Preliminary observations on escape swimming and giant neurons in Aglantha digitale (Hydromedusae: Trachylina)

1980 ◽  
Vol 58 (4) ◽  
pp. 549-552 ◽  
Author(s):  
S. Donaldson ◽  
G. O. Mackie ◽  
A. Roberts
Keyword(s):  
Action Potentials ◽  
Giant Axon ◽  
Synaptic Delay ◽  
Giant Axons ◽  
A Value ◽  
Giant Synapses ◽  
Run Up

Aglantha can swim in two ways, one of which, fast swimming, is evoked by contact with predators and serves for escape. The response consists of two or three violent contractions of which the first propels the animal a distance equivalent to five body lengths. Peak velocities in the range 0.3–0.4 m s−1 were measured. Drag is reduced by contraction of the tentacles.Coordination of escape swimming and tentacle contraction is achieved by a system of giant axons. A giant axon runs down each tentacle; action potentials in these elements show a one-for-one correspondence with potentials recorded from a ring-shaped axon lying in the margin near the tentacle bases. The ring giant synapses with eight motor giants which run up the subumbrella innervating the swimming muscles.Conduction velocities in the giant axons may be as high as 4.0 m s−1 in the case of the largest (40 μm diameter) axons. A value of 1.6 ms was obtained for minimum synaptic delay between the ring and motor giant axons.

Microelectrode Study of the Resting and Action Potentials of the Cockroach Giant Axon with Special Reference to the Role Played by the Nerve Sheath

1967 ◽  
Vol 47 (2) ◽  
pp. 357-373
Author(s):  
Y. PICHON ◽  
J. BOISTEL
Keyword(s):  
Action Potential ◽  
Action Potentials ◽  
Maximum Rate ◽  
Diffusion Processes ◽  
Extracellular Fluid ◽  
Giant Axon ◽  
Resting Potential ◽  
Giant Axons ◽  
The Mean ◽  
Nerve Cords

1. The use of very fine-tipped and mechanically strong microelectrodes has allowed reliable recordings of resting and action potentials to be made in cockroach giant axons in sheathed and desheathed nerve cords. 2. When the microelectrode was withdrawn from a giant axon in an intact connective the first positive change in the potential from the resting level, was in most cases followed by a negative deflexion to the original zero level, the ‘sheath potential’. The values of this ‘sheath potential’ together with the resting potential, the action potential, the maximum rate of rise and maximum rate of fall of the action potential have been measured in three different salines. 3. In normal saline, resting potentials were lower in sheathed preparations (58·1 ± 55·4 mV.) than in desheathed ones (67·4 ± 6·2 mV.), whereas action potentials were higher in the former (103±5·9 mV.) than in the latter (85·9±4·6 mV.). 4. Elevation of K+ and Ca2+ concentrations in the saline to the haemolymph level resulted in a decrease of resting and action potentials in desheathed cords, to 57·3±5·3 mV. and 36·5±7·6 mV. respectively. No alterations in the membrane potentials were recorded in intact connectives bathed in this saline, the mean resting potential being 55·6±4·2 mV. and the mean action potential 107·9±6·0 mV. Local desheathing of the nerve cord led only to local disturbance of the resting and action potentials, thus indicating that diffusion processes along the extracellular spaces were very slow. 5. The use of a saline in which cation concentrations have been elevated to the extracellular level resulted in normal resting potentials (64·6±3·3 mV.) and action potentials (90·9±7·2 mV.) in desheathed cords, despite the relatively high potassium concentration (17·1 mM./l.). 6. Recordings of the maximum rates of rise and rates of fall showed that there was no significant modification in the shape of the action potential in these different experimental conditions. 7. The values of the ‘sheath potential’ were very variable from one impalement to another and it is suggested that this potential might be related to variations of the microelectrode tip potential bathed in different ionic solutions. 8. The low resting potentials and high action potentials of giant axons in intact nerve cords may result from an excess of inorganic cations in the extracellular fluid.

