Excitation of identified serotonergic neurons by escape command neurons in lobsters.

1997 ◽  
Vol 200 (14) ◽  
pp. 2017-2033 ◽  
Author(s):  
M Hörner ◽  
W A Weiger ◽  
D H Edwards ◽  
E A Kravitz
Keyword(s):  
Action Potentials ◽  
Giant Axon ◽  
Homarus Americanus ◽  
Excitatory Input ◽  
Plateau Phase ◽  
Command Neurons ◽  
Substantial Variation ◽  
Giant Fiber ◽  
Neurosecretory Neurons ◽  
Sufficient Magnitude

Serotonin-containing neurosecretory neurons in the first abdominal ganglion (A1 5-HT cells) of the lobster (Homarus americanus) ventral nerve cord have been shown previously to function as 'gain setters' in postural, slow muscle, command neuron circuitries. Here we show that these same amine neurons receive excitatory input from lateral (LG) and medial (MG) giant axons, which are major interneurons in phasic, fast muscle systems. Activation of either LG or MG axons elicits short-latency, non-fatiguing, long-lasting excitatory postsynaptic potentials (EPSPs) in A1 5-HT cells which follow stimulus frequencies of up to 100 Hz in a 1:1 fashion. Single spikes triggered in either giant axon can produce EPSPs in the A1 5-HT cells of sufficient magnitude to cause the cells to spike and to fire additional action potentials after variable latencies; action potentials elicited in this way reset the endogenous spontaneous spiking rhythm of the A1 5-HT neurons. The giant-axon-evoked EPSP amplitudes show substantial variation from animal to animal. In individual preparations, the variation of EPSP size from stimulus to stimulus was small over the first 25 ms of the response, but increased considerably in the later, plateau phase of each response. When tested in the same preparation, EPSPs in A1 5-HT cells evoked by firing the LG axons were larger, longer-lasting and more variable than those triggered by firing the MGs. Firing A1 5-HT cells through an intracellular electrode, prior to activation of the giant fiber pathway, significantly reduced the size of LG-evoked EPSPs in A1 5-HT cells. Finally, morphological and physiological results suggest that similarities exist between giant fiber pathways in lobsters and crayfish. The possible functional significance of an involvement of these large amine-containing neurosecretory neurons in both tonic and phasic muscle circuitries will be discussed.

Interneurons between giant axons and motoneurons in crayfish escape circuitry

1981 ◽  
Vol 45 (3) ◽  
pp. 550-573 ◽  
Author(s):  
A. P. Kramer ◽  
F. B. Krasne ◽  
J. J. Wine
Keyword(s):  
Motor Pattern ◽  
Excitatory Input ◽  
Inhibitory Input ◽  
Command Neurons ◽  
Giant Fiber ◽  
Flexor Muscle ◽  
Giant Axons ◽  
Formal Level ◽  
The One

