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.

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.

Electrophysiological evidence from glutamate microapplications for local excitatory circuits in the CA1 area of rat hippocampal slices

1988 ◽  
Vol 59 (1) ◽  
pp. 110-123 ◽  
Author(s):  
E. P. Christian ◽  
F. E. Dudek
Keyword(s):  
Hippocampal Neurons ◽  
Hippocampal Slices ◽  
Pyramidal Cells ◽  
Inhibitory Synapses ◽  
Excitatory Synapses ◽  
Recording Site ◽  
Postsynaptic Potentials ◽  
Inhibitory Postsynaptic Potentials ◽  
Ca1 Area ◽  
Transverse Slice

1. Evidence for local excitatory synaptic connections in CA1 of the rat hippocampus was obtained by recording excitatory postsynaptic potentials (EPSPs) intracellularly from pyramidal cells during local microapplications of glutamate. 2. Experiments were performed in hippocampal slices cut parallel to (transverse slice) or perpendicular to (longitudinal slice) alvear fibers. In normal solutions, glutamate microdrops (10–20 mM, 10–20 micron diam) applied in CA1 within 400 micron of recorded cells sometimes increased the frequency of inhibitory postsynaptic potentials for 5–10 s in both transverse and longitudinal slices. Increases in EPSP frequency were also occasionally observed, but only in transverse slices. Tetrodotoxin (1 microgram/ml) blocked glutamate-induced increases in PSP frequency, thus indicating that they were not caused by subthreshold effects on presynaptic terminals. Increases in PSP frequency were interpreted to result from glutamate activation of hippocampal neurons with inhibitory and excitatory connections to recorded neurons. 3. In both slice orientations, local excitatory circuits were studied in more isolated conditions by surgically separating CA1 from CA3 (transverse slices) and by blocking GABAergic inhibitory synapses with picrotoxin (5–10 microM). Microdrops were systematically applied at 200 and 400 micron on each side of the recording site. Significant glutamate-induced increases in EPSP frequency were observed in neurons from both slice orientations to microdrops in at least one of the locations. This provided evidence that excitatory synapses are present in both transverse and longitudinal slices. 4. Substantial increases in EPSP frequency only occurred in neurons from longitudinal slices when glutamate was microapplied 200 micron or less from the recording site. In transverse slices, however, large increases in EPSP frequency were observed to glutamate microapplications at 200 or 400 micron. These data suggest that CA1 local excitatory connections project for longer distances in the transverse than in the longitudinal plane of section. 5. Increases in EPSP frequency, averaged across cells, did not differ significantly in the four microapplication sites in either transverse or longitudinal slices. Thus local excitation in CA1 does not appear to be asymmetrically arranged in the way suggested for CA3. 6. The densities of local excitatory circuits in CA1 versus CA3 were studied by quantitatively comparing glutamate-induced increases in EPSP frequency.(ABSTRACT TRUNCATED AT 400 WORDS)

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.

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.

Synaptic integrative properties at hyperbaric pressure

1988 ◽  
Vol 60 (4) ◽  
pp. 1497-1512 ◽  
Author(s):  
Y. Grossman ◽  
J. J. Kendig
Keyword(s):  
Synaptic Transmission ◽  
Motor Neurons ◽  
Repetitive Stimulation ◽  
Inhibitory Synapses ◽  
Synaptic Connections ◽  
Paired Pulse ◽  
Inhibitory Transmission ◽  
Inhibitory Synaptic Transmission ◽  
Hyperbaric Pressure ◽  
Per Se

