Currents in the presynaptic terminal arbors of barnacle photoreceptors

1993 ◽  
Vol 10 (2) ◽  
pp. 261-270 ◽  
Author(s):  
Jon H. Hayashi ◽  
Ann E. Stuart

AbstractWe have described the currents flowing across the presynaptic membranes of the four median photoreceptors of the giant barnacle, Balanus nubilus, using a quasi-voltage clamp arrangement. Membrane potential, measured in the terminal region of one photoreceptor, was controlled in all four terminals by feedback current supplied through the nerve containing the photoreceptors’ axons. The [Ca2+] ∘ in the saline was reduced to decrease the Ca2+ current, enabling better voltage control, and tetraethylammonium ion (TEA, 20 mM) was added to block a fast voltage-dependent K+ conductance.Depolarizing voltage steps from the resting potential in the dark (−60 mV) evoked slow, inward Ca2+-dependent currents which could be blocked by Co2+, Mg2+, or Cd2+. The Ca2+ currents were followed by large outward currents that persisted for many seconds after the offset of moderate or large pulses. These tail currents increased in magnitude and duration with pulse duration and reversed at about −80 mV, consistent with previous evidence for a Ca2+-activated K+ conductance in this membrane. When the Ca2+-activated outward current was reduced to zero by increasing the [K+]∘ so as to set EK at −20 mV, and then stepping the voltage to this value, the step evoked a steady inward Ca2+ current. Thus, the Ca2+ current did not show voltage- or Ca2+-dependent inactivation. When Ba2+ was substituted for Ca2+, 500-ms depolarizing steps evoked steady inward currents but no outward currents. In any given experiment, the activation voltage of the Ca2+ or Ba2+ current did not depend on holding potential.At the barnacle photoreceptor’s synapse, the postsynaptic cell adapts to maintained presynaptic voltage by a mechanism that is not understood. We conclude that neither Ca2+ current inactivation nor a shift in activation voltage with holding potential can account for this adaptation.

1995 ◽  
Vol 74 (4) ◽  
pp. 1485-1497 ◽  
Author(s):  
J. Schmidt ◽  
S. Gramoll ◽  
R. L. Calabrese

1. The effects of Phe-Met-Arg-Phe (FMRF)amide (10(-6) M) on membrane properties of heart interneurons in the third, fourth, and fifth segmental ganglia [HN(3), HN(4), and HN(5) cells, respectively] of the leech were studied using discontinuous current-clamp and single-electrode voltage-clamp techniques. FMRFamide was focally applied onto the soma of the cell under investigation. 2. Application of FMRFamide depolarized HN(3) and HN(4) cells by evoking an inward current. These responses were subject to pronounced desensitization. The inward currents evoked by application of FMRFamide were associated with an increase in membrane conductance and appeared to be voltage dependent. Currents were enhanced at more depolarized potentials. 3. The responsiveness of the HN(3) and HN(4) cells was not affected when the Ca2+ concentration in the bath saline was reduced from normal (1.8 mM) to 0.1 mM. The depolarizing response on application of FMRFamide was blocked when Co2+ was substituted for Ca2+. 4. HN(3) and HN(4) cells did not respond to FMRFamide application in Na(+)-free solution. Inward currents were largely reduced when bath saline with 30% of the normal Na+ concentration was used. When Li+ was substituted for Na+ in the saline, application of FMRFamide still evoked depolarizing responses in HN(3) and HN(4) cells. 5. We conclude that focal application of FMRFamide onto the somata of HN(3) and HN(4) cells evokes a voltage-dependent inward current, carried largely by Na+. 6. Focal application of FMRFamide onto somata of HN(5) cells hyperpolarized these cells by activating a voltage-dependent outward current. 7. HN(5) cells were loaded with Cl- until inhibitory postsynaptic potentials carried by Cl- reversed. Cl(-)-loaded cells still responded with a hyperpolarization when FMRFamide was applied onto their somata. Therefore the outward current evoked by FMRFamide appears to be mediated by a K+ conductance increase. 8. Application of FMRFamide onto the somata of HN(5) cells enhanced outward currents that were evoked by depolarizing voltage steps from a holding potential of -45 mV. 9. We conclude that the hyperpolarizing response of HN(5) cells to focal application of FMRFamide onto their somata is the result of an up-regulation of a voltage-dependent K+ current.