1. Crayfish giant fibers are generally believed to generate tailflip movements by means of direct connections to two classes of phasic flexor muscle motoneurons, the motor giants (MoGs) and the nongiant fast flexor motoneurons (FFs). It is shown here that the giants also stimulate a network of interneurons that make connections with the FFs. 2. This network includes an intraganglionic neuron, the segmental giant (SG), in each abdominal hemisegment and a number of intersegmental neurons, two of which (I2 and I3) were studied in detail. 3. The SGs are driven reliably by the giant fibers and they in turn drive the FFs of their hemisegment about as effectively as do the giant fibers themselves; it is possible that the giant fibers excite the FFs mainly by way of the SGs. The SGs also have an efferent first root axon whose peripheral targets we have been unable to determine. 4. I2 and I3 originate in the second and third abdominal ganglia, respectively, and descend to the last ganglion. In their ganglia of origin they are reliably driven by the giant fibers and by the SGs. In addition, I2 weakly excites I3 and both receive weak, apparently direct, excitatory input from FFs as well as less direct excitatory and inhibitory input from unidentified afferent sources. Both weakly excite most FFs in ganglia behind the one in which they originate. This excitation adds to that produced directly by giant fibers and SGs and, we believe, is sometimes decisive in causing FF firing. Their firing also causes inhibition involved in suppressing effects of reafference, as do the giant fibers themselves. 5. I3 strongly excites the motoneurons of certain tail fan muscles (the ventral and posterior telson flexors). However, the contraction of these muscles would be maladaptive during some giant fiber-mediated tailflips. Accordingly, when the giant fibers, which always recruit I3, fire, they cause an inhibition of the motoneurons that nullifies the excitatory input from I3. At a formal level this means that the giants, viewed as command neurons, not only drive but also alter or modulate the subordinate motor pattern-generating network that they control. 6. Tailflips that are less stereotyped than those mediated by giant fibers are known to occur without participation of the giants. It is suggested that the presence of complex circuitry mediating between giant fibers and FFs may be related to the use of portions of this circuitry as well as the FFs themselves in production of nongiant tailflips.

Prolonged response of skeletal muscle in the absence of penetrating anions

1960 ◽  
Vol 198 (2) ◽  
pp. 289-299 ◽  
Author(s):  
Gertrude Falk ◽  
Jorge F. Landa
Keyword(s):  
Action Potentials ◽  
Critical Concentration ◽  
Relaxation Oscillations ◽  
Plateau Phase ◽  
Slow Oscillations ◽  
Mechanical Responses ◽  
External Potassium ◽  
Prolonged Response ◽  
Plateau Level ◽  
Potassium Addition

Replacement of Ringer's chloride by a variety of nonpenetrating anions results in prolonged electrical and mechanical responses of muscle to stimulation. The ‘negative after-potential’ is characterized by a slowly increasing secondary depolarization which reaches a stable plateau lasting as long as 2 minutes. After-discharge frequently occurs during early depolarization. In most fibers repolarization is relatively abrupt, but in some, slow oscillations resembling relaxation oscillations arise following the plateau, grow gradually in amplitude and, only when they are of sufficient amplitude, does the membrane repolarize. Prolonged depolarization can still be produced when the spike has failed. At times, fibers may respond with short-duration action potentials, but may be primed to give prolonged responses by previous stimuli or by increase of external potassium. Addition of chloride has no effect below a critical concentration. Reduction of sodium to 25% of normal does not change plateau level or duration. Duration of the plateau phase is decreased by potassium.

Segmental differences in pathways between crayfish giant axons and fast flexor motoneurons

1985 ◽  
Vol 53 (1) ◽  
pp. 252-265 ◽  
Author(s):  
L. A. Miller ◽  
G. Hagiwara ◽  
J. J. Wine
Keyword(s):  
High Probability ◽  
Behavior Pattern ◽  
Excitatory Input ◽  
Conclusive Evidence ◽  
Spatial Patterning ◽  
Command Neurons ◽  
Additional Input ◽  
Premotor Neurons ◽  
Escape Trajectories ◽  
Escape Responses