1. Because hyperbaric pressure profoundly depresses excitatory synaptic transmission, it has proved difficult to account for its excitatory effects in the CNS. We tested the hypothesis that hyperbaric pressure might increase excitation by enhancing facilitation and potentiation during repetitive synaptic activation, and/or by selectively depressing inhibitory synaptic transmission. Intracellular microelectrode recordings were obtained from crustacean muscle fibers innervated by single identifiable excitor and inhibitor motor neurons; the preparations were exposed to pressures of 0.1-10.1 MPa. 2. Hyperbaric pressure reduced the amplitude of the singly evoked excitatory junctional potential (EJP), enhanced paired-pulse facilitation, and increased the potentiation elicited by trains of stimuli. The potentiated EJP at 10.1 MPa approached the comparable response evoked at normobaric pressure. 3. Hyperbaric pressure also depressed inhibitory synaptic transmission, measured as depression of the EJP by the inhibitor motor neuron. However, pressure depressed excitatory and inhibitory synaptic transmission to the same extent. Thus there appears to be no selective effect of pressure on the GABA-activated chloride channel. The amplitude of the inhibited EJP at 10.1 MPa remained below that at normobaric pressure, even during repetitive stimulation. 4. The results do not support the hypothesis that pressure increases central excitation by selectively depressing inhibitory transmission per se; enhancement of potentiation, however, probably plays an important role. In this preparation, in which inhibitory transmission also displays facilitation, pressure did not increase overall excitation or alter the balance between excitation and inhibition. 5. These results predict that a pressure-excitable network should encompass excitatory synaptic connections which exhibit pronounced facilitation and inhibitory synapses with little or no facilitation.

Voltage-activated potassium currents in isolated motor neurons from the jellyfish Polyorchis penicillatus

1994 ◽  
Vol 72 (2) ◽  
pp. 1010-1019 ◽  
Author(s):  
J. Przysiezniak ◽  
A. N. Spencer
Keyword(s):  
Motor Neurons ◽  
Action Potentials ◽  
Voltage Dependence ◽  
Primary Cultures ◽  
Potassium Currents ◽  
Whole Cell ◽  
Time To Peak ◽  
Polyorchis Penicillatus ◽  
Slow Onset

1. We describe two voltage-activated potassium currents in the swim motor neurons (SMNs) of the hydrozoan jellyfish, Polyorchis penicillatus. Recordings from neurons isolated in primary cultures were made using the tight-seal, whole-cell technique. 2. One current, IK-fast, turned on rapidly (time to peak = 6–15 ms), was half-activated at -10 to 0 mV, decayed with two exponential phases (tau were approximately 70 ms and approximately 1 s), and was half-inactivated by prepulses around -53 mV. It likely plays an important role in regulating the duration of SMN action potentials. IK-fast has features shared by delayed rectifiers and A-like currents in other invertebrates and vertebrates. 3. Another current, IK-slow, elicited from a holding potential of -30 mV, exhibited a slow onset (tau = 65–250 ms), was half-activated approximately +24 mV, exhibited a shallower voltage dependence than IK-fast, and did not inactivate. It was slower than most known delayed rectifiers.

Studies on hexactinellid sponges. II. Excitability, conduction and coordination of responses in rhabdocalyptus dawsoni (lambe, 1873)

1983 ◽  
Vol 301 (1107) ◽  
pp. 401-418 ◽  
Keyword(s):  
Electrical Stimulation ◽  
Refractory Period ◽  
Conduction System ◽  
Conduction Time ◽  
Pumping Power ◽  
Chemical Signalling ◽  
Conduction Pathway ◽  
Electrical Impulses ◽  
Effector Response ◽  
Hexactinellid Sponges