1982 ◽  
Vol 79 (2) ◽  
pp. 187-209 ◽  
Author(s):  
J E Lisman ◽  
G L Fain ◽  
P M O'Day

The voltage-dependent conductances of Limulus ventral photoreceptors have been investigated using a voltage-clamp technique. Depolarization in the dark induces inward and outward currents. The inward current is reduced by removing Na+ or Ca2+ and is abolished by removing both ions. These results suggest that both Na+ and Ca2+ carry voltage-dependent inward current. Inward current is insensitive to tetrodotoxin but is blocked by external Ni2+. The outward current has a large transient component that is followed by a smaller maintained component. Intracellular tetraethylammonium preferentially reduces the maintained component, and extracellular 4-amino pyridine preferentially reduces the transient component. Neither component is strongly affected by removal of extracellular Ca2+ or by intracellular injection of EGTA. It is concluded that the photoreceptors contain at least three separate voltage-dependent conductances: 1) a conductance giving rise to inward currents; 2) a delayed rectifier giving rise to maintained outward K+ current; and 3) a rapidly inactivating K+ conductance similar to the A current of molluscan neurons.


1993 ◽  
Vol 69 (1) ◽  
pp. 241-247 ◽  
Author(s):  
W. Muller ◽  
H. D. Lux

1. Numerical methods were used to evaluate voltage space-clamp performance in the investigation of a voltage-dependent inward current similar to the noninactivating Ca current. In addition, the cell is equipped with a repolarizing system, represented by leak and outwardly rectifying outward conductances. The electrotonically compact model cell is represented by a cable with an electrotonic length of 1 space constant under control conditions, but that becomes effectively only 0.33 space constants during a 90% reduction of the leak and outward conductance. The cable is perfectly voltage clamped at one end. 2. The apparent voltage dependence, activation, and inactivation of the clamp current depend on the distribution of the membrane slope conductance along the cable; this depends on 1) the distribution of the inward current along the cable and 2) the amplitude of the inward current relative to the amplitudes of the leak and voltage-dependent outward currents. 3. Under control conditions, the membrane voltage decays steeply with distance from the command voltage at the clamp site to almost resting potential for most of the rest of the cable. This is because the leak and outward current are dominant over the inward current. The inward current is activated primarily at the clamped part of the cable. Clamp currents are activated instantaneously. The clamp-current current-voltage (I-V) relation is less steep with depolarization because the membrane potential for locations away from the clamp site lags behind the clamp potential. 4. When the conductances for leak and outward current are reduced by 90%, these conductances lose their dominance. The membrane slope conductance now has a range with negative values.(ABSTRACT TRUNCATED AT 250 WORDS)


2010 ◽  
Vol 104 (3) ◽  
pp. 1566-1577 ◽  
Author(s):  
Thomas M. Hamm ◽  
Vladimir V. Turkin ◽  
Neha K. Bandekar ◽  
Derek O'Neill ◽  
Ranu Jung

We report here the first direct measurements of persistent inward currents (PICs) in rat hindlimb motoneurons, obtained from ketamine–xylazine anesthetized rats during slow voltage ramps performed by single-electrode somatic voltage clamp. Most motoneurons expressed PICs and current–voltage ( I– V) relations often contained a negative-slope region (NSR; 13/19 cells). PICs activated at −52.7 ± 3.89 mV, 9 mV negative to spike threshold. NSR onset was −44.2 ± 4.1 mV. PIC amplitudes were assessed by maximum inward currents measured relative to extrapolated leak current and to NSR-onset current. PIC conductance at potentials just positive to activation was assessed by the relative change in slope conductance ( gin/ gleak). PIC amplitudes varied widely; some exceeded 5 and 10 nA relative to current at NSR onset or leak current, respectively. PIC amplitudes did not vary significantly with input conductance, but PIC amplitudes normalized by recruitment current decreased with increasing input conductance. Similarly, gin/ gleak decreased with increasing input conductance. Currents near resting potential on descending limbs of I– V relations were often outward, relative to ascending-limb currents. This residual outward current was correlated with increases in leak conductance on the descending limb and with input conductance. Excluding responses with accommodation, residual outward currents matched differences between recruitment and derecruitment currents, suggesting a role for residual outward current in frequency adaptation. Comparison of potentials for PIC activation and NSR onset with interspike trajectories during discharge demonstrated correspondence between PIC activation and frequency–current ( f– I) range boundaries. Contributions of persistent inward and outward currents to motoneuron discharge characteristics are discussed.