We have used electrophysiological techniques to document segmental differences in the pathways between the giant, escape command axons, lateral giants (LG) and medial giants (MG), and the nongiant, fast flexor (FF) motoneurons. We found no difference in the input from LG and MG axons to FF motoneurons in the posterior (4th and 5th) ganglia. Since flexor motor output in these segments would be inconsistent with the LG-evoked behavior pattern, this finding was puzzling. Electromyographic (EMG) recordings during escape responses by intact unrestrained animals confirm that the FF muscles innervated by the posterior ganglia are not excited during LG-mediated tailflips, but are excited during MG-mediated tailflips. In the 2nd and 3rd ganglia, the command axons fire the FF motoneurons with high probability, in part via electrical excitatory postsynaptic potentials (EPSPs) from premotor neurons, the segmental giants (SG). In the 4th and 5th ganglia, the equivalent pathway is much less effective. Single, directly elicited impulses in SGs in ganglia 2 and 3 fire their respective FF motoneurons with high probability, while those in ganglia 4 and 5 rarely fire FF motoneurons. The command axons fire the SGs reliably in all segments. The amplitude of the SG-evoked EPSP in FF motoneurons is significantly smaller in posterior vs. anterior ganglia. For technical reasons, we are unable to present conclusive evidence on ganglionic variations in FF-motoneuron thresholds. The FF motoneurons receive additional excitatory input from intersegmental interneurons recruited by the command neurons. Motoneurons in ganglia 4 and 5 are excited by large interneurons that do not synapse on motoneurons in ganglia 2 and 3, but this additional input is not sufficient to compensate for the weaker effect of SG input. Unlike the all-or-none segmental differences demonstrated previously for the LG-to-motor giant pathway (24), the SG-to-FF pathway changes gradually, retains significant though subthreshold strength in posterior ganglia, and is common to both LGs and MGs. These features provide opportunities for variation in the spatial patterning of flexion and in the resulting escape trajectories.

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.

Calcium-dependent potassium conductance in rat supraoptic nucleus neurosecretory neurons

1985 ◽  
Vol 54 (6) ◽  
pp. 1375-1382 ◽  
Author(s):  
C. W. Bourque ◽  
J. C. Randle ◽  
L. P. Renaud
Keyword(s):  
Time Constant ◽  
Action Potentials ◽  
Supraoptic Nucleus ◽  
Potassium Conductance ◽  
Reversal Potential ◽  
Input Resistance ◽  
Mean Amplitude ◽  
Progressive Increase ◽  
Calcium Dependent ◽  
Neurosecretory Neurons

Intracellular recordings of rat supraoptic nucleus neurons were obtained from perfused hypothalamic explants. Individual action potentials were followed by hyperpolarizing afterpotentials (HAPs) having a mean amplitude of -7.4 +/- 0.8 mV (SD). The decay of the HAP was approximated by a single exponential function having a mean time constant of 17.5 +/- 6.1 ms. This considerably exceeded the cell time constant of the same neurons (9.5 +/- 0.8 ms), thus indicating that the ionic conductance underlying the HAP persisted briefly after each spike. The HAP had a reversal potential of -85 mV and was unaffected by intracellular Cl- ionophoresis of during exposure to elevated extracellular concentrations of Mg2+. In contrast, the peak amplitude of the HAP was proportional to the extracellular Ca2+ concentration and could be reversibly eliminated by replacing Ca2+ with Co2+, Mn2+, or EGTA in the perfusion fluid. During depolarizing current pulses, evoked action potential trains demonstrated a progressive increase in interspike intervals associated with a potentiation of successive HAPs. This spike frequency adaptation was reversibly abolished by replacing Ca2+ with Co2+, Mn2+, or EGTA. Bursts of action potentials were followed by a more prolonged afterhyperpolarization (AHP) whose magnitude was proportional to the number of impulses elicited (greater than 20 Hz) during a burst. Current injection revealed that the AHP was associated with a 20-60% decrease in input resistance and showed little voltage dependence in the range of -70 to -120 mV. The reversal potential of the AHP shifted with the extracellular concentration of K+ [( K+]o) with a mean slope of -50 mV/log[K+]o.(ABSTRACT TRUNCATED AT 250 WORDS)

scholarly journals Ca2+-activated Cl− current in sheep lymphatic smooth muscle

2000 ◽  
Vol 279 (5) ◽  
pp. C1327-C1335 ◽  
Author(s):  
H. M. Toland ◽  
K. D. McCloskey ◽  
K. D. Thornbury ◽  
N. G. McHale ◽  
M. A. Hollywood
Keyword(s):  
Smooth Muscle ◽  
Carboxylic Acid ◽  
Patch Clamp ◽  
Action Potentials ◽  
Channel Blocker ◽  
Equilibrium Potential ◽  
Plateau Phase ◽  
Current Clamp ◽  
Patch Clamp Technique ◽  
Perforated Patch Clamp