scholarly journals Central circuitry in the jellyfish Aglantha. II: The ring giant and carrier systems

1995 ◽  
Vol 198 (11) ◽  
pp. 2271-2278 ◽  
Author(s):  
G Mackie ◽  
R Meech
Keyword(s):  
Conduction Velocity ◽  
Action Potentials ◽  
Giant Axon ◽  
Nerve Ring ◽  
Carrier System ◽  
Close Collaboration ◽  
Giant Axons ◽  
Dense Fluid ◽  
Conduction Velocities ◽  
Carrier Systems

1. The ring giant axon in the outer nerve ring of the jellyfish Aglantha digitale is a multinucleate syncytium 85 % of which is occupied by an electron-dense fluid-filled vacuole apparently in a Gibbs­Donnan equilibrium with the surrounding band of cytoplasmic cortex. Micropipette recordings show small (-15 to -25 mV) and large (-62 to -66 mV) resting potentials. Low values, obtained with a high proportion of the micropipette penetrations, are assumed to be from the central vacuole; high values from the cytoplasmic cortex. Background electrical activity includes rhythmic oscillations and synaptic potentials representing hair cell input caused by vibration. 2. After the ring giant axon has been cut, propagating action potentials evoked by stimulation are conducted past the cut and re-enter the axon on the far side. The system responsible (the carrier system) through-conducts at a velocity approximately 25 % of that of the ring giant axon and is probably composed of small neurones running in parallel with it. Numerous small neurones are seen by electron microscopy, some making one-way and some two-way synapses with the ring giant. 3. Despite their different conduction velocities, the two systems normally appear to fire in synchrony and at the velocity of the ring giant axon. We suggest that, once initiated, ring giant spikes propagate rapidly around the margin, firing the carrier neurones through serial synapses and giving them, in effect, the same high conduction velocity. Initiation of ring giant spikes can, however, require input from the carrier system. The spikes are frequently seen to be mounted on slow positive potentials representing summed carrier postsynaptic potentials. 4. The carrier system fires one-for-one with the giant axons of the tentacles and may mediate impulse traffic between the latter and the ring giant axon. We suggest that the carrier system may also provide the pathways from the ring giant to the motor giant axons used in escape swimming. 5. The findings show that the ring giant axon functions in close collaboration with the carrier system, increasing the latter's effective conduction velocity, and that interactions with other neuronal sub-systems are probably mediated exclusively by the carrier system.

scholarly journals Withdrawal Reflex and Conduction Block in the Giant Axons of a Sabellid Worm (Pseudopotamilla Occelata)

1986 ◽  
Vol 126 (1) ◽  
pp. 433-444
Author(s):  
TAKASHIRO HIGUCHI ◽  
HIROYUKI NAKAMURA ◽  
KATSUHIKO SAWAUCHI ◽  
HIROSHI OKUMURA
Keyword(s):  
Action Potentials ◽  
Conduction Block ◽  
Giant Axon ◽  
The Body ◽  
Axon Membrane ◽  
Histological Studies ◽  
Giant Axons ◽  
Withdrawal Reflex ◽  
Anterior Half ◽  
Longitudinal Muscles

1. Body contraction in the sabellid worm, Pseudopotamilla occelata, during the rapid withdrawal reflex occurred only in the anterior half of the body. End-to-end shortening was never observed. The longitudinal muscles are well-developed in the anterior half, and poorly developed in the posterior half. 2. Conduction of action potentials along the giant axons was blocked at the midbody, and was responsible for the anteriorly restricted body contraction. 3. Electrophysiological and histological studies excluded the possibility that conduction block resulted from a safety factor attributable to the special geometry of the axons. 4. Current injection across the giant axon membrane in the region of the conduction block indicated that changes in the properties of the membrane were responsible for the conduction block.

scholarly journals THE FUNCTION OF THE PROXIMAL SYNAPSES OF THE SQUID STELLATE GANGLION

