scholarly journals Dopamine as a Neuroactive Substance in the Jellyfish Polyorchis Penicillatus

1991 ◽  
Vol 156 (1) ◽  
pp. 433-451
Author(s):  
JUN-MO CHUNG ◽  
ANDREW N. SPENCER
Keyword(s):  
Motor Neurons ◽  
Reversal Potential ◽  
Inhibitory Effect ◽  
Cellular Level ◽  
Potassium Ions ◽  
Current Clamp ◽  
Polyorchis Penicillatus ◽  
Outward Currents ◽  
Neuroactive Substance ◽  
Current Clamp Mode

Recent studies have shown that nerve-rich tissues in the margin of Polyorchis penicillatus (Eschscholtz), one of the hydromedusae, contain dopamine. The present experiments were conducted to determine the physiological action of dopamine at the cellular level. In the current-clamp mode, dopamine, ranging from 10−8 to 10−3moll−1, applied to cultured swimming motor neurons of this jellyfish produced hyperpolarizations accompanied by a decrease of firing rate or complete inhibition of spiking produced by anodal break excitation. Dopamine in the voltage-clamp mode elicited outward currents at more positive levels than −55 mV, which is the reversal potential of the response. The results of a series of ionic experiments suggest that the inhibitory effect of dopamine is caused by an increased permeability to potassium ions.

Modulation of Jellyfish Potassium Channels by External Potassium Ions

1999 ◽  
Vol 82 (4) ◽  
pp. 1728-1739 ◽  
Author(s):  
Nikita G. Grigoriev ◽  
J. David Spafford ◽  
Andrew N. Spencer
Keyword(s):  
Potassium Channels ◽  
Motor Neurons ◽  
Fruit Fly ◽  
Site Directed Mutagenesis ◽  
High Threshold ◽  
Extracellular Potassium ◽  
Potassium Ions ◽  
Polyorchis Penicillatus ◽  
State Dependent ◽  
Inactivation Mechanism

The amplitude of an A-like potassium current ( I Kfast) in identified cultured motor neurons isolated from the jellyfish Polyorchis penicillatus was found to be strongly modulated by extracellular potassium ([K+]out). When expressed in Xenopus oocytes, two jellyfish Shaker-like genes, jShak1 and jShak2, coding for potassium channels, exhibited similar modulation by [K+]out over a range of concentrations from 0 to 100 mM. jShak2-encoded channels also showed a decreased rate of inactivation and an increased rate of recovery from inactivation at high [K+]out. Using site-directed mutagenesis we show that inactivation of jShak2 can be ascribed to an unusual combination of a weak “implicit” N-type inactivation mechanism and a strong, fast, potassium-sensitive C-type mechanism. Interaction between the two forms of inactivation is responsible for the potassium dependence of cumulative inactivation. Inactivation of jShak1 was determined primarily by a strong “ball and chain” mechanism similar to fruit fly Shaker channels. Experiments using fast perfusion of outside-out patches with jShak2 channels were used to establish that the effects of [K+]out on the peak current amplitude and inactivation were due to processes occurring at either different sites located at the external channel mouth with different retention times for potassium ions, or at the same site(s) where retention time is determined by state-dependent conformations of the channel protein. The possible physiological implications of potassium sensitivity of high-threshold potassium A-like currents is discussed.

scholarly journals A Comparative Voltage and Current-Clamp Analysis of Feedback and Feedforward Synaptic Transmission in the Striatal Microcircuit In Vitro

2006 ◽  
Vol 95 (2) ◽  
pp. 737-752 ◽  
Author(s):  
Nicholas Gustafson ◽  
Elakkat Gireesh-Dharmaraj ◽  
Uwe Czubayko ◽  
Kim T. Blackwell ◽  
Dietmar Plenz
Keyword(s):  
Reversal Potential ◽  
Current Clamp ◽  
Movement Initiation ◽  
Gramicidin D ◽  
Current Clamp Mode ◽  
State Potential ◽  
Fast Spiking ◽  
Cortical Inputs ◽  
Time Critical