Freshly dispersed sheep mesenteric lymphatic smooth muscle cells were studied at 37°C using the perforated patch-clamp technique with Cs+- and K+-filled pipettes. Depolarizing steps evoked currents that consisted ofl-type Ca2+ [ I Ca(L)] current and a slowly developing current. The slow current reversed at 1 ± 1.5 mV with symmetrical Cl− concentrations compared with 23.2 ± 1.2 mV ( n = 5) and −34.3 ± 3.5 mV ( n = 4) when external Cl− was substituted with either glutamate (86 mM) or I− (125 mM). Nifedipine (1 μM) blocked and BAY K 8644 enhanced I Ca(L), the slow-developing sustained current, and the tail current. The Cl− channel blocker anthracene-9-carboxylic acid (9-AC) reduced only the slowly developing inward and tail currents. Application of caffeine (10 mM) to voltage-clamped cells evoked currents that reversed close to the Cl− equilibrium potential and were sensitive to 9-AC. Small spontaneous transient depolarizations and larger action potentials were observed in current clamp, and these were blocked by 9-AC. Evoked action potentials were triphasic and had a prominent plateau phase that was selectively blocked by 9-AC. Similarly, fluid output was reduced by 9-AC in doubly cannulated segments of spontaneously pumping sheep lymphatics, suggesting that the Ca2+-activated Cl− current plays an important role in the electrical activity underlying spontaneous activity in this tissue.

Cloning and characterization of an electrogenic Na/HCO3− cotransporter from the squid giant fiber lobe

2007 ◽  
Vol 292 (6) ◽  
pp. C2032-C2045 ◽  
Author(s):  
Peter M. Piermarini ◽  
Inyeong Choi ◽  
Walter F. Boron
Keyword(s):  
Giant Axon ◽  
Predicted Amino Acid Sequence ◽  
Giant Fiber ◽  
Reading Frame ◽  
Excitable Membranes ◽  
Current Voltage ◽  
Partial Cdna ◽  
Partial Cdna Clone ◽  
Current Voltage Relationship

The squid giant axon is a classic model system for understanding both excitable membranes and ion transport. To date, a Na+-driven Cl-HCO3− exchanger, sqNDCBE—related to the SLC4 superfamily and cloned from giant fiber lobe cDNA—is the only HCO3−-transporting protein cloned and characterized from a squid. The goal of our study was to clone and characterize another SLC4-like cDNA. We used degenerate PCR to obtain a partial cDNA clone (squid fiber clone 3, SF3), which we extended in both the 5′ and 3′ directions to obtain the full-length open-reading frame. The predicted amino-acid sequence of SF3 is similar to sqNDCBE, and a phylogenetic analysis of the membrane domains indicates that SF3 clusters with electroneutral Na+-coupled SLC4 transporters. However, when we measure pHi and membrane potential—or use two-electrode voltage clamping to measure currents—on Xenopus oocytes expressing SF3, the oocytes exhibit the characteristics of an electrogenic Na/HCO3− cotransporter, NBCe. That is, exposure to extracellular CO2/HCO3− not only causes a fall in pHi, followed by a robust recovery, but also causes a rapid hyperpolarization. The current-voltage relationship is also characteristic of an electrogenic NBC. The pHi recovery and current require HCO3− and Na+, and are blocked by DIDS. Furthermore, neither K+ nor Li+ can fully replace Na+ in supporting the pHi recovery. Extracellular Cl− is not necessary for the transporter to operate. Therefore, SF3 is an NBCe, representing the first NBCe characterized from an invertebrate.

