ~2/3 of neurons. Although SMOCs superficially resembled inhibitory postsynaptic currents (IPSCs), they had slower risetimes and decay times than spontaneous IPSCs. SMOCs required intracellular Ca2+ release from ryanodine receptors and were also dependent on the influx of extracellular Ca2+. SMOCs were unaffected by apamin but were partially blocked by iberiotoxin and charybdotoxin, indicating that SMOCs were mediated by big-conductance Ca2+-activated K+ channels. Application of the sarco/endoplasmic Ca2+ ATPase inhibitor cyclopiazonic acid blocked the generation of SMOCs and also increased neural excitability. Neurons with SMOCs had significantly broader action potentials, slower membrane time constants, and higher input resistance than neurons without SMOCs. Thus, SMOCs may serve as a mechanism to regulate action potential threshold in a majority of neurons within the newt medullary reticular formation. NEW & NOTEWORTHY The medullary reticular formation exerts a powerful influence on sensorimotor integration and subsequent motor behavior, yet little is known about the neurons involved. In this study, we identify a transient potassium current that regulates action potential threshold in a majority of medullary reticular neurons.

Nitric oxide in glutamate-induced compound action potential threshold shifts

2008 ◽  
Vol 239 (1-2) ◽  
pp. 54-59 ◽  
Author(s):  
Mihir R. Patel ◽  
Jocelyn C. Stamat ◽  
Carlton J. Zdanski ◽  
Charles S. Ebert ◽  
Jiri Prazma
Keyword(s):  
Nitric Oxide ◽  
Action Potential ◽  
Compound Action Potential ◽  
Action Potential Threshold ◽  
Potential Threshold ◽  
Compound Action

Electrical Communication Within a Neuron

2017 ◽  
Author(s):  
Peggy Mason
Keyword(s):  
Action Potential ◽  
Action Potentials ◽  
Single Neuron ◽  
Spatial Summation ◽  
Periodic Paralysis ◽  
Demyelinating Diseases ◽  
Dynamic Polarization ◽  
Length Constant ◽  
Action Potential Threshold ◽  
Potential Threshold

Postsynaptic potentials integrate across time and space within a single neuron. The influence of the length constant on spatial summation and of the time constant on temporal summation is described. Whereas passive properties give rise to graded potentials, the voltage-gated sodium channel (VGSC) supports the all-or-none action potential. The action potential can be used to conduct information across long distances and is therefore used in the majority of neurons that have axons. How the inactivated state of VGSCs gives rise to the refractory period and dynamic polarization is described. The meaning of the action potential threshold is fully considered and then applied to understand the clinical condition of hyperkalemic periodic paralysis. Trains of action potentials carry information, and degradation of the spike train compromises the message. The speed of action potential conduction along both unmyelinated and myelinated axons is explored. In closing, an overview of demyelinating diseases is offered.

scholarly journals D-type potassium channels normalize action potential firing between dorsal and ventral CA1 neurons of the mouse hippocampus

2019 ◽  
Vol 121 (3) ◽  
pp. 983-995 ◽  
Author(s):  
Gregory J. Ordemann ◽  
Christopher J. Apgar ◽  
Darrin H. Brager
Keyword(s):  
Potassium Channels ◽  
Action Potential ◽  
Functional Expression ◽  
Action Potential Firing ◽  
Ca1 Neurons ◽  
Potential Output ◽  
Mouse Hippocampus ◽  
Potential Firing ◽  
Action Potential Threshold ◽  
Potential Threshold

Specific memory processes and neurological disorders can be ascribed to different dorsoventral regions of the hippocampus. Recently, differences in the anatomical and physiological properties between dorsal and ventral hippocampal CA1 neurons were described for both the rat and mouse hippocampus and have greatly contributed to our understanding of these processes. While differences in the subthreshold properties were similar between rat and mouse neurons, differences in action potential output between dorsal and ventral neurons were strikingly less divergent in mouse compared with rat CA1 neurons. Here, we investigate the mechanism underlying the lack of difference in action potential firing between dorsal and ventral CA1 pyramidal neurons in mouse hippocampus. Consistent with rat, we found that ventral CA1 neurons had a more depolarized resting membrane potential and higher input resistance than dorsal CA1 neurons in the mouse hippocampus. Despite these differences, action potential output in response to current injection was not significantly different. We found that ventral neurons have a more depolarized action potential threshold compared with dorsal neurons and that threshold in ventral neurons was more sensitive to block of KV1 channels compared with dorsal neurons. Outside-out voltage-clamp recordings found that slowly inactivating K+ currents were larger in ventral CA1 neurons. These results suggest that, despite differences in subthreshold properties between dorsal and ventral CA1 neurons, action potential output is normalized by the differential functional expression of D-type K+ channels. NEW & NOTEWORTHY Understanding differences in neurons within a brain region is integral in the reliable interpretation of comparative studies. Our findings identify a novel mechanism by which D-type potassium channels normalize action potential firing between dorsal and ventral CA1 neurons of mouse hippocampus despite differences in subthreshold intrinsic properties. Action potential threshold in ventral neurons is influenced by a greater functional expression of D-type potassium channels resulting in a depolarized action potential threshold compared with dorsal hippocampus.

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