Persistent sodium conductance contributes to orexin-A-mediated modulation of membrane excitability in neonatal rat mesencephalic V neurons

2021 ◽  
pp. 135846
Author(s):  
Susumu Tanaka ◽  
Soju Seki ◽  
Yudai Ono ◽  
Akifumi Enomoto ◽  
Mikihiko Kogo
Keyword(s):  
Neonatal Rat ◽  
Membrane Excitability ◽  
Orexin A ◽  
Sodium Conductance ◽  
Persistent Sodium Conductance

Conditions Sufficient for Nonsynaptic Epileptogenesis in the CA1 Region of Hippocampal Slices

2002 ◽  
Vol 87 (1) ◽  
pp. 62-71 ◽  
Author(s):  
Marom Bikson ◽  
Scott C. Baraban ◽  
Dominique M. Durand
Keyword(s):  
Neuronal Excitability ◽  
Epileptiform Activity ◽  
Hippocampal Slices ◽  
Seizure Threshold ◽  
Ion Selective Electrodes ◽  
Receptor Antagonists ◽  
Sodium Conductance ◽  
Ca1 Region ◽  
Persistent Sodium Conductance

Nonsynaptic mechanisms exert a powerful influence on seizure threshold. It is well-established that nonsynaptic epileptiform activity can be induced in hippocampal slices by reducing extracellular Ca2+ concentration. We show here that nonsynaptic epileptiform activity can be readily induced in vitro in normal (2 mM) Ca2+ levels. Those conditions sufficient for nonsynaptic epileptogenesis in the CA1 region were determined by pharmacologically mimicking the effects of Ca2+ reduction in normal Ca2+ levels. Increasing neuronal excitability, by removing extracellular Mg2+ and increasing extracellular K+ (6–15 mM), induced epileptiform activity that was suppressed by postsynaptic receptor antagonists [d-(−)-2-amino-5-phosphonopentanoic acid, picrotoxin, and 6,7-dinitroquinoxaline-2,3-dione] and was therefore synaptic in nature. Similarly, epileptiform activity induced when neuronal excitability was increased in the presence of KCaantagonists (verruculogen, charybdotoxin, norepinephrine, tetraethylammonium salt, and Ba2+) was found to be synaptic in nature. Decreases in osmolarity also failed to induce nonsynaptic epileptiform activity in the CA1 region. However, increasing neuronal excitability (by removing extracellular Mg2+ and increasing extracellular K+) in the presence of Cd2+, a nonselective Ca2+channel antagonist, or veratridine, a persistent sodium conductance enhancer, induced spontaneous nonsynaptic epileptiform activity in vitro. Both novel models were characterized using intracellular and ion-selective electrodes. The results of this study suggest that reducing extracellular Ca2+ facilitates bursting by increasing neuronal excitability and inhibiting Ca2+ influx, which might, in turn, enhance a persistent sodium conductance. Furthermore, these data show that nonsynaptic mechanisms can contribute to epileptiform activity in normal Ca2+ levels.

Properties of persistent sodium conductance and calcium conductance of layer V neurons from cat sensorimotor cortex in vitro

1985 ◽  
Vol 53 (1) ◽  
pp. 153-170 ◽  
Author(s):  
C. E. Stafstrom ◽  
P. C. Schwindt ◽  
M. C. Chubb ◽  
W. E. Crill
Keyword(s):  
Voltage Clamp ◽  
Sensorimotor Cortex ◽  
Potassium Currents ◽  
Spike Threshold ◽  
Sodium Conductance ◽  
Blocking Agents ◽  
Calcium Conductance ◽  
Layer V ◽  
Persistent Sodium Conductance

Properties of the persistent sodium conductance and the calcium conductance of layer V neurons from cat sensorimotor cortex were examined in an in vitro slice preparation by use of a single microelectrode, somatic voltage clamp, current clamp, intra- and extracellular application of blocking agents, and extracellular ion substitution. The persistent sodium current (INaP) attained its steady level within 2-4 ms of a step change in voltage at every potential where it could be examined directly [to about 40 mV positive to resting potential (RP)]. Because of its fast onset INaP can be activated during a single excitatory postsynaptic potential (EPSP) and can influence the subsequent voltage time course and cell excitability. Application of a depolarizing holding potential greater than or equal to 20 mV positive to RP could inactivate spikes, thus allowing examination of INaP at voltages positive to spike threshold. At every potential where INaP was visible, it was mixed with a slow outward current. After depressing potassium currents with blocking agents, INaP could be observed during depolarizations to about 40 mV positive to RP where it is normally hidden by the larger outward currents. Indirect evidence suggests that INaP is present and large during prolonged depolarizations greater than 50 mV positive to RP. INaP was blocked by intracellular injection of the lidocaine derivative QX-314, as well as by extracellular tetrodotoxin (TTX). INaP was much more sensitive to QX-314 than was the height and rate of rise of the spike. This observation and the results in paragraph 3 above are best explained by separate INaP and spike sodium channels. After blockade of INaP and sodium spikes, Ca2+ spikes could be evoked only if potassium currents were first depressed. The Ca2+-dependent nature of the regenerative potentials was indicated by their disappearance when Co2+ or Mn2+ was substituted for Ca2+ in the perfusate and by the appearance of greatly enhanced potentials of similar form when Ba2+ was substituted for Ca2+. Ba2+ substitution greatly enhanced evoked and spontaneous synaptic potentials. Prolonged-plateau action potentials could be evoked in the presence of TTX and Ba2+. Ca2+ spike threshold was 30-40 mV positive to RP, which is significantly more positive than sodium spike threshold. Results of voltage clamp in the normal perfusate and in the presence of Ca2+-blockers or Ba2+ indicated that little or no Ca2+ conductance is activated in the voltage range 25 mV positive to RP where INaP is the dominant ionic current.(ABSTRACT TRUNCATED AT 400 WORDS)