1959 ◽  
Vol 42 (3) ◽  
pp. 609-616 ◽  
Author(s):  
S. H. Bryant
Keyword(s):  
Synaptic Transmission ◽  
Intracellular Recording ◽  
Stellate Ganglion ◽  
Synaptic Delay ◽  
Postsynaptic Potentials ◽  
Giant Axons ◽  
Temporal Form ◽  
Giant Synapses ◽  
Spike Initiation ◽  
Giant Synapse

In the oxygenated excised squid (Loligo pealii) stellate ganglion preparation one can produce excitation of the stellar giant axons by stimulating the second largest (accessory fiber, Young, 1939) or other smaller preganglionic giant axons. Impulse transmission is believed to occur at the proximal synapses of the stellar giant axons rather than the distal (giant) synapses which are excited by the largest giant preaxon. Proximal synaptic transmission is more readily depressed by hypoxia and can be fatigued independently of, and with fewer impulses than, the giant synapses. Intracellular recording from the last stellar axon at its inflection in the ganglion reveals both proximal and distal excitatory postsynaptic potentials EPSP's). The synaptic delay, temporal form of the EPSP, and depolarization for spike initiation were similar for both synapses. If the proximal EPSP occurs shortly after excitation by the giant synapse it reduces the undershoot and adds to the falling phase of the spike. If it occurs later it can produce a second spike. Parallel results were obtained when the proximal EPSP's arrived earlier than the EPSP of the giant synapse. In fatigued preparations it was possible to sum distal and proximal or two proximal EPSP's and achieve spike excitation.

Synaptic potentials and threshold currents underlying spike production in motor giant axons of Aglantha digitale

1995 ◽  
Vol 74 (4) ◽  
pp. 1662-1670 ◽  
Author(s):  
R. W. Meech ◽  
G. O. Mackie
Keyword(s):  
Neuromuscular Junctions ◽  
Sodium Current ◽  
Giant Axon ◽  
Nerve Ring ◽  
Synaptic Delay ◽  
Similar Distribution ◽  
Axon Membrane ◽  
Postsynaptic Potentials ◽  
Giant Axons ◽  
Inward Currents

1. Motor giant axons that excite swimming muscles in the jelly-fish Aglantha digitale interface with units of the inner and outer nerve rings in the margin at the base of the bell. External recording electrodes were used to monitor electrical activity at different sites within the nerve ring while events in the motor giant axon were recorded with intracellular micropipettes placed within 100 microns of the synaptic area. In some experiments, 4- to 6-micron-diam patch pipettes were used to record in situ from ion channel clusters at different locations along the axon. 2. Independently propagating calcium and sodium spikes in the motor giant axon were found to arise from different excitatory postsynaptic potentials (EPSPs). Two separate inputs were identified; one EPSP class represented an input from the pacemaker system in the inner nerve ring, whereas another represented an input from the giant axon in the outer nerve ring. EPSPs from the two nerve rings had significantly different time courses and amplitudes. EPSPs from the ring giant axon reached a peak in little more than 1 ms, whereas EPSPs from the pacemaker system reached a maximum in approximately 7 ms. These slower EPSPs may be compound events composed of postsynaptic potentials from multiple synapses excited in series by the passage of the pacemaker neuron signal. 3. The threshold for the production of calcium spikes by the slow EPSPs of the pacemaker system (-51 +/- 2.2 mV, mean +/- SD; n = 5) corresponded well with the voltage at which a net inward “T”-type calcium current first appeared in recordings from axon membrane patches (-55 to -50 mV); the threshold for the initiation of the sodium spike by the fast EPSPs of the ring giant system (-32 +/- 1.2 mV, mean +/- SD; n = 6) corresponded well with the voltage at which a net inward sodium current first appeared (-35 to -30 mV). 4. Inward currents were rarely observed in membrane patches formed using pipettes with tips of < 1 micron OD. Even with 4-micron pipettes, patches of membrane were sometimes obtained with a channel population consisting exclusively of potassium channels; calcium and sodium currents were found in highly discrete areas (“hot spots”). Preliminary findings on the undersurface of the axon, which makes synaptic contact with the myoepithelium, are consistent with a similar distribution. 5. The pathway by which the ring giant excites the motor giant axon is not definitely known. The synaptic delay between the peak of the ring giant action potential (monitored externally) and the initial rise of the fast EPSP (1.64 +/- 0.15 ms, mean +/- SD; n = 21) would allow for transmission at two synapses, because single synaptic delays at neuromuscular junctions in Aglantha are approximately 0.7 ms at 12 degrees C. The mean synaptic delay at the slow EPSP synapse was 0.88 +/- 0.09 (SD) ms (n = 12). 6. The delay between the impulse in the ring giant axon and the subsequent excitation of the motor giant axon may permit the animal to withdraw its tentacles and so lower the drag that would otherwise reduce the effectiveness of any escape swim and might induce tentacle autotomy.