Striatal spiny projection (SP) neurons control movement initiation by integrating cortical inputs and inhibiting basal ganglia outputs. Central to this control lies a “microcircuit” that consists of a feedback pathway formed by axon collaterals between GABAergic SP neurons and a feedforward pathway from fast spiking (FS) GABAergic interneurons to SP neurons. Here, somatically evoked postsynaptic potentials (PSPs) and currents (PSCs) were compared for both pathways with dual whole cell patch recording in voltage- and current-clamp mode using cortex-striatum-substantia nigra organotypic cultures. On average, feedforward inputs were 1 ms earlier, more reliable, and about twice as large in amplitude compared with most feedback inputs. On the other hand, both pathways exhibited widely varying, partially overlapping amplitude distributions. This variability was already established for single FS neurons targeting many SP neurons. In response to precisely timed action potential bursts, feedforward and feedback inputs consistently showed short-term depression ≤50–70% in voltage-clamp, although feedback inputs also displayed strong augmentation in current-clamp in line with previous reports. The augmentation of feedback inputs was absent in gramicidin D perforated-patch recording, which also showed the natural reversal potential for both inputs to be near firing threshold. Preceding depolarizing feedback inputs during the down state did not consistently change subsequent postsynaptic action potentials. We conclude that feedback and feedforward inputs have their dominant effect during the up-state. The reversal potential close to the up-state potential, which supports shunting operation with millisecond precision and the strong synaptic depression, should enable both pathways to carry time-critical information.

Outward currents in heart motor neurons of the medicinal leech

1995 ◽  
Vol 74 (6) ◽  
pp. 2524-2537 ◽  
Author(s):  
C. A. Opdyke ◽  
R. L. Calabrese
Keyword(s):  
Voltage Clamp ◽  
Motor Neurons ◽  
Reversal Potential ◽  
Input Resistance ◽  
Medicinal Leech ◽  
Transient Current ◽  
Bathing Solution ◽  
Outward Currents ◽  
Maximal Activation ◽  
Electrode Voltage

1. Outward currents were studied in isolation in heart motor neurons in the medicinal leech, using the single-electrode voltage-clamp technique. The currents were divided into four distinct types on the basis of their time and voltage characteristics and sensitivity to external Ca2+ concentration. 2. The four types were a fast transient current, IKA; a slow transient current. IK1; a noninactivating current, IK2, all measured in a bathing solution in which Co2+ was substituted for Ca2+; and a calcium-sensitive current. IK1Cal which was revealed in a bathing solution containing normal levels of Ca2+. 3. The outward currents in heart motor neurons studied in different ganglia possessed differences of quality. For example, heart motor neurons from ganglia 3 or 4 had significantly less IK2 and IK1 than neurons recorded from more posterior ganglia. Heart motor neurons from ganglion 3 often had little or no IK1. Soma input resistance, electrotonic length, and soma capacitance measured in heart motor neurons from both anterior and posterior ganglia exhibited no significant differences. 4. IKA started to activate near -45 mV with half-maximal activation at about -20 mV and was fully inactivated by 0 mV: IK1 started to activate near -45 mV with half-maximal activation at about -10 mV and was not fully inactivated by 0 mV; IK2 started to activate near -50 mV; IK1Cal started to activate near -35 mV. The time constant of removal of inactivation for IKA was 25 ms, measured at -80 mV, and that for IK1 was 380 ms, measured at -40 mV. 5. Tetraethylammonium acetate (TEA) allowed to diffuse from the inside of the recording microelectrode effectively blocked IKA, IK1, and IK2. Bath-applied TEA (25 mM) acted similarly but was less effective, particularly at blocking Ik2. Bath-applied 4-aminopyridine effectively blocked the transient currents IKA and IK1. A reversal potential of -65 mV was found for the outward currents, corresponding to a mix of IK1 and IK2.

A new inhibitory pathway in the jellyfish Polyorchis penicillatus

2012 ◽  
Vol 90 (2) ◽  
pp. 172-181 ◽  
Author(s):  
G.O. Mackie ◽  
R.W. Meech ◽  
A.N. Spencer
Keyword(s):  
Motor Neurons ◽  
Stimulus Frequency ◽  
Reversal Potential ◽  
Potassium Acetate ◽  
Inhibitory Synapses ◽  
Polyorchis Penicillatus ◽  
Inhibitory Postsynaptic Potentials ◽  
Conduction Pathway ◽  
Ring Canals ◽  
Electrical Impulses

