The development of voltege-dependent ionic conductances In murine spinal cord neurones in culture

1988 ◽  
Vol 66 (10) ◽  
pp. 1328-1336 ◽  
Author(s):  
C. Krieger ◽  
T. A. Sears
Keyword(s):  
Spinal Cord ◽  
Sodium Current ◽  
Potassium Conductance ◽  
Calcium Currents ◽  
Delayed Rectifier ◽  
Patch Clamp Technique ◽  
Calcium Dependent ◽  
Ionic Conductances ◽  
Voltage Dependent

The development of voltage-dependent ionic conductances of foetal mouse spinal cord neurones was examined using the whole-cell patch-clamp technique on neurones cultured from embryos aged 10–12 days (E10–E12) which were studied between the first day in vitro (V1) to V10. A delayed rectifier potassium conductance (IK) and a leak conductance were observed in neurones of E10.V1, E11, V1, and E12, V1 as well as in neurones cultured for longer periods. A rapidly activating and inactivating potassium conductance (IA) was seen in neurones from E11, V2 and E12, V1 and at longer times in vitro. A tetrodotoxin (TTX) sensitive sodium-dependent inward current was observed in neurones of E11 and E12 from V1 onwards. Calcium-dependent conductances were not detectable in these neurones unless the external calcium concentration was raised 10- to 20-foid and potassium conductances were blocked. Under these conditions calcium currents could be observed as early as E11, V3 and E12, V2 and at subsequent times in vitro. The pattern of development of voltage-dependent ionic conductances in murine spinal neurones is such that initially leak and potassium currents are present followed by sodium current and subsequently calcium current.

scholarly journals Effect of FMRFamide on voltage-dependent currents in identified centrifugal neurons of the optic lobe of the cuttlefish, Sepia officinalis

2020 ◽  
Author(s):  
Abdesslam Chrachri
Keyword(s):  
Visual Processing ◽  
Calcium Current ◽  
Optic Lobe ◽  
Low Voltage ◽  
Sodium Current ◽  
Calcium Currents ◽  
Delayed Rectifier ◽  
Outward Currents ◽  
Voltage Dependent ◽  
Inward Currents

AbstractWhole-cell patch-clamp recordings from identified centrifugal neurons of the optic lobe in a slice preparation allowed the characterization of five voltage-dependent currents; two outward and three inward currents. The outward currents were; the 4-aminopyridine-sensitive transient potassium or A-current (IA), the TEA-sensitive sustained current or delayed rectifier (IK). The inward currents were; the tetrodotoxin-sensitive transient current or sodium current (INa). The second is the cobalt- and cadmium-sensitive sustained current which is enhanced by barium and blocked by the dihydropyridine antagonist, nifedipine suggesting that it could be the L-type calcium current (ICaL). Finally, another transient inward current, also carried by calcium, but unlike the L-type, this current is activated at more negative potentials and resembles the low-voltage-activated or T-type calcium current (ICaT) of other preparations.Application of the neuropeptide FMRFamide caused a significant attenuation to the peak amplitude of both sodium and sustained calcium currents without any apparent effect on the transient calcium current. Furthermore, FMRFamide also caused a reduction of both outward currents in these centrifugal neurons. The fact that FMRFamide reduced the magnitude of four of five characterized currents could suggest that this neuropeptide may act as a strong inhibitory agent on these neurons.SummaryFMRFamide modulate the ionic currents in identified centrifugal neurons in the optic lobe of cuttlefish: thus, FMRFamide could play a key role in visual processing of these animals.

Voltage-dependent calcium channels in ventricular cells of rainbow trout: effect of temperature changes in vitro

2000 ◽  
Vol 278 (6) ◽  
pp. R1524-R1534 ◽  
Author(s):  
Catherine S. Kim ◽  
Mary D. Coyne ◽  
Judith K. Gwathmey
Keyword(s):  
Rainbow Trout ◽  
Calcium Channels ◽  
Temperature Sensitivity ◽  
Calcium Currents ◽  
Temperature Dependency ◽  
Patch Clamp Technique ◽  
Ventricular Cells ◽  
Voltage Dependent ◽  
Voltage Dependent Calcium Channels

