Medial Giant Research Articles

«В БЕЗУМНОМ МИРЕ ЗУМА КАЖДЫЙ ОКАЗАЛСЯ В ДВОЙНОЙ РОЛИ – ЗРИТЕЛЯ И АКТЕРА ОДНОВРЕМЕННО»

Oksana Bulgakowa is a researcher of visual culture, a film critic, a screenwriter, a director, and a professor at the Johannes Gutenberg University Mainz. She has taught at the Humboldt University of Berlin, the Leipzig Graduate School of Music and Theater, the Free University of Berlin, Stanford University and the University of California Berkeley. Author of the books “FEKS: Die Fabrik des exzentrischen Schauspielers” (1996), “Sergei Eisenstein – drei Utopien. Architekturentwürfe zur Filmtheorie” (1996), “Sergej Eisenstein. Eine Biographie” (1998), “The Gesture Factory” (2005, a renewed edition to be published by NLO publishing house in 2021), “The Soviet hearing eye: cinema and its sensory organs” (2010), “The Voice as a cultural phenomenon”(2015), “SINNFABRIK/FABRIK DER SINNE” (2015), “The Fate of the Battleship: The Biography of Sergei Eisenstein” (2017). Author of the network projects “The Visual Universe of Sergei Eisenstein” (2005), “Sergei Eisenstein: My Art in Life. Google Arts and Culture” (in collaboration with Dietmar Hochmuth, 2017–2018), and the films “Stalin – eine Mosfilmproduktion” (in collaboration with Enno Patalas, 1993), “Different Faces of Sergei Eisenstein” (in collaboration with Dietmar Hochmuth, 1997). In this issue of P&I, Oksana Bulgakowa talks about medial giants and midgets, obscene gestures of Elvis Presley, “voice-over discourse” of TV presenters, and the birth of Eisenstein’s “Method” from psychosis and neurosis. Interview by Ekaterina Maksimova. Photo by Dietmar Hochmuth.

Not so fast: giant interneurons control precise movements of antennal scales during escape behavior of crayfish.

High-speed video recordings of escape responses in freely behaving crayfish revealed precisely coordinated movements of conspicuous head appendages, the antennal scales, during tail-flips that are produced by giant interneurons. For tail-flips that are generated by the medial giants (MG) in response to frontal attacks, the scales started to extend immediately after stimulation and extension was completed before the animal began to propel backwards. For tail-flips that are elicited by caudal stimuli and controlled by the lateral giants (LG), scale extensions began with significant delay after the tail-flip movement was initiated, and full extension of the scales coincided with full flexion of the tail. When we used implanted electrodes and stimulated the giant neurons directly, we observed the same patterns of scale extensions and corresponding timing. In addition, single action potentials of MG and LG neurons evoked with intracellular current injections in minimally restrained preparations were sufficient to activate scale extensions with similar delays as seen in freely behaving animals. Our results suggest that the giant interneurons, which have been assumed to be part of hardwired reflex circuits that lead to caudal motor outputs and stereotyped behavior, are also responsible for activating a pair of antennal scales with high temporal precision.

Effects of Ethanol on Sensory Inputs to the Medial Giant Interneurons of Crayfish.

Crayfish are capable of two rapid, escape reflexes that are mediated by two pairs of giant interneurons, the lateral giants (LG) and the medial giants (MG), which respond to threats presented to the abdomen or head and thorax, respectively. The LG has been the focus of study for many decades and the role of GABAergic inhibition on the escape circuit is well-described. More recently, we demonstrated that the LG circuit is sensitive to the acute effects of ethanol and this sensitivity is likely mediated by interactions between ethanol and the GABAergic system. The MG neurons, however, which receive multi-modal sensory inputs and are located in the brain, have been less studied despite their established importance during many naturally occurring behaviors. Using a combination of electrophysiological and neuropharmacological techniques, we report here that the MG neurons are sensitive to ethanol and experience an increase in amplitudes of post-synaptic potentials following ethanol exposure. Moreover, they are affected by GABAergic mechanisms: the facilitatory effect of acute EtOH can be suppressed by pretreatment with a GABA receptor agonist whereas the inhibitory effects resulting from a GABA agonist can be occluded by ethanol exposure. Together, our findings suggest intriguing neurocellular interactions between alcohol and the crayfish GABAergic system. These results enable further exploration of potentially conserved neurochemical mechanisms underlying the interactions between alcohol and neural circuitry that controls complex behaviors.