1997 ◽  
Vol 78 (6) ◽  
pp. 3125-3132 ◽  
Author(s):  
Abdesslam Chrachri ◽  
Roddy Williamson

Chrachri, Abdesslam and Roddy Williamson. Voltage-dependent conductances in primary sensory hair cells. J. Neurophysiol. 78: 3125–3132, 1997. Cephalopods, such as sepia, squid, and octopus, show a well-developed and sophisticated control of balance particularly during prey capture and escape behaviors. There are two separate areas of sensory epithelium in cephalopod statocysts, a macula/statolith system, which detects linear accelerations (gravity), and a crista/cupula system, which detects rotational movements. The aim of this study is to characterize the ionic conductances in the basolateral membrane of primary sensory hair cells. These were studied using a whole cell patch-clamp technique, which allowed us to identify five ionic conductances in the isolated primary hair cells; an inward sodium current, an inward calcium current, and three potassium outward currents. These outward currents were distinguishable on the basis of their voltage-dependence and pharmacological sensitivities. First, a transient outward current ( I A) was elicited by depolarizing voltage steps from a holding potential of −60 mV, was inactivated by holding the cell at −40 mV, and was blocked by 4-aminopyridine. A second, voltage-sensitive, outward current with a sustained time course was identified. This current was not blocked by 4-aminopyridine nor inactivated at a holding potential of −40 mV and hence could be separated from I A using these protocols. A third outward current that depended on Ca2+ entry for its activation was detected, this current was identified by its sensitivity to Ca2+ channel blockers such as Co2+ and Cd2+ and by the N-shaped profile of its current-voltage curve. Inward currents were studied using cesium aspartate solution in the pipette to block the outward currents. Two inward currents were observed in the primary sensory hair cells. A fast transient inward current, which is presumably responsible for spike generation. This inward current appeared as a rapidly activating inward current; this was strongly voltage dependent. Three lines of evidence suggest that this fast transient inward current is a Na+ current ( I Na). First, it was blocked by tetrodotoxin (TTX); second, it also was blocked by Na+-free saline; and third, it was inactivated when primary hair cells were held at a potential more than −40 mV. The sustained inward current was not affected by TTX and was increased in amplitude 5 min after equimolar Ba2+ replaced Ca2+ as a charge carrier. This inward current also was blocked after external application of 2 mmol/l Co2+ or Cd2+. Furthermore, this current was reduced significantly in a dose-dependent manner by nifedipine, suggesting that it is an L-type Ca2+ current ( I Ca).


1998 ◽  
Vol 275 (6) ◽  
pp. H1979-H1992 ◽  
Author(s):  
Andrew C. Zygmunt ◽  
Robert J. Goodrow ◽  
Charlene M. Weigel

The contributions of electrogenic sodium/calcium exchange current ( I NaCa), calcium-activated chloride conductance [ I Cl(Ca)], and calcium-activated nonselective cation conductance to delayed afterdepolarizations (DAD) were examined. Nonselective cation channels were absent in canine M cells, since inhibition of I NaCa and I Cl(Ca)eliminated all calcium-activated currents without abolishing cell shortening. After the cells were treated with isoproterenol and ouabain to increase calcium loading, I NaCa was 168 ± 30 × 10−3 pC/pF and I Cl(Ca) was 114 ± 24 × 10−3pC/pF. Transient overlapping inward and outward currents were evoked positive to the chloride reversal potential ( E Cl). Outward current was chloride sensitive, and inward current was blocked by replacement of external sodium with lithium. When E Cl was −50 mV, triggered activity occurred in normal external sodium and persisted after inhibition of I NaCa. Steps to −80 mV revealed oscillating inward currents in normal sodium and chloride, which persisted after inhibition of I NaCa. When E Cl was equal to −113 mV, I Cl(Ca) opposed I NaCa at the resting potential. DAD occurred in normal sodium, and inhibition of outward I Cl(Ca)provoked triggered activity. We conclude that I NaCa represents ∼60% of the total calcium-activated current at resting potentials but that both I NaCa and I Cl(Ca) work in concert to cause DAD in calcium-overloaded cells.


2020 ◽  
Author(s):  
Abdesslam Chrachri

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.


