Acute effects of thyroid hormone on sodium currents in neonatal myocytes

1990 ◽  
Vol 10 (3) ◽  
pp. 309-315 ◽  
Author(s):  
W. Craelius ◽  
W. L. Green ◽  
D. R. Harris
Keyword(s):  
Thyroid Hormone ◽  
Action Potential ◽  
Action Potentials ◽  
Acute Exposure ◽  
Na Channels ◽  
Neonatal Rats ◽  
Sodium Currents ◽  
Acute Effects ◽  
Na Current ◽  
20 Nm

Sodium currents and action potentials were recorded from myocytes of neonatal rats during acute exposure to thyroid hormone (5–20 nM). One to 5 minutes after addition of thyroid hormone to the bath, decay from peak Na current was slowed, with the fractional current flowing 20 ms after onset (relative to peak current) increasing from 6±5% to 17±13% (p<0.01, n=12). Action potential durations were increased from 55±14 to 86±36 msec (p<0.05, n=6). The effects of thyroid hormone were partially reversed by lidocaine (60 μM, n=5), a specific blocker of a slow sub-population of Na channels. Thus thyroid hormone interacts directly with myocyte membrane, probably by slowing of inactivation of Na channels.

Basis for tetrodotoxin and lidocaine effects on action potentials in dog ventricular myocytes

1988 ◽  
Vol 254 (6) ◽  
pp. H1157-H1166 ◽  
Author(s):  
J. A. Wasserstrom ◽  
J. J. Salata
Keyword(s):  
Action Potential ◽  
Action Potentials ◽  
Ventricular Myocytes ◽  
Ionic Currents ◽  
Detectable Effect ◽  
Na Channel ◽  
Na Current ◽  
Voltage Range ◽  
Purkinje Fibers ◽  
Ventricular Cells

We studied the effects of tetrodotoxin (TTX) and lidocaine on transmembrane action potentials and ionic currents in dog isolated ventricular myocytes. TTX (0.1-1 x 10(-5) M) and lidocaine (0.5-2 x 10(-5) M) decreased action potential duration, but only TTX decreased the maximum rate of depolarization (Vmax). Both TTX (1-2 x 10(-5) M) and lidocaine (2-5 x 10(-5) M) blocked a slowly inactivating toward current in the plateau voltage range. The voltage- and time-dependent characteristics of this current are virtually identical to those described in Purkinje fibers for the slowly inactivating inward Na+ current. In addition, TTX abolished the outward shift in net current at plateau potentials caused by lidocaine alone. Lidocaine had no detectable effect on the slow inward Ca2+ current and the inward K+ current rectifier, Ia. Our results indicate that 1) there is a slowly inactivating inward Na+ current in ventricular cells similar in time, voltage, and TTX sensitivity to that described in Purkinje fibers; 2) both TTX and lidocaine shorten ventricular action potentials by reducing this slowly inactivating Na+ current; 3) lidocaine has no additional actions on other ionic currents that contribute to its ability to abbreviate ventricular action potentials; and 4) although both agents shorten the action potential by the same mechanism, only TTX reduces Vmax. This last point suggests that TTX produces tonic block of Na+ current, whereas lidocaine may produce state-dependent Na+ channel block, namely, blockade of Na+ current only after Na+ channels have already been opened (inactivated-state block).

scholarly journals Acute exposure to thyroid hormone increases Na + current and intracellular Ca 2+ in cat atrial myocytes

2003 ◽  
Vol 546 (2) ◽  
pp. 491-499 ◽  
Author(s):  
Yong G. Wang ◽  
Elena N. Dedkova ◽  
Jon P. Fiening ◽  
Kaie Ojamaa ◽  
Lothar A. Blatter ◽  
...  
Keyword(s):  
Thyroid Hormone ◽  
Acute Exposure ◽  
Atrial Myocytes ◽  
Na Current ◽  
Intracellular Ca