Novel neurobiological properties of elements in the escape circuitry of the shrimp.

Escape behaviors in penaeid shrimp are mediated by large myelinated medial giant fibers which course from the brain to the last abdominal ganglion in the ventral nerve cord. In each abdominal segment, the medial giant axons make synaptic connections with paired myelinated motor giant axons that excite the abdominal deep flexor muscles and drive the tailflips that constitute the escape behavior. I examined (1) anatomical features of the abdominal motor giant fibers and (2) electrical properties of both the medial and motor giant axons in the pink shrimp, Farfantepenaeus duorarum The motor giant axons in the paired third roots of shrimp abdominal ganglia emerge from a single fused neurite that originates from two clusters of cell bodies within the ganglion. Injection of large positive currents into the abdominal medial giant fibers generates action potentials that are transmitted to the opposite medial giant axon through putative collateral synapses within the ganglia. Transmission across the medial-to-motor giant synapse is fast and resistant to fatigue, with synaptic delays equal to or less than those previously documented at the lateral-to-motor giant electrical synapse in crayfish. Transmission was found to be extremely reliable even with presynaptic spike frequencies as high as 250 Hz. While action potentials within the medial giant fibers are transmitted across the medial-to-motor giant synapse with a large safety factor, neither prolonged positive nor prolonged negative currents pass through the synaptic nexus, irrespective of the site of injection. The lack of DC current passage along with the inability of neurobiotin or biocytin to spread through the synaptic nexus raises the possibility that the synaptic mechanism may be capacitative.

Loss of escape responses and giant neurons in the tailflipping circuits of slipper lobsters, Ibacus spp. (Decapoda, Palinura, Scyllaridae)

In many decapod crustaceans, escape tailflips are triggered by lateral giant (LG) and medial giant (MG) interneurons, which connect to motor giant (MoG) abdominal flexor neurons. Several decapods have lost some or all of these giant neurons, however. Because escape-related giant neurons have not been documented in palinurans, I examined tailflipping and abdominal nerve cords for giant neurons in two scyllarid lobster species, Ibacus peronii and Ibacus alticrenatus. Unlike decapods with giant neurons, Ibacus do not tailflip in response to sudden taps. Ibacus can perform non-giant tailflipping: the frequency of tailflips during swimming is adjusted by altering the gap between each individual tailflip. Abdominal nerve cord sections show no LG or MG interneurons. Backfilling nerve 3 of abdominal ganglia revealed no MoG neurons, and the fast flexor motor neuron population is otherwise identical to that described for crayfish. The loss of giant neurons in Ibacus represents an independent deletion of these cells compared to other reptantian decapods known to have lost these giant neurons. This loss is correlated with the normal posture in scyllarids, in which the last two abdominal segments are flexed, and an alternative defensive strategy, concealment by digging into sand.

Biotin staining in the giant fiber systems of the lobster.

The avidin-biotin-complex method is a popular immunocytochemical technique. This method labels consistently a group of neurons in the lobster ventral nerve cord in the absence of primary antibodies. The specific staining is due to a relatively high level of endogenous biotin (or biocytin) in these neurons. These biotin-positive neurons are located in the supraesophageal, thoracic, and abdominal ganglia. Intraaxonal injection of Lucifer yellow followed by Texas red-conjugated streptavidin staining reveals that the neurons are members of the medial giant (MG) and lateral giant (LG) systems, which are important in mediating rapid tail flipping during escape maneuvers. In neuronal somata, staining is restricted to the cytoplasm. Within MG axons, staining appears as punctate, subaxolemmal structures. Preincubating nerve cords in biocytin or direct intraaxonal injection of biocytin enhances staining of these punctate organelles. In LG axons, staining is localized to fragments of braided filamentous structures that also appear to be associated with the axolemma. Preincubation of ventral nerve cords in various concentrations of biocytin results in the appearance of additional groups of stained neurons, suggesting that there are subsets of neurons with specific biocytin-uptake or -retention mechanisms. In the crayfish, biotin-positive staining is confined to the MG neurons; the LG neurons are not stained. In the earthworm, no staining is observed in the MG and LG axon escape systems. In the goldfish, no biotin-staining is seen in the Mauthner neurons and their axons. The significance of specific localization of biotin or biocytin to subsets of neurons is unclear. It may reflect the presence of high levels of biocytin moieties on biotin-dependent enzymes. Biotin is an important cofactor in the catalytic functions of several decarboxylases crucial in energy production and lipogenesis. Axons of the giant fiber systems in lobsters and crayfish may have high energy and fatty acid synthesis requirements. Increased levels of biotin accumulation may also be related to other functions of the giant axon systems, such as the formation of electrical synapses among themselves and with phasic motoneurons.