Voltage-dependent calcium channels (VDCC) in ventricular myocytes from rainbow trout ( Oncorhynchus mykiss) were investigated in vitro using the perforated patch-clamp technique, which maintains the integrity of the intracellular milieu. First, we characterized the current using barium as the charge carrier and established the doses of various pharmacological agents to use these agents in additional studies. Second, we examined the current at several physiological temperatures to determine temperature dependency. The calcium currents at 10°C (acclimation temperature) were identified as l-type calcium currents based on their kinetic behavior and response to various calcium channel agonists and antagonists. Myocytes were chilled (4°C) and warmed (18 and 22°C), and the response of VDCC to varying temperatures was observed. There was no significant dependency of the current amplitude and kinetics on temperature. Amplitude decreased 25–36% at 4°C (Q10 ∼1.89) and increased 18% at 18°C (Q10 ∼1.23) in control, Bay K8644 (Bay K)-, and forskolin-enhanced currents. The inactivation rates (τi) did not demonstrate a temperature sensitivity for the VDCC (Q10 1.23–1.92); Bay K treatment, however, increased temperature sensitivity of τi between 10 and 18°C (Q10 3.98). The low Q10 values for VDCC are consistent with a minimal temperature sensitivity of trout myocytes between 4 and 22°C. This low-temperature dependency may provide an important role for sarcolemmal calcium channels in adaptation to varying environmental temperatures in trout.

Ionic Currents Underlying Difference in Light Response Between Type A and Type B Photoreceptors

2006 ◽  
Vol 95 (5) ◽  
pp. 3060-3072 ◽  
Author(s):  
K. T. Blackwell
Keyword(s):  
Sodium Current ◽  
Light Response ◽  
Type A ◽  
Ionic Currents ◽  
Firing Frequency ◽  
Delayed Rectifier ◽  
Type B ◽  
Calcium Dependent ◽  
Fast Sodium Current

In Hermissenda crassicornis, the memory of light associated with turbulence is stored as changes in intrinsic and synaptic currents in both type A and type B photoreceptors. These photoreceptor types exhibit qualitatively different responses to light and current injection, and these differences shape the spatiotemporal firing patterns that control behavior. Thus the objective of the study was to identify the mechanisms underlying these differences. The approach was to develop a type B model that reproduced characteristics of type B photoreceptors recorded in vitro, and then to create a type A model by modifying a select number of ionic currents. Comparison of type A models with characteristics of type A photoreceptors recorded in vitro revealed that type A and type B photoreceptors have five main differences, three that have been characterized experimentally and two that constitute hypotheses to be tested with experiments in the future. The three differences between type A and type B photoreceptors previously characterized include the inward rectifier current, the fast sodium current, and conductance of calcium-dependent and transient potassium channels. Two additional changes were required to produce a type A photoreceptor model. The very fast firing frequency observed during the first second after light onset required a faster time constant of activation of the delayed rectifier. The fast spike adaptation required a fast, noninactivating calcium-dependent potassium current. Because these differences between type A and type B photoreceptors have not been confirmed in comparative experiments, they constitute hypotheses to be tested with future experiments.

Studies of solitary semicircular canal hair cells in the adult pigeon. II. Voltage-dependent ionic conductances

1989 ◽  
Vol 62 (4) ◽  
pp. 935-945 ◽  
Author(s):  
D. G. Lang ◽  
M. J. Correia
Keyword(s):  
Hair Cells ◽  
Semicircular Canal ◽  
Potassium Conductance ◽  
Outward Current ◽  
Resting Membrane Potential ◽  
Calcium Dependent ◽  
Ionic Conductances ◽  
Voltage Dependent ◽  
Steady State Inactivation ◽  
Inward Currents