On the binding of iabelled saxitoxin to the squid giant axon

1984 ◽  
Vol 222 (1227) ◽  
pp. 147-153 ◽  
Keyword(s):  
Binding Sites ◽  
Binding Capacity ◽  
Giant Axon ◽  
Squid Giant Axon ◽  
Giant Axons ◽  
A Value ◽  
Saturable Binding ◽  
Mean Diameter ◽  
Loligo Forbesi

Measurement of the maximum saturable binding capacity for 3 H-labelled saxitoxin in well cleaned giant axons from Loligo forbesi gave a value of 290 ± 65 (s. e. m.) binding sites per square micrometre of membrane. In samples of the fin nerve the total saturable uptake was 12.4 ± 2.4 fmol mg -1 wet mass, corresponding to 94 sites per square micrometre for fibres whose mean diameter after fixation and embedding was estimated as 16 µm.

The form and dimensions of the giant synapse of squids

1986 ◽  
Vol 312 (1155) ◽  
pp. 355-377 ◽  
Keyword(s):  
Stellate Ganglion ◽  
Giant Axon ◽  
Giant Fibre ◽  
Cobalt Ions ◽  
Synaptic Contacts ◽  
Giant Axons ◽  
Giant Synapses ◽  
Giant Fibres ◽  
Well Differentiated ◽  
Giant Synapse

A study was made of the distal giant synapse, and of proximal synapses, in the stellate ganglion of the squid, Loligo vulgaris . For this purpose we injected iontophoretically dyes or cobalt ions into the pre- or postsynaptic axon. The intra-axonal movement of visible dyes was measured. Both presynaptic fibres, the main second order giant axon and the largest accessory axon, branched to make multiple synaptic contacts on the giant motor axons from near the perikarya down to near the exit of the stellar nerves from the ganglion. There were considerable individual variations in the branching patterns of the presynaptic giant axon and in the course and number of the postsynaptic giant axons. More than one accessory axon made contact with the largest motor axon. Fine structural details of the synapse are presented. The size of the contact area made by the main presynaptic axon on the last postsynaptic axon of a medium-sized animal was estimated from low power electron micrographs. We measured and counted synaptic contacts, synaptic vesicles and mitochondria. The fine structure of proximal synapses was found to be very similar to that of the distal synapse. Cobalt- or dye-injected ganglia showed that the perikarya of the axons which fuse to form the postsynaptic giant axons are located in diffuse and overlapping areas of the giant fibre lobe. In freshly hatched larvae the giant synapse was well differentiated; a gradient of differentiation from brain to periphery was detectable. The distal giant synapses of the oegopsid squid Todarodes sagittatus and of Sepia officinalis differed from the Loligo synapse. In Todarodes and Sepia collaterals and processes from both the presynaptic and the postsynaptic giant fibres are shown to meet in numerous contacts in the enlarged sheath surrounding the third order axon. In several respects the Loligo giant fibre system appears to represent in phylogenetical order the more evolved neuronal network.

Electrical interactions between the giant axons of a polychaete worm (Sabella penicillus L.)