Contribution of Na+/Ca2+ exchange to action potential of human atrial myocytes

1996 ◽  
Vol 271 (3) ◽  
pp. H1151-H1161 ◽  
Author(s):  
A. Benardeau ◽  
S. N. Hatem ◽  
C. Rucker-Martin ◽  
B. Le Grand ◽  
L. Mace ◽  
...  
Keyword(s):  
Action Potential ◽  
Action Potentials ◽  
Time Course ◽  
Significant Proportion ◽  
Type A ◽  
Plateau Phase ◽  
Type B ◽  
Atrial Myocytes ◽  
Human Atrial Myocytes ◽  
Delayed Afterdepolarizations

The Ca2+ dye indo 1 was used to record internal Ca2+ (Cai) transients in order to investigate the role of the Na+/Ca2+ exchange current (INa/Ca) in whole cell patch-clamped human atrial myocytes After the activation of the L-type Ca2+ current by test pulses (20 ms) at +20 mV, a tail current (I(tail)) was activated at a holding potential of -80 mV with a density of -1.29 +/- 0.06 pA/pF. The time course of I(tail) followed that of Cai transients I(tail) was suppressed by dialyzing cells with ethylene glycol-bis(beta-aminoethyl ether)-N,N,N',N'-tetraacetic acid, applying 5 mM caffeine, or substituting external Na+ with Li+, indicating that this current was mainly generated by INa/Ca. Two types of action potential were recorded: type A, which is characterized by a narrow early plateau followed by a late low plateau phase, and type B, which is characterized by a small initial peak followed by a prolonged high plateau phase. Type B action potentials were found in larger cells than type A action potentials (membrane capacitance 81.8 +/- 4.5 and 122.4 +/- 7.0 pF in types A and B, respectively, P < 0.001). Substitution of external Na+ with Li+ shortened the late plateau of the type A action potential and the prolonged plateau of the type B action potential. Suppression of Cai transients by caffeine shortens the late part of both types of action potentials, whereas its lengthening effect on the initial phase of action potentials can result from several different mechanisms. The beat-to-beat dependent relationship between Cai transients and action potentials could be mediated by Ina/Ca- Delayed afterdepolarizations were present in a significant proportion of atrial myocytes in our experimental conditions. They were reversibly suppressed by Li+ substitution for Na+, suggesting that they are generated by INa/Ca. We conclude that INa/Ca plays a major role in the development of action potentials and delayed afterdepolarizations in isolated human atrial myocytes.

scholarly journals Molecular identification of SqKv1A. A candidate for the delayed rectifier K channel in squid giant axon.

1996 ◽  
Vol 108 (3) ◽  
pp. 207-219 ◽  
Author(s):  
J J Rosenthal ◽  
R G Vickery ◽  
W F Gilly
Keyword(s):  
Time Course ◽  
Xenopus Oocytes ◽  
Giant Axon ◽  
K Channel ◽  
Delayed Rectifier ◽  
Giant Fiber ◽  
Western Blots ◽  
Internal Solution ◽  
Giant Axons ◽  
K Currents

We have cloned the cDNA for a squid Kvl potassium channel (SqKv1A). SqKv1A mRNA is selectively expressed in giant fiber lobe (GFL) neurons, the somata of the giant axons. Western blots detect two forms of SqKv1A in both GFL neuron and giant axon samples. Functional properties of SqKv1A currents expressed in Xenopus oocytes are very similar to macroscopic currents in GFL neurons and giant axons. Macroscopic K currents in GFL neuron cell bodies, giant axons, and in Xenopus oocytes expressing SqKv1A, activate rapidly and inactivate incompletely over a time course of several hundred ms. Oocytes injected with SqKv1A cRNA express channels of two conductance classes, estimated to be 13 and 20 pS in an internal solution containing 470 mM K. SqKv1A is thus a good candidate for the "20 pS" K channel that accounts for the majority of rapidly activating K conductance in both GFL neuron cell bodies and the giant axon.

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