1. The ionic conductances present in putative type II hair cells enzymatically dissociated from the anterior, posterior, and lateral semicircular canal cristae of the white king pigeon (Columba livia) vestibule were studied under whole cell voltage clamp. 2. Two classes of voltage-dependent potassium conductances were distinguishable on the basis of the time course of activation and inactivation and pharmacologic sensitivity. The rapid potassium conductance, IA, as inhibited by 6 mM 4-aminopyridine (4-AP), whereas the slow potassium conductance, IK, was inhibited by 50 mM tetraethylammonium (TEA). These conductances were not affected by extracellular calcium removal. IA was quite similar to the rapidly-inactivating A-current of molluscan soma, whereas IK was more like the delayed rectifier of molluscan soma. 3. The steady-state inactivation of IA occurred over a potential range from -100 to -40 mV. The threshold for activation of IA occurred between -60 and -50 mV. The slope conductance of the I-V curve over a range of -50 to -20 mV was 13.7 nS when the conditioning pulse was -100 mV, and we estimate it to be approximately 1-2 nS from the resting membrane potential of -56 mV. 4. The steady-state inactivation of IK was approximately 60% at -40 mV and was completely removed at -80 mV. The threshold for activation of IK was between -50 and -40 mV. The slope conductance of the I-V curve over a range of -50 to -20 mV was 10.5 nS when the conditioning pulse was -80 mV, and we estimate it to be approximately 6-7 nS from the resting potential of -56 mV. 5. At -56 mV (the average resting membrane potential of putative type II semicircular canal hair cells), approximately 10-14% of IA channels and approximately 57-70% of IK channels were not inactivated: thus IA and IK can contribute to the outward current during small depolarizations from rest. 6. A small calcium-dependent outward current, IK(Ca), could be elicited during step depolarizations from a holding potential of -40 mV. This calcium-dependent current was active over the range of -20 to +40 mV. 7. Inward currents could not be detected when the cells were exposed to normal physiological solutions. However, when the outward currents were blocked with internal cesium and the external solution contained 20 mM barium, sustained inward currents with rapid activation kinetics could be detected. The threshold for activation of the inward current occurred at -40 mV, and the I-V relationship peaked at -10 mV.(ABSTRACT TRUNCATED AT 400 WORDS)

Calcium currents and transmitter output in cultured spinal cord and dorsal root ganglion neurons

1986 ◽  
Vol 56 (5) ◽  
pp. 1257-1267 ◽  
Author(s):  
M. Jia ◽  
P. G. Nelson
Keyword(s):  
Spinal Cord ◽  
Dorsal Root Ganglion ◽  
Dorsal Root ◽  
Calcium Currents ◽  
Dorsal Root Ganglion Neurons ◽  
Ion Concentration ◽  
Drg Neurons ◽  
Voltage Dependent ◽  
Ganglion Neurons

The effects of repetitive activation upon voltage-dependent calcium currents (ICa) and transmitter release were studied in dissociated cell cultures of fetal mouse spinal cord and dorsal root ganglion. Sodium and potassium currents were suppressed with tetrodotoxin (TTX) and tetraethylammonium (TEA) ions, 4-aminopyridine (4-AP), and cesium sulfate. Calcium currents were compared under voltage clamp before and after a series of depolarizing clamp pulses in spinal cord (SC) and dorsal root ganglion (DRG) neurons. Repetitive activation resulted in an exponential decline in ICa, with the decrease in ICa being much more marked in DRG compared with SC neurons. Both voltage-dependent inactivation and inactivation related to the intracellular movement of Ca2+ appeared to be involved in the decrement in ICa with repetitive activation. A decrease in transmitter output occurred with repetitive activation in DRG neurons but not in SC neurons (either excitatory or inhibitory). DRG neuron synaptic boutons had fewer mitochondria than did the boutons of either excitatory or inhibitory of SC neurons. The decrement in both ICa and synaptic transmitter output in DRG neurons could last for prolonged periods (at least minutes) following repetitive activation. We hypothesize that this vulnerability of DRG neurons to repetitive activation may be related, at least in part, to a relative incapacity to maintain a low intracellular calcium ion concentration [Ca]i during periods of increased calcium ingress associated with excitation. Such an incapacity to buffer [Ca]i may be one mechanism leading to the inactive synapses seen in some studies in vitro and in vivo of synaptic transmission.

Beyond Hodgkin and Huxley: Calcium and Calcium-Dependent Potassium Currents

1998 ◽  
Author(s):  
Christof Koch
Keyword(s):  
Sodium Current ◽  
Second Messengers ◽  
Giant Axon ◽  
Firing Frequency ◽  
Squid Giant Axon ◽  
Molecular Techniques ◽  
Calcium Dependent ◽  
Ionic Conductances ◽  
Voltage Dependent ◽  
Set Up