Contact of food with the manubrial lips in the genus Polyorchis A. Agassiz, 1862 evokes trains of electrical impulses (E potentials) that propagate to the margin. E potentials are also produced by food stimuli at the margin and tentacle bases. E potentials are shown to be associated with inhibitory postsynaptic potentials (ipsps) in the swimming motor neurons and contribute to the arrest of swimming during feeding. The conduction pathway for E potentials is a nerve plexus located in the endodermal walls of the stomach and radial and ring canals. We have explored the conducting properties of the system; the conduction velocity varies with stimulus frequency but is about 15 cm/s when stimuli are more than 50 s apart. Neurites belonging to the E system run around the margin adjacent to the inner nerve ring, where the swimming pacemaker neurons are located. We suggest that they may make inhibitory synapses on to the swimming motor neurons, but this has yet to be demonstrated anatomically. The reversal potential for ipsps, recorded intracellularly with potassium acetate micropipettes, was estimated to be about –69 mV. Swimming inhibition mediated by this endodermal pathway is distinct from that observed during protective “crumpling” behaviour and that associated with contractions of the radial muscles seen during feeding, though it may accompany the latter.

Ca2+ sparks and BK currents in gallbladder myocytes: role in CCK-induced response

2002 ◽  
Vol 282 (1) ◽  
pp. G165-G174 ◽  
Author(s):  
María J. Pozo ◽  
Guillermo J. Pérez ◽  
Mark T. Nelson ◽  
Gary M. Mawe
Keyword(s):  
Smooth Muscle ◽  
Ryanodine Receptor ◽  
Outward Current ◽  
Bk Channels ◽  
Transient Outward Current ◽  
Induced Response ◽  
Current Clamp ◽  
Current Activity ◽  
Outward Currents ◽  
Current Clamp Mode

We sought to elucidate the regulation of gallbladder smooth muscle (GBSM) excitability by localized Ca2+ release events (sparks) and large-conductance Ca2+-dependent (BK) channels by determining whether sparks exist in GBSM and, if so, whether they activate BK channels. Sparks were identified in isolated GBSM loaded with fluo 4. Each spark was associated with a transient outward current, suggesting communication of ryanodine receptor (RyR) channels with BK channels. This was confirmed by the inhibition of outward currents with iberiotoxin (100 nM), thapsigargin (200 nM), and ryanodine (10 μM). In current clamp mode, the transient BK currents were associated with brief membrane hyperpolarizations (10.9 ± 1.3 mV). Because transient BK currents could dampen GBSM excitability, we tested whether CCK attenuates these events. CCK (10 nM) reduced the amplitude and frequency of transient BK currents, and subsequent caffeine application restored transient BK current activity. These results support the concept that RyRs and BK channels contribute to the regulation of GBSM excitability and that CCK can act in part by inhibiting this pathway.

scholarly journals Activation of Slo2.1 channels by niflumic acid

2010 ◽  
Vol 135 (3) ◽  
pp. 275-295 ◽  
Author(s):  
Li Dai ◽  
Vivek Garg ◽  
Michael C. Sanguinetti
Keyword(s):  
Voltage Dependence ◽  
Reversal Potential ◽  
Niflumic Acid ◽  
Flufenamic Acid ◽  
Channel Activation ◽  
Outward Currents ◽  
Transmembrane Voltage ◽  
High K ◽  
Charged Residues ◽  
K Current

Slo2.1 channels conduct an outwardly rectifying K+ current when activated by high [Na+]i. Here, we show that gating of these channels can also be activated by fenamates such as niflumic acid (NFA), even in the absence of intracellular Na+. In Xenopus oocytes injected with <10 ng cRNA, heterologously expressed human Slo2.1 current was negligible, but rapidly activated by extracellular application of NFA (EC50 = 2.1 mM) or flufenamic acid (EC50 = 1.4 mM). Slo2.1 channels activated by 1 mM NFA exhibited weak voltage dependence. In high [K+]e, the conductance–voltage (G-V) relationship had a V1/2 of +95 mV and an effective valence, z, of 0.48 e. Higher concentrations of NFA shifted V1/2 to more negative potentials (EC50 = 2.1 mM) and increased the minimum value of G/Gmax (EC50 = 2.4 mM); at 6 mM NFA, Slo2.1 channel activation was voltage independent. In contrast, V1/2 of the G-V relationship was shifted to more positive potentials when [K+]e was elevated from 1 to 300 mM (EC50 = 21.2 mM). The slope conductance measured at the reversal potential exhibited the same [K+]e dependency (EC50 = 23.5 mM). Conductance was also [Na+]e dependent. Outward currents were reduced when Na+ was replaced with choline or mannitol, but unaffected by substitution with Rb+ or Li+. Neutralization of charged residues in the S1–S4 domains did not appreciably alter the voltage dependence of Slo2.1 activation. Thus, the weak voltage dependence of Slo2.1 channel activation is independent of charged residues in the S1–S4 segments. In contrast, mutation of R190 located in the adjacent S4–S5 linker to a neutral (Ala or Gln) or acidic (Glu) residue induced constitutive channel activity that was reduced by high [K+]e. Collectively, these findings indicate that Slo2.1 channel gating is modulated by [K+]e and [Na+]e, and that NFA uncouples channel activation from its modulation by transmembrane voltage and intracellular Na+.