Inhibition by a actinomycin D of the denervation-induced action potential in frog slow muscle fibres

1973 ◽  
Vol 184 (1074) ◽  
pp. 91-95 ◽  
Keyword(s):  
Sciatic Nerve ◽  
Action Potential ◽  
Action Potentials ◽  
Rna Synthesis ◽  
Actinomycin D ◽  
Slow Muscle ◽  
Muscle Fibres ◽  
Na Channels ◽  
Potential Mechanism ◽  
Slow Muscle Fibres

Pyriformis muscles of the frog were denervated by section of the sciatic nerve. About three weeks later all slow muscle fibres examined had become capable of generating action potentials. However, the action potential mechanism failed to develop if actinomycin D was injected early after the operation. It is suggested that RNA synthesis is required for the formation of ‘Na channels’ in the membrane of denervated slow muscle fibres.

scholarly journals Action potentials in Xenopus oocytes triggered by blue light

2020 ◽  
Vol 152 (5) ◽  
Author(s):  
Florian Walther ◽  
Dominic Feind ◽  
Christian vom Dahl ◽  
Christoph Emanuel Müller ◽  
Taulant Kukaj ◽  
...  
Keyword(s):  
Membrane Potential ◽  
Action Potential ◽  
Blue Light ◽  
Action Potentials ◽  
Xenopus Oocytes ◽  
Na Channel ◽  
Xenopus Laevis Oocytes ◽  
Na Channels ◽  
Excitable Cells ◽  
Voltage Gated

Voltage-gated sodium (Na+) channels are responsible for the fast upstroke of the action potential of excitable cells. The different α subunits of Na+ channels respond to brief membrane depolarizations above a threshold level by undergoing conformational changes that result in the opening of the pore and a subsequent inward flux of Na+. Physiologically, these initial membrane depolarizations are caused by other ion channels that are activated by a variety of stimuli such as mechanical stretch, temperature changes, and various ligands. In the present study, we developed an optogenetic approach to activate Na+ channels and elicit action potentials in Xenopus laevis oocytes. All recordings were performed by the two-microelectrode technique. We first coupled channelrhodopsin-2 (ChR2), a light-sensitive ion channel of the green alga Chlamydomonas reinhardtii, to the auxiliary β1 subunit of voltage-gated Na+ channels. The resulting fusion construct, β1-ChR2, retained the ability to modulate Na+ channel kinetics and generate photosensitive inward currents. Stimulation of Xenopus oocytes coexpressing the skeletal muscle Na+ channel Nav1.4 and β1-ChR2 with 25-ms lasting blue-light pulses resulted in rapid alterations of the membrane potential strongly resembling typical action potentials of excitable cells. Blocking Nav1.4 with tetrodotoxin prevented the fast upstroke and the reversal of the membrane potential. Coexpression of the voltage-gated K+ channel Kv2.1 facilitated action potential repolarization considerably. Light-induced action potentials were also obtained by coexpressing β1-ChR2 with either the neuronal Na+ channel Nav1.2 or the cardiac-specific isoform Nav1.5. Potential applications of this novel optogenetic tool are discussed.

Influence of streptomycin on spontaneous activity of clusters of cultured cardiac cells from neonatal rats

1980 ◽  
Vol 58 (4) ◽  
pp. 433-435 ◽  
Author(s):  
M. D. Payet ◽  
G. Bkaily ◽  
O. F. Schanne ◽  
E. Ruiz-Ceretti
Keyword(s):  
Action Potential ◽  
Action Potentials ◽  
Maximum Rate ◽  
Cardiac Cells ◽  
Neonatal Rats ◽  
Slow Response ◽  
Diastolic Depolarization ◽  
Beating Rate ◽  
Maximum Rate Of Rise ◽  
Diastolic Potential