The cornerstone of modern biophysics is the comprehensive analysis by Hodgkin and Huxley (1952a,b,c,d) of the generation and propagation of action potentials in the squid giant axon. The basis of their model is a fast sodium current INa and a delayed potassium current IK (which here we also refer to as IDR)- The last 40 years of research have shown that impulse conduction along axons can be successfully analyzed in terms of one or both of these currents. Nonetheless, their equations do not capture—nor were they intended to capture—a number of important biophysical phenomena, such as adaptation of the firing frequency to long-lasting stimuli or bursting, that is, the generation of two to five spikes within 5-20 msec. Moreover, the transmission of electrical signals within and between neurons involves more than the mere circulation of stereotyped pulses. These impulses must be set up and generated by subthreshold processes. The differences between the firing behavior of most neurons and the squid giant axon reflect the roles of other voltage-dependent ionic conductances than the two described by Hodgkin and Huxley. Over the last two decades, more than several dozen membrane conductances have been characterized (Hagiwara, 1983; Llinás, 1988; Hille, 1992). They differ in principal carrier, voltage, and time dependence, dependence on the presence of intracellular calcium and on their susceptibility to modulation by synaptic inputs and second messengers. Our knowledge of these conductances and the role they play in impulse formation has accelerated rapidly in recent years as a result of various technical innovations such as single-cell isolation, patch clamping, and molecular techniques. We will here describe the most important of these conductances and briefly characterize each one. In order to understand more completely the functional role of these conductances in determining the response of the cell to input, empirical equations that approximate their behavior under physiological conditions must be developed and compared against the physiological preparations. In a remarkable testimony to the power and the generality of the Hodgkin-Huxley approach, the majority of such phenomenological models has used their methodology of describing individual ionic conductances in terms of activating and inactivating particles with first-order kinetics (see Chap. 6).

scholarly journals On The Mechanism of Spontaneous Impulse Generation in the Pacemaker of the Heart

1961 ◽  
Vol 45 (2) ◽  
pp. 317-330 ◽  
Author(s):  
Wolfgang Trautwein ◽  
Donald G. Kassebaum
Keyword(s):  
Sodium Current ◽  
Potassium Conductance ◽  
Rhythmic Activity ◽  
Current Strength ◽  
Heart Beat ◽  
Free Medium ◽  
Pacemaker Potential ◽  
Impulse Generation ◽  
Sodium Conductance ◽  
Voltage Dependent

Rhythmic activity in Purkinje fibers of sheep and in fibers of the rabbit sinus can be produced or enhanced when a constant depolarizing current is applied. When extracellular calcium is reduced successively, the required current strength is less, and eventually spontaneous beating occurs. These effects are believed due to an increase in steady-state sodium conductance. A significant hyperpolarization occurs in fibers of the rabbit sinus bathed in a sodium-free medium, suggesting an appreciable sodium conductance of the "resting" membrane. During diastole, there occurs a voltage-dependent and, to a smaller extent, time-dependent reduction in potassium conductance, and a pacemaker potential occurs as a result of a large resting sodium conductance. It is postulated that the mechanism underlying the spontaneous heart beat is a high resting sodium current in pacemaker tissue which acts as the generator of the heart beat when, after a regenerative repolarization, the decrease in potassium conductance during diastole reestablishes the condition of threshold.

Serotonin has different effects on two classes of Betz cells from the cat

1994 ◽  
Vol 72 (4) ◽  
pp. 1925-1937 ◽  
Author(s):  
W. J. Spain
Keyword(s):  
Firing Rate ◽  
Potassium Conductance ◽  
Membrane Conductance ◽  
Constant Current ◽  
Repetitive Firing ◽  
Calcium Dependent ◽  
Constant Current Stimulation ◽  
Ionic Mechanisms ◽  
Betz Cells

1. Intracellular recording from cat Betz cells in vitro revealed a strong correlation between the dominant effect of serotonin (5-HT) and the Betz cell subtype in which it occurred. In large Betz cells that show posthyperpolarization excitation (termed PHE cells), 5-HT evoked a long-lasting membrane depolarization, whereas 5-HT evoked an initial hyperpolarization of variable duration in smaller Betz cells that show posthyperpolorization inhibition (termed PHI cells). 2. Voltage-clamp studies revealed that 5-HT caused a depolarizing shift of activation of the cation current Ih, which resulted in the depolarization in PHE cells, whereas the hyperpolarization in PHI cells is caused by an increase in a resting potassium conductance. 3. The effect of 5-HT on firing properties during constant current stimulation also differed consistently in the two types of Betz cells. In PHE cells the initial firing rate increased after 5-HT application, but the steady firing was unaffected. The depolarizing shift of Ih activation caused the increase of initial firing rate. 4. In PHI cells 5-HT caused a decrease in spike frequency adaptation. The decrease in adaptation was caused by a combination of two conductance changes. First, 5-HT caused a slow afterdepolarization in PHI cells that could trigger repetitive firing in the absence of further stimulation. The sADP depended on calcium entry through voltage-gated channels and was associated with a decrease in membrane conductance. Second, 5-HT caused reduction of a slow calcium-dependent potassium current that normally contributes to slow adaptation. 5. In conclusion, the effect of 5-HT on excitability differs systematically in Betz cell subtypes in part because they have different dominant ionic mechanisms that are modulated. If we assume that PHE cells and PHI cells represent fast and slow pyramidal tract (PT) neurons respectively, 5-HT will cause early recruitment of fast PT cells and delay recruitment of slow PT cells during low levels of synaptic excitation.