Cholecystokinin-gated currents in neurons of the rat solitary complex in vitro

1993 ◽  
Vol 70 (6) ◽  
pp. 2584-2595 ◽  
Author(s):  
P. Branchereau ◽  
J. Champagnat ◽  
M. Denavit-Saubie
Keyword(s):  
Voltage Clamp ◽  
Potassium Current ◽  
Reversal Potential ◽  
Input Resistance ◽  
Calcium Currents ◽  
Equilibrium Potential ◽  
Potassium Ions ◽  
Nernst Equation ◽  
Membrane Hyperpolarization ◽  
Cckb Receptor

1. Ionic conductances controlled by type A and type B cholecystokinin (CCK) receptors were studied in neurons of the rat nucleus tractus solitarius (NTS) and dorsal motor nucleus of the vagus (DMNV), using intracellular and whole-cell patch clamp recordings in current or voltage clamp configuration during bath application of agonists (CCK8, CCK4, BC 264) and antagonists. 2. CCKA receptor-related inhibition was associated with a membrane hyperpolarization and a decrease in input resistance that developed 2-6 min after the arrival of drug into the extracellular medium. These effects were induced by 5 nM CCK8 but not BC 264 and they were blocked by the CCKA antagonist, L-364,718, but not by the CCKB antagonist, L-365,260. 3. CCKA receptor-related inhibition was generated by a potassium current that reversed at a reversal potential E(rev) of -73 +/- 1 (mean +/- SE) mV with bathing potassium concentration [K+]o = 6 mM and at -88 +/- 1 with [K+]o = 3 mM, in agreement with the Nernst equation for potassium ions. 4. CCKB receptor-related excitation was associated with a membrane depolarization and an increase of the input resistance induced by the following agonists at threshold concentrations: CCK8 (0.2 nM) > or = BC 264 (0.4 nM) > CCK4 (10.9 nM). The increase of input resistance was abolished by L-365,260 and was maintained after blockade of the CCKA current by L-364,718. 5. CCKB receptor-related excitation, in the neurons (30% of cases) in which clear response reversal was observed, appeared to be generated by a decrease of a potassium conductance. Responses showed a reversal potential E(rev) of -68 +/- 4 mV with [K+]o = 6 mM and -89 +/- 1 mV with [K+]o = 3 mM, verifying predictions from the Nernst equation applied to potassium ions. However, in 70% of cases, clear reversal was not observed at membrane potentials negative to the theoretical potassium equilibrium potential EK. 6. In voltage clamp studies, CCK8 induced a 181 +/- 17 pA inward current associated with a 26 +/- 4% decrease in the instantaneous current (I(ins)) generated by hyperpolarizing voltage steps. This effect on I(ins) was demonstrated in the absence of effects on the outward noninactivating potassium current (IM) and on the inward noninactivating cationic current (IQ). 7. CCKB receptor-mediated excitation was not suppressed by cobalt, a blocker of calcium currents, and was not associated with a change of the calcium-dependent potassium current (IK(Ca)).(ABSTRACT TRUNCATED AT 400 WORDS)

Lysophosphatidic acid, serum, and hyposmolarity activate Cl- currents in corneal keratocytes

1995 ◽  
Vol 269 (6) ◽  
pp. C1385-C1393 ◽  
Author(s):  
M. A. Watsky
Keyword(s):  
Lysophosphatidic Acid ◽  
Reversal Potential ◽  
Flufenamic Acid ◽  
Disulfonic Acid ◽  
Hypotonic Stress ◽  
Outward Currents ◽  
Fetal Bovine ◽  
Patch Technique ◽  
Corneal Keratocytes ◽  
In Cells