1980 ◽  
Vol 88 (1) ◽  
pp. 293-304 ◽  
Author(s):  
YOUKO SATOW ◽  
CHING KUNG

Late K-outward currents upon membrane depolarization were recorded in Paramecium tetraurelia under a voltage clamp. A Ca-induced K-outward component is demonstrated by subtracting the value of the outward current in a pawn A mutant lacking functional Ca-channels (pwA500). The Ca-induced K-outward current activates slowly, reaching a peak after 100 to 1000 ms. The current then remains steady or reaches the steady state after a decline of several seconds. EGTA2- injection experiments show that the Ca-induced K-outward current is dependent on the internal Ca2+ concentration. The current is shown to depend on the voltage-dependent Ca conductance, by study of the leaky pawn A mutant (pwA132), which has a lowered Ca conductance as well as a lowered Ca-induced K-current. The Ca-induced GK is thus indirectly dependent on the voltage. The maximal GK is about 40 nmho/cell at + 7 mV in 4 mM-K+. The Ca-induced K current is sustained throughout the prolonged depolarization and the prolonged ciliary reversal.


2020 ◽  
Vol 21 (14) ◽  
pp. 4876
Author(s):  
Zbigniew Burdach ◽  
Agnieszka Siemieniuk ◽  
Waldemar Karcz

In contrast to the well-studied effect of auxin on the plasma membrane K+ channel activity, little is known about the role of this hormone in regulating the vacuolar K+ channels. Here, the patch-clamp technique was used to investigate the effect of auxin (IAA) on the fast-activating vacuolar (FV) channels. It was found that the macroscopic currents displayed instantaneous currents, which at the positive potentials were about three-fold greater compared to the one at the negative potentials. When auxin was added to the bath solution at a final concentration of 1 µM, it increased the outward currents by about 60%, but did not change the inward currents. The imposition of a ten-fold vacuole-to-cytosol KCl gradient stimulated the efflux of K+ from the vacuole into the cytosol and reduced the K+ current in the opposite direction. The addition of IAA to the bath solution with the 10/100 KCl gradient decreased the outward current and increased the inward current. Luminal auxin reduced both the outward and inward current by approximately 25% compared to the control. The single channel recordings demonstrated that cytosolic auxin changed the open probability of the FV channels at the positive voltages to a moderate extent, while it significantly increased the amplitudes of the single channel outward currents and the number of open channels. At the positive voltages, auxin did not change the unitary conductance of the single channels. We suggest that auxin regulates the activity of the fast-activating vacuolar (FV) channels, thereby causing changes of the K+ fluxes across the vacuolar membrane. This mechanism might serve to tightly adjust the volume of the vacuole during plant cell expansion.


2006 ◽  
Vol 96 (5) ◽  
pp. 2189-2199 ◽  
Author(s):  
J. H. Sun ◽  
B. Yang ◽  
D. F. Donnelly ◽  
C. Ma ◽  
R. H. LaMotte

Previous experimental results from our laboratory demonstrated that monocyte chemoattractant protein-1 (MCP-1) depolarizes or increases the excitability of nociceptive neurons in the intact dorsal root ganglion (DRG) after a chronic compression of the DRG (CCD), an injury that upregulates neuronal expression of both MCP-1 and mRNA for its receptor CCR2. We presently explore the ionic mechanisms underlying the excitatory effects of MCP-1. MCP-1 (100 nM) was applied, after CCD, to acutely dissociated small DRG neurons with nociceptive properties. Under current clamp, the proportion of neurons depolarized was similar to that previously observed for CCD-treated neurons in the intact ganglion, although the magnitude of depolarization was greater. MCP-1 induced a decrease in rheobase by 44 ± 10% and some cells became spontaneously active at resting potential. Action potential width at a voltage equal to 10% of the peak height was increased from 4.94 ± 0.23 to 5.90 ± 0.47 ms. In voltage clamp, MCP-1 induced an inward current in 27 of 50 neurons held at −60 mV, which increased with concentration over the range of 3 to 300 nM (EC50= 45 nM). The MCP-1–induced current was not voltage dependent and had an estimated reversal potential of −27 mV. In addition, MCP-1 inhibited a voltage-dependent, noninactivating outward current, presumably a delayed rectifier type K+conductance. We conclude that MCP-1 enhances excitability in CCD neurons by, at least, two mechanisms: 1) activation of a nonvoltage-dependent depolarizing current with characteristics similar to a nonselective cation conductance and 2) inhibition of a voltage-dependent outward current.


Sign in / Sign up

Export Citation Format

Share Document