1980 ◽  
Vol 84 (1) ◽  
pp. 119-136
Author(s):  
D. Mellon ◽  
J. E. Treherne ◽  
N. J. Lane ◽  
J. B. Harrison ◽  
C. K. Langley
Keyword(s):  
Safety Factor ◽  
Nerve Cord ◽  
Action Potentials ◽  
Divalent Cations ◽  
Muscular Contraction ◽  
The Body ◽  
The Other ◽  
Intracellular Recordings ◽  
Giant Axons ◽  
Other Hand

Intracellular recordings demonstrated a transfer of impulses between the paired giant axons of Sabella, apparently along narrow axonal processes contained within the paired commissures which link the nerve cords in each segment of the body. This transfer appears not to be achieved by chemical transmission, as has been previously supposed. This is indicated by the spread of depolarizing and hyperpolarizing voltage changes between the giant axons, the lack of effects of changes in the concentrations of external divalent cations on impulse transmission and by the effects of hyperpolarization in reducing the amplitude of the depolarizing potential which precedes the action potentials in the follower axon. The ten-to-one attenuation of electronic potentials between the giant axons argues against the possibility of an exclusively passive spread of potential along the axonal processes which link the axons. Observation of impulse traffic within the nerve cord commissures indicates, on the other hand, that transmission is achieved by conduction of action potentials along the axonal processes which link the giant axons. At least four pairs of intact commissures are necessary for inter-axonal transmission, the overall density of current injected at multiple sites on the follower axon being, it is presumed, sufficient to overcome the reduction in safety factor imposed by the geometry of the system in the region where axonal processes join the giant axons. The segmental transmission between the giant axons ensures effective synchronization of impulse traffic initiated in any region of the body and, thus, co-ordination of muscular contraction, during rapid withdrawal responses of the worm.

Vesicle-Mediated Restoration of a Plasmalemmal Barrier in Severed Axons

Physiology ◽  
2003 ◽  
Vol 18 (3) ◽  
pp. 115-118 ◽  
Author(s):  
Harvey M. Fishman ◽  
George D. Bittner
Keyword(s):  
Action Potentials ◽  
Mammalian Cells ◽  
Molecular Mechanisms ◽  
Giant Axons ◽  
Permeable Barrier ◽  
Endocytotic Vesicles ◽  
Severed Axons

Ca2+-induced endocytotic vesicles undergo protein-mediated interactions to restore a selectively permeable barrier and propagated action potentials in severed invertebrate giant axons. Similar barrier-restoration phenomena observed in cultured mammalian cells with transected neurites suggest that cellular/molecular mechanisms that repair plasmalemmal damage are phylogenetically conserved.

Coordinated Excitation of Flexor Inhibitors in the Crayfish

1980 ◽  
Vol 86 (1) ◽  
pp. 187-195
Author(s):  
CHIKAO UYAMA ◽  
TAKASHI MATSUYAMA
Keyword(s):  
Giant Axon ◽  
Experimental Results ◽  
Abdominal Ganglion ◽  
Giant Axons ◽  
The Third ◽  
Nerve Cords

In isolated abdominal nerve cords of crayfish, the medial or lateral giant axons were stimulated at a position just rostral to the first abdominal ganglion. Recordings of the impulse sequences of the flexor inhibitor (FI) were made from the anterior five ganglia, three ganglia at a time. In 20% of our preparations, one giant axon impulse caused one to four FI impulses in every abdominal third root. An equal number of FI impulses were usually produced by each abdominal ganglion for any given stimulation. The earliest FI impulse was observed at the third root of the fourth ganglion. FI impulses occurred with increasing latencies rostrally and caudally from the fourth ganglion. The FI responses to medial and lateral giant axons stimulation were essentially equivalent. FI impulses were recorded from the rostral three abdominal ganglia, while the caudal ganglia were cut off one after another from the sixth to the third ganglion. Little change was noted until after the removal of the fourth ganglion, which usually caused all FI impulses to disappear. From these experimental results, we propose a model of central mechanisms for FI excitation.

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