Rhabdocalyptus can arrest its feeding current. The response is initiated by mechanical or electrical stimulation, and is coordinated through the sponge by a conduction system, having a precise excitability threshold and conducting on an all-or-none basis. All parts are excitable and conduct. Individuals in colonial assemblages are coordinated. Spontaneous as well as evoked arrests are observed. There is evidence of scattered pacemaker sites. Conduction is diffuse and unpolarized, and occurs with a velocity of 0.26 ± 0.07 cm s -1 at 11 °C. The conduction system is probably the trabecular syncytium. Isolated dermal membrane (‘pure’ trabecular tissue, without flagella or contractile elements) conducts. Mechanical and chemical signalling mechanisms are discussed. It is concluded that they cannot account for the phenomena observed, but that conduction must involve electrical impulses. The effectors responsible for current arrests are almost certainly the flagella of the flagellated chambers. It is assumed that they stop beating on receiving an arrest signal through the conduction pathway. The waveforms of arrests recorded with a thermistor flowmeter are best interpreted in terms of sudden, all-or-none cessation of pumping, with slow, gradual recovery of full pumping power. The flagella probably beat feebly at first on becoming active again following an arrest. The effector response shows a refractory period of 30 s. Responses occur with short latency. Delays are attributable to conduction time. The system is fatigueable. Numerous parallels exist with the behaviour of the stigmatal cilia in the ascidian branchial sac, both in the characteristics of the effector response and in the mechanism of coordination.

scholarly journals Probing the structure of the conduction pathway of the sheep cardiac sarcoplasmic reticulum calcium-release channel with permeant and impermeant organic cations.

1993 ◽  
Vol 102 (6) ◽  
pp. 1107-1129 ◽  
Author(s):  
A Tinker ◽  
A J Williams
Keyword(s):  
Sarcoplasmic Reticulum ◽  
Relative Permeability ◽  
Single Channel ◽  
Reversal Potential ◽  
Organic Cations ◽  
Rate Theory ◽  
Calcium Release Channel ◽  
Release Channel ◽  
Cardiac Sarcoplasmic Reticulum ◽  
Conduction Pathway

The sarcoplasmic reticulum Ca(2+)-release channel plays a central role in cardiac muscle function by providing a ligand-regulated pathway for the release of sequestered Ca2+ to initiate contraction following cell excitation. The efficiency of the channel as a Ca(2+)-release pathway will be influenced by both gating and conductance properties of the system. In the past we have investigated conduction and discrimination of inorganic mono- and divalent cations with the aim of describing the mechanisms governing ion handling in the channel (Tinker, A., A.R. G. Lindsay, and A.J. Williams. 1992. Journal of General Physiology. 100:495-517.). In the present study, we have used permeant and impermeant organic cations to provide additional information on structural features of the conduction pathway. The use of permeant organic cations in biological channels to explore structural motifs underlying selectivity has been an important tool for the electrophysiologist. We have examined the conduction properties of a series of monovalent organic cations of varying size in the purified sheep cardiac sarcoplasmic reticulum Ca(2+)-release channel. Relative permeability, determined from the reversal potential measured under bi-ionic conditions with 210-mM test cation at the cytoplasmic face of the channel and 210 mM K+ at the luminal, was related inversely to the minimum circular cation radius. The reversal potential was concentration-independent. The excluded area hypothesis, with and without a term for solute-wall friction, described the data well and gave a lower estimate for minimum pore radius of 3.3-3.5 A. Blocking studies with the impermeant charged derivative of triethylamine reveal that this narrowing occurs over the first 10-20% of the voltage drop when crossing from the lumen of the SR to the cytoplasm. Single-channel conductances were measured in symmetrical 210 mM salt. Factors other than relative permeability determine conductance as ions with similar relative permeability can have widely varying single-channel conductance. Permeant ions, such as the charged derivatives of trimethylamine and diethylmethylamine, can also inhibit K+ current. The reduction in relative conductance with increasing concentrations of these two ions at a holding potential of 60 mV was described by a rectangular hyperbola and revealed higher affinity binding for diethylmethylamine as compared to trimethylamine. It was possible to describe the complex permeation properties of these two ions using a single-ion four barrier, three binding site Eyring rate theory model. In conclusion, these studies reveal that the cardiac Ca(2+)-release channel has a selectivity filter of approximately 3.5-A radius located at the luminal face of the protein.(ABSTRACT TRUNCATED AT 400 WORDS)

scholarly journals Locomotor deficits in ALS mice are paralleled by loss of V1-interneuron-connections onto fast motor neurons