Thoracic Connections Between Crayfish Giant Fibres and Motor Giant Neurones Reverse Abdominal Pattern

ABSTRACT The escape tail-flip of the crayfish is ‘commanded’ by two bilaterally paired sets of giant fibre (GF) interneurones, the lateral giant (LG) and medial giant (MG) (see e.g. Wine, 1984, for a review). The two classes of GF respond to different stimuli and initiate tail-flips with different kinematic forms. An arousal stimulus applied to the front of the animal initiates a spike in the MG system, and this causes a tail-flip that drives the animal directly backwards, away from the stimulus. An arousal stimulus applied to the rear of the animal initiates a spike in the LG system, and this causes a tail-flip that drives the animal upwards and forwards, again moving it away from the stimulus. The major motor output path from the GFs is through monosynaptic rectifying electrical connections to a class of powerful trunk flexor motor neurones called the motor giant (MoG) neurones (Furshpan and Potter, 1959a). There is one MoG neurone in each hemisegment of the thorax and abdomen.

The role of the legs in the lateral giant fibre escape of the crayfish Cherax destructor (Crustacea: Decapoda: Astacura)

AbstractIt is known that leg positioning is important for reducing drag during escape mediated by the medial giant (MG) axon of the crayfish (Cooke and Macmillian, '85). This report examines the question of whether the legs also have a role in escape mediated by the lateral giant (LG) neuron. The trajectory and the dynamics of the lateral giant (LG) escape behaviour of the crayfish Cherax destructor were analyzed using high speed cinematographic techniques. The LG escape flip was found to be stereotyped for each particular animal but rested animals produce their own characteristic trajectories. We tested to see if denervation of the legs would alter the escape trajectory. Interference with the articulating membrane at the base of the legs alters escape performance and a new set of displacement curves characteristic of each animal is produced. This is the outcome whether or not the nerves are severed. Electrophysiological recordings confirmed earlier latency measurements (Cooke, '85) and indicate that the efferent signals to the legs evoked by LG activation arrive too late to position them to influence the escape trajectory. We suggest that operations on the articulating membrane produce their effects by altering the starting position of the legs. We provide some preliminary evidence that supports this hypothesis.

Photoinactivation of the crayfish segmental giant neuron reveals a direct giant-fiber to fast-flexor connection with a chemical component

The escape tail flip of the crayfish is "commanded" by 2 sets of giant-fiber (GF) interneurons. In each hemisegment, these drive the motor giant (MoG) abdominal flexor motor-neuron through a monosynaptic electrical connection, but the remaining 8 or 9 fast-flexor (FF) motorneurons receive most of their input via a disynaptic electrical pathway through the segmental giant (SG) neuron. We have investigated a monosynaptic GF-FF pathway, which operates in parallel to the disynaptic GF-SG-FF pathway, by using dye-mediated photoinactivation to remove the SGs from the tail-flip circuit. SG photoinactivation involves an initial broadening of the spike, leading to a long-duration, massively depolarized plateau. This is followed by loss of spike capability, a gradual reduction in the resting potential, and eventual total loss of electrical responsiveness. After bilateral photoinactivation of the SGs, a spike in one set of GFs, the medial giants (MGs), produces little if any effect in FFs in any ganglion. A spike in the other set, the lateral giants (LGs), produces an EPSP in FFs with a declining anterior-to-posterior segmental gradient in amplitude. These differences in LG and MG outputs, which are obscured in the intact circuit by the common MG/LG-SG-FF pathway, give clues to a probable early evolutionary form of the circuit. The LG-FF connection in anterior ganglia has a significant electrical component. However, it also has an apparent monosynaptic chemical component, as revealed by the response to saline containing cadmium ions, and to cooling the preparation. This is the first physiological evidence for chemical output from a crayfish GF.