In clusters of trypsinized ventricle cells from neonatal rats which exhibit slow response action potentials, streptomycin in concentrations from 0.17 to 5.5 mM significantly inhibits the beating rate. Microelectrode experiments performed at a concentration of 5.5 mM revealed a reduction in the slope of diastolic depolarization from 149 to 53 mV/s whereas the maximum diastolic potential depolarized from −42.4 to −33.6 mV which entailed a decrease in overshoot and maximum rate of rise of the action potential. We conclude that the decrease of the slope of diastolic depolarization mainly determines the slowing of the beating rate and that streptomycin interferes with the pacemaker mechanism usually associated with the slow response.

scholarly journals Na+ current in presynaptic terminals of the crayfish opener cannot initiate action potentials

2016 ◽  
Vol 115 (1) ◽  
pp. 617-621 ◽  
Author(s):  
Jen-Wei Lin
Keyword(s):  
Patch Clamp ◽  
Neuromuscular Junction ◽  
Action Potential ◽  
Action Potentials ◽  
Peak Amplitude ◽  
High Threshold ◽  
Na Current ◽  
Presynaptic Terminals ◽  
Activation Rate ◽  
Fast Activation

Action potential (AP) propagation in presynaptic axons of the crayfish opener neuromuscular junction (NMJ) was investigated by simultaneously recording from a terminal varicosity and a proximal branch. Although orthodromically conducting APs could be recorded in terminals with amplitudes up to 70 mV, depolarizing steps in terminals to −20 mV or higher failed to fire APs. Patch-clamp recordings did detect Na+ current ( INa) in most terminals. The INa exhibited a high threshold and fast activation rate. Local perfusion of Na+-free saline showed that terminal INa contributed to AP waveform by slightly accelerating the rising phase and increasing the peak amplitude. These findings suggest that terminal INa functions to “touch up” but not to generate APs.

scholarly journals Differential Effects of NGF and BDNF on Axotomy-Induced Changes in GABAA-Receptor-Mediated Conductance and Sodium Currents in Cutaneous Afferent Neurons

1997 ◽  
Vol 78 (1) ◽  
pp. 31-42 ◽  
Author(s):  
Adetokunbo A. Oyelese ◽  
Marco A. Rizzo ◽  
Stephen G. Waxman ◽  
Jeffery D. Kocsis
Keyword(s):  
Sciatic Nerve ◽  
Action Potential ◽  
Action Potentials ◽  
Afferent Neurons ◽  
Sodium Currents ◽  
Drg Neurons ◽  
Differential Effects ◽  
Action Potential Waveform ◽  
Induced Changes ◽  
Potential Waveform

Oyelese, Adetokunbo A., Marco A. Rizzo, Stephen G. Waxman, and Jeffery D. Kocsis. Differential effects of NGF and BDNF on axotomy-induced changes in GABAA-receptor-mediated conductance and sodium currents in cutaneous afferent neurons. J. Neurophysiol. 78: 31–42, 1997. The effects of nerve growth factor (NGF) and brain-derived neurotrophic factor (BDNF) on injury-induced changes in the electrophysiological properties of adult rat cutaneous afferent dorsal root ganglion (DRG) neurons were examined. Whole cell patch-clamp techniques were used to study γ-aminobutyric acid-A (GABAA)-receptor-mediated conductance, voltage-dependent sodium currents, and action potential waveform in cutaneous afferent neurons (35–60 μm diam) cultured from control and axotomized animals. Cutaneous afferent neuronswere identified by retrograde labeling with hydroxy-stilbamidine (Fluoro-gold, a fluorescent retrograde axonal tracer); the sciatic nerve was transected 1 wk after Fluoro-gold injection and L4/L5 DRG neurons were cultured 2–3 wk after axotomy. NGF, BDNF, or Ringer (vehicle) solution was delivered in vivo directly to the transected sciatic nerve stump in axotomized rats via an osmotic pump. Recordings were obtained from neurons 5–24 h after culture. Axotomized neurons from rats treated with vehicle solution displayed a twofold increase in GABA-induced conductance and a prominent reduction in the proportion of neurons expressing action potentials that had inflections on the falling phase. The expression of kinetically slow tetrodotoxin (TTX)-resistant sodium current was markedly reduced and an increased expression of kinetically fast TTX-sensitive current was observed in neurons from vehicle-treated, axotomized rats. Treatment with NGF (0.25 μg/μl at 12 μl/day for 14 days) in axotomized animals resulted in an increase in the proportion of neurons expressing TTX-resistant, slow sodium currents and inflected action potentials, but had no effect on GABA-induced conductance. Treatment with BDNF (0.5 μg/μl at 12 μl/day for 14 days) attenuated the axotomy-induced increase in GABAA-receptor-mediated conductance while minimally affecting action potential waveform. The observed neurotrophin effects occurred independently of cell size changes. These findings indicate a differential regulation of GABAA receptor and sodium channel properties in axotomized rat cutaneous afferent neurons by specific neurotrophic factors.