Hippocampal pyramidal cells: significance of dendritic ionic conductances for neuronal function and epileptogenesis

1979 ◽  
Vol 42 (2) ◽  
pp. 476-496 ◽  
Author(s):  
R. D. Traub ◽  
R. Llinas
Keyword(s):  
Hot Spots ◽  
Potassium Conductance ◽  
Pyramidal Cells ◽  
Calcium Currents ◽  
Membrane Properties ◽  
Repetitive Firing ◽  
Published Data ◽  
Neuronal Responses ◽  
Voltage Dependent ◽  
Hippocampal Pyramidal Cells

1. Starting with published data derived mainly from hippocampal slice preparations, we have used computer-modeling techniques to study hippocampal pyramidal cells (HPCs). 2. The dendrites of the HPC apparently have a short electrotonic length. Calcium spikes are apparently generated by a voltage-dependent mechanism whose kinetics are slow in comparison with those generating sodium spikes of the soma. Inward calcium currents are assumed to trigger a long-lasting potassium conductance. This slow calcium-potassium system, which in our model is located predominantly on the dendrites, provides a heuristic model to describe the mechanism for a) the after-depolarization following an HPC soma (sodium) spike, b) the long afterhyperpolarization following repetitive firing, c) bursts of spikes that sometimes occur after orthodromic or antidromic stimulation, and d) the buildup of the "depolarizing shift" during the strong synaptic input presumed to occur during seizures. 3. Fast prepotentials or d-spikes are shown to arise most probably from dendritic "hot spots" of sodium-regenerative membrane. The limited amplitude and short duration of these prepotentials imply that the hot spots are located on small dendrites. 4. Dendritic electroresponsiveness, first postulated for the HPC by Spencer and Kandel (52), is analyzed quantitatively here and is shown to provide rich integrative possibilities for this cell. Our model suggests that, for these nerve cells, alterations in specific membrane properties, particularly calcium electroresponsiveness, can lead to bursting behavior that resembles epileptogenic neuronal responses.

Characterization of voltage-dependent calcium currents in mouse motoneurons

1992 ◽  
Vol 68 (1) ◽  
pp. 85-92 ◽  
Author(s):  
M. Mynlieff ◽  
K. G. Beam
Keyword(s):  
Voltage Dependence ◽  
Low Voltage ◽  
Calcium Currents ◽  
Patch Clamp Technique ◽  
Maximal Amplitude ◽  
Time To Peak ◽  
Whole Cell Patch Clamp ◽  
Voltage Dependent ◽  
Channel Currents

1. Calcium channel currents were measured with the whole-cell patch clamp technique in cultured, identified mouse motoneurons. Three components of current were operationally defined on the basis of voltage dependence, kinetics, and pharmacology. 2. Test potentials to -50 mV or greater (10 mM external Ca2+) elicited a low-voltage activated T-type current that was transient (decaying to baseline in less than 200 ms) and had a relatively slow time to peak (20-50 ms). A 1-s prepulse to -45 mV produced approximately half-maximal inactivation of this T current. 3. Two high-voltage activated (HVA) components of current (1 transient and 1 sustained) were activated by test potentials to -20 mV or greater (10 mM external Ca2+). A 1-s prepulse to -35 mV produced approximately half-maximal inactivation of the transient component without affecting the sustained component. 4. When Ba2+ was substituted for Ca2+ as the charge carrier, activation of the HVA components was shifted in the hyperpolarizing direction, and the relative amplitude of the transient HVA component was reduced. 5. Amiloride (1-2 mM) caused a reversible, partial block of the T current without affecting the HVA components. 6. The dihydropyridine agonist isopropyl 4-(2,1,3-benzoxadiazol-4-yl)-1,4-dihydro-2,6-dimethyl-5-nitro-3- pyridine-carboxylate [(+)-SDZ 202-791, 100 nM-1 microM)] shifted the activation of the sustained component of HVA current to more negative potentials and increased its maximal amplitude. Additionally, (+)-SDZ 202-791 caused the appearance of a slowed component of tail current.(ABSTRACT TRUNCATED AT 250 WORDS)

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