The influence of serum, lysophosphatidic acid (LPA), and hyposmotic stress on the ion channel activity of normal and cryo-injured rabbit corneal keratocytes was investigated. Whole cell currents were examined using the amphotericin perforated-patch technique. In cells from wounded corneas, fetal bovine serum activated large, holding voltage-insensitive, fast-activating, 4,4'-diisothiocyanostilbene-2,2'-disulfonic acid (DIDS)-, flufenamic acid-, and 5-nitro-2-(3-phenylpropylamino)benzoic acid (NPPB)-blockable outward currents showing inactivation at depolarized voltages. LPA activated identical currents, also only in cells from wounded corneas. Blocker and reversal potential experiments characterized the current as a Cl- currents (Icl). Lysophosphatidylcholine (10 microM) failed to activate the current. An identical current was activated by hyposmotic stimulation in cells from control and wounded corneas. Hyposmotic stimulation also activated Icl in cells from wounded corneas that were unresponsive to LPA. We conclude that serum, LPA, and hypotonic stress activate Icl in keratocytes from wounded corneas. We also conclude that LPA is a serum factor that can activate Icl and that hyposmotic activation may work through a signaling pathway separate from that of LPA.

Aplysia ink release: central locus for selective sensitivity to long-duration stimuli

1979 ◽  
Vol 42 (5) ◽  
pp. 1223-1232 ◽  
Author(s):  
E. Shapiro ◽  
J. Koester ◽  
J. H. Byrne
Keyword(s):  
Motor Neuron ◽  
Spike Train ◽  
Motor Neurons ◽  
Neural Circuit ◽  
Reversal Potential ◽  
Secretory Process ◽  
Neuron Activity ◽  
Long Duration ◽  
Noxious Stimuli ◽  
Selective Sensitivity

1. A behavioral and electrophysiological analysis of defensive ink release in Aplysia californica was performed to examine the response of this behavior and its underlying neural circuit to various-duration noxious stimuli. 2. Three separate behavioral protocols were employed using electrical shocks to the head as noxious stimuli to elicit ink release. Ink release was found to be selectively responsive to longer duration stimuli, and to increase in a steeply graded fashion as duration is increased. 3. Intracellular stimulation of ink motor neurons revealed that ink release is a linear function of motor neuron spike train duration, indicating that the selective sensitivity of the behavior to long-duration stimuli is not due to a nonlinearity in the glandular secretory process. 4. In contrast, electrophysiological examination of ink motor neuron activity in response to sustained head shock revealed an accelerating spike train. During the later part of the spike train, compound excitatory synaptic potentials show a positive shift in reversal potential. 5. Our results suggest a central locus for the mechanisms that determine sensitivity of inking behavior to stimulus duration. 6. In contrast to ink release, defensive gill withdrawal was found to be extremely sensitive to short-duration stimuli.

scholarly journals Studies on the interaction of growth regulators with potassium ions in some physiological processes in bean (Phaseolus vulgaris L.). III The effect of growth regulators on growth, chlorophyll level and transpiration depending on potassium concentration

2014 ◽  
Vol 55 (4) ◽  
pp. 577-588
Author(s):  
Jadwiga Stopińska
Keyword(s):  
Growth Regulators ◽  
Potassium Concentration ◽  
Leaf Growth ◽  
Inhibitory Effect ◽  
Physiological Effect ◽  
Potassium Ions ◽  
Phaseolus Vulgaris L ◽  
Physiological Processes ◽  
Bean Plants ◽  
Chlorophyll Level

Leaf growth and chlorophyll level in GA<sub>3</sub>-treated bean, and leaf growth and transpiration intensity in ABA-treated bean plants were studied at two potassium concentrations in the medium (1 and 3 mM KNO<sub>3</sub>). The plants were grown on Hoagland's solution and growth regulators were applied to the shoot growth apexes. Both GA<sub>3</sub> and K<sup>+</sup> ions were found to stimulate growth of primary leaves and increase their potassium amount. GA<sub>3</sub> contrary to K<sup>+</sup> slightly decreased the potassium content in leaves Both factors reduced the chlorophyll content but did not affect the total chlorophyll amount in these organs Interaction between GA<sub>3</sub> and K<sup>+</sup> ions was of additive nature. The effect of ABA and K<sup>+</sup> ions on growth of both kinds of leaves and on the amount and content of potassium in them were antagonistic. The inhibitory effect of the hormone was stronger at higher potassium concentration in the medium. Either factor reduced transpiration intensity in leaves, however, the inhibitory effect of the growth regulator was stronger at lower potassium concentration. The potassium level modified both the physiological effect of the regulators and the sensitivity of bean particularly to ABA.

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