Neuropeptide Y modulates membrane excitability in neonatal rat mesencephalic V neurons

2020 ◽  
Vol 98 (5) ◽  
pp. 921-935
Author(s):  
Soju Seki ◽  
Susumu Tanaka ◽  
Saori Yamada ◽  
Tadataka Tsuji ◽  
Akifumi Enomoto ◽  
...  
Keyword(s):  
Neuropeptide Y ◽  
Neonatal Rat ◽  
Membrane Excitability

scholarly journals Control of Neuronal Persistent Activity by Voltage-Dependent Dendritic Properties

2008 ◽  
Vol 100 (3) ◽  
pp. 1278-1286 ◽  
Author(s):  
Erwin Idoux ◽  
Daniel Eugène ◽  
Antoine Chambaz ◽  
Christophe Magnani ◽  
John A. White ◽  
...  
Keyword(s):  
Cell Types ◽  
Dynamic Clamp ◽  
Persistent Activity ◽  
Type B ◽  
Sodium Conductance ◽  
Type D ◽  
Voltage Dependent ◽  
Prepositus Hypoglossi ◽  
Sodium Ion Channels ◽  
Persistent Sodium Conductance

Neural integrators and working memory rely on persistent activity, a widespread neural phenomenon potentially involving persistent sodium conductances. Using a unique combination of voltage-clamp, dynamic-clamp, and frequency-domain techniques, we have investigated the role of voltage-dependent conductances on the dendritic electrotonic structure of neurons of the prepositus hypoglossi nucleus (PHN), which is known to be involved in oculomotor integration. The PHN contains two main neuronal populations: type B neurons with a double afterhyperpolarization and type D neurons, which not only are oscillatory but also have a greater electrotonic length than that of type B neurons. The persistent sodium conductance is present in all PHN neurons, although its effect on the dynamic electrotonic structure is shown to significantly differ in the two major cell types present in the nucleus. The electrotonic differences are such that the persistent sodium conductance can be almost perfectly manipulated in a type B neuron using an on-line dynamic clamp to add or subtract virtual sodium ion channels. The dynamic-clamp results are confirmed by data-fitted models, which suggest that the persistent sodium conductance has two different roles depending on its somatic versus dendritic location: perisomatic conductances could play a major role in maintaining action potential discharge and dendritic conductances would be more involved in other computational properties, such as those involving remote synaptic processing or bistable events.

scholarly journals Regulation of membrane excitability: a convergence on voltage-gated sodium conductance

2014 ◽  
Vol 51 (1) ◽  
pp. 57-67 ◽  
Author(s):  
Wei-Hsiang Lin ◽  
Richard A. Baines
Keyword(s):  
Membrane Excitability ◽  
Voltage Gated ◽  
Sodium Conductance

scholarly journals Subcellular distribution of persistent sodium conductance in cortical pyramidal neurons

2021 ◽  
pp. JN-RM-2989-20
Author(s):  
Arik Shvartsman ◽  
Oron Kotler ◽  
Ohad Stoler ◽  
Yana Khrapunsky ◽  
Israel Melamed ◽  
...  
Keyword(s):  
Subcellular Distribution ◽  
Pyramidal Neurons ◽  
Sodium Conductance ◽  
Cortical Pyramidal Neurons ◽  
Persistent Sodium Conductance

Cytochemical Evidence for Presynatic β-Adrenergic Regulation of Secretion in the Developing Rat Submandibular Gland

1977 ◽  
Vol 35 ◽  
pp. 430-431
Author(s):  
L.S. Cutler
Keyword(s):  
Cyclic Amp ◽  
Adenylate Cyclase ◽  
Submandibular Gland ◽  
Neonatal Rat ◽  
Cyclase Activity ◽  
Adenylate Cyclase Activity ◽  
Parotid Glands ◽  
Adrenergic Agonist ◽  
Rat Submandibular Gland

Many studies previously have shown that the B-adrenergic agonist isoproterenol and the a-adrenergic agonist norepinephrine will stimulate secretion by the adult rat submandibular (SMG) and parotid glands. Recent data from several laboratories indicates that adrenergic agonists bind to specific receptors on the secretory cell surface and stimulate membrane associated adenylate cyclase activity which generates cyclic AMP. The production of cyclic AMP apparently initiates a cascade of events which culminates in exocytosis. During recent studies in our laboratory it was observed that the adenylate cyclase activity in plasma membrane fractions derived from the prenatal and early neonatal rat submandibular gland was retractile to stimulation by isoproterenol but was stimulated by norepinephrine. In addition, in vitro secretion studies indicated that these prenatal and neonatal glands would not secrete peroxidase in response to isoproterenol but would secrete in response to norepinephrine. In contrast to these in vitro observations, it has been shown that the injection of isoproterenol into the living newborn rat results in secretion of peroxidase by the SMG (1).

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