2020 ◽  
Author(s):  
Ilary Allodi ◽  
Roser Montañana-Rosell ◽  
Raghavendra Selvan ◽  
Peter Löw ◽  
Ole Kiehn
Keyword(s):  
Motor Neuron ◽  
Motor Neurons ◽  
Inhibitory Synapses ◽  
Neuron Death ◽  
Spinal Interneurons ◽  
Pathway Interaction ◽  
Fast Twitch Muscle ◽  
Motor Neuron Death ◽  
Locomotor Deficits ◽  
Induced Changes

AbstractALS is characterized by progressive inability to execute movements. Motor neurons innervating fast-twitch muscle fibers exhibit preferential degeneration. The reason for differential vulnerability of fast motor neurons, and its consequence on motor output is not known. Here, we show that fast motor neurons receive more inhibitory synaptic inputs than slow motor neurons, and loss of inhibitory synapses onto fast motor neurons precedes disease progression in the SOD1G93A mouse model of ALS. Loss of inhibitory synapses on fast motor neurons is accounted for by a loss of synapses from inhibitory V1 spinal interneurons. Deficits in V1-motor neuron connectivity appear prior to motor neuron death and are paralleled by development of specific SOD1G93A locomotor deficits. These distinct SOD1G93A locomotor deficits are phenocopied by silencing of inhibitory V1 spinal interneurons in wild-type mice. Silencing inhibitory V1 spinal interneurons does not exacerbate SOD1G93A locomotor deficits, suggesting phenotypic pathway interaction. Our study identifies a potential cell non-autonomous source of motor neuronal vulnerability in ALS, and links ALS-induced changes in locomotor phenotypes to inhibitory V1 interneurons.

Inhibitory control of excitable dendrites in neocortex

1995 ◽  
Vol 74 (4) ◽  
pp. 1810-1814 ◽  
Author(s):  
H. G. Kim ◽  
M. Beierlein ◽  
B. W. Connors
Keyword(s):  
Pyramidal Cells ◽  
Inhibitory Synapses ◽  
Type I ◽  
Relative Timing ◽  
Inhibitory Postsynaptic Potentials ◽  
Glutamate Receptor Antagonists ◽  
Apical Dendrites ◽  
Whole Cell Recordings ◽  
Reversal Potentials ◽  
Stimulation Of

1. Many dendrites of pyramidal cells in mature neocortex express active Na+ and Ca2+ conductances. Dendrites are also the target of numerous inhibitory synapses. We examined the interactions between the intrinsic excitability of dendrites and synaptic inhibition using whole cell recordings from the apical dendrites of layer 5 pyramidal cells. Experiments were performed on slices of somatosensory cortex from mature rats. Slices were bathed in the glutamate receptor antagonists 2-amino-5-phosphonopentanoic acid and 6,7-dinitroquinoxaline-2,3-dione, and maintained at 32-36 degrees C. 2. In agreement with previous findings, intradendritic current injection evoked two distinct types of dendritic firing. Type I dendrites generated monophasic fast spikes, whereas type II dendrites showed more complex firing patterns, consisting of fast and slow spike components. 3. Stimulation of cortical layers 2/3 evoked fast inhibitory postsynaptic potentials (IPSPs) in all dendrites tested. IPSP reversal potentials were bimodally distributed, with means of about -53 and -85 mV when recorded with high-Cl(-)-concentration-filled electrodes. Interestingly, IPSP reversal potentials were correlated with the type of dendritic spiking pattern. 4. IPSPs were able to delay, completely block, or partially block spiking in dendrites, depending on the relative timing between inhibition and dendritic spiking. Slow, Ca(2+)-dependent spike components could be blocked selectively by IPSPs. Furthermore, inhibition could either phase advance or phase delay repetitive patterns of dendritic spiking, depending on the timing of the IPSP.

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