Acute Effects of Thyroid Hormone Analogs on Sodium Currents in Neonatal Rat Myocytes

1999 ◽  
Vol 31 (4) ◽  
pp. 881-893 ◽  
Author(s):  
Chien-Jung Huang ◽  
Herbert M. Geller ◽  
William L. Green ◽  
William Craelius
Keyword(s):  
Thyroid Hormone ◽  
Neonatal Rat ◽  
Sodium Currents ◽  
Acute Effects ◽  
Rat Myocytes ◽  
Hormone Analogs

The Local Anesthetic n-Butyl-p-Aminobenzoate Selectively Affects Inactivation of Fast Sodium Currents in Cultured Rat Sensory Neurons

1995 ◽  
Vol 82 (6) ◽  
pp. 1463-1473. ◽  
Author(s):  
R. J. Van den Berg ◽  
P. F. Van Soest ◽  
Z. Wang ◽  
R. J. E. Grouls ◽  
H. H. M. Korsten
Keyword(s):  
Action Potential ◽  
Sensory Neurons ◽  
Local Anesthetic ◽  
Action Potentials ◽  
Sodium Current ◽  
Short Exposure ◽  
Na Channels ◽  
Firing Threshold ◽  
Na Currents ◽  
Ganglion Neurons

Background Aqueous suspensions of the local anesthetic n-butyl-p-aminobenzoate (BAB), epidurally applied in terminal cancer patients, resulted in a sensory blockade, lasting up to several months. To investigate the mechanism of action on the cellular level, the effect of 100 microM BAB on Na+ action potentials and on Na+ currents in dorsal root ganglion neurons from neonatal rats was studied. Methods Small neurons grown in cell culture were selected for patch-clamp measurements. Both Na+ action potentials, evoked by current pulses of increasing amplitude (current clamp) and Na+ currents, activated at different membrane potentials (voltage clamp), were investigated in the absence and presence of 100 microM BAB. The local anesthetic was applied by external perfusion for 2 or 10 min. Results In the presence of 100 microM BAB, either the firing threshold was raised or the action potential was abolished. The maximal peak conductances, underlying the fast sodium current INa,F and the slow sodium current INa,5, were not changed. However, the inactivation of INa,F was increased by BAB. The sigmoid inactivation curve shifted 12 mV toward hyperpolarizing membrane voltages, whereas no changes were found for the inactivation of the slow Na+ current. Only at short exposure times of 2 min, the effects of BAB could be reversed during a 10-min wash-out. Conclusions BAB dramatically increased the firing threshold, and in part of the sensory neurons, it blocked the action potential. The inactivation of the fast Na+ channels, but not of the slow Na+ channels, was increased by BAB. Thus, the block of fast Na+ channels by BAB may contribute to epidural analgesia. At exposure times of 10 min, the effect of BAB was not reversible. This probably originates from its high lipid-solubility, which may be an important factor in determining the duration of the block in vivo.

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