Mechanisms of depolarizing inhibition at the crayfish giant motor synapse. II. Quantitative reconstruction

1. The relative strengths of four mechanisms of depolarizing synaptic inhibition described in the previous paper were evaluated with an electrical model of the giant motor synapse (GMS) and postsynaptic region of the motor giant motoneuron (MoG). 2. The model consists of one compartment that represents the presynaptic region of the medial giant (MG) interneuron and three compartments that represent the postsynaptic region and proximal axon of the MoG. The presynaptic MG compartment is linked to a postsynaptic MoG compartment by a rectifying conductance that represents the GMS. Each compartment consists of parallel paths to ground for active and/or passive membrane currents. 3. Parameter values of the model were set so the MG compartment would replicate an MG impulse and the MoG compartments would replicate the current-clamp, voltage-clamp, and synaptic responses of a single MoG neuron described in the previous paper. The Hodgkin-Huxley equations described voltage-sensitive sodium and potassium currents. 4. Comparison of the MoG compartment currents that mediate an inhibited excitatory postsynaptic potential (EPSP) [triggered during a depolarizing inhibitory postsynaptic potential (d-IPSP)] with those of an uninhibited EPSP indicate that all four mechanisms have significant inhibitory effects. Reverse bias of the GMS by the d-IPSP reduced the GMS current by 65 nA (12%). The remaining inward current was further reduced by a 243-nA outward current through the inhibitory postsynaptic conductance. The d-IPSP inactivated sodium conductance so the inward sodium current evoked by the EPSP was reduced by 319 nA (-68%). The d-IPSP reduced the latency for potassium activation by the EPSP so that the outward potassium current coincided with the inward sodium current and reduced the net inward current by 100 nA. Together, these mechanisms reduced the EPSP amplitude by 69%. 5. The resting potential of MoG is normally 15 mV more positive than MG rest potential, but in some preparations this difference may be as much as 25 mV or as little as 0 mV. Corresponding differences in the rest potentials of the MoG and MG models have little effect on the amplitude of the model MoG EPSP because changes in the inward synaptic and sodium currents are balanced by corresponding changes in the outward potassium current.

The Telson Flexor Neuromuscular System of the Crayfish: III. The Role of Feedforward Inhibition in Shaping a Stereotyped Behaviour Pattern

ABSTRACT The telson flexor system is homologous to the fast flexor system of anterior ganglia (Dumont & Wine, 1986a), but important differences exist in connections to the telson motor giants (MoGs) (Dumont & Wine, 1986b). In this paper, we describe additional differences in connections to the telson non-giant fast flexor (FF) motor neurones and to the telson flexor inhibitor (FI). The telson FF motor neurones in ganglion 6 (G6) receive inputs similar to those in G4 and G5 (Miller, Hagiwara & Wine, 1985). The escape command neurones (lateral giants, LGs, and medial giants, MGs) in common provide weak disynaptic input via the telson segmental giant (SG6), and relatively strong tri-synaptic input via SG2, SG3 and the corollary discharge interneurones 12 and 13. There may also be some direct input from the MGs, but it, as well as the connections from SG6, appears to vary in different preparations. The compound PSP produced in telson FFs by a single LG or MG impulse was suprathreshold in only five of 55 experiments in isolated abdominal nerve cords, but the probability that a motor neurone would fire increased with additional giant axon impulses, showing that temporal summation of excitation outweighed the possible recruitment of inhibition. Firing probability was higher in semi-intact preparations, where at least one posterior telson FF was fired by a single LG impulse 50% of the time. As was pointed out previously (Dumont & Wine, 1986b), telson flexion would disrupt the behaviour pattern expected from LG commands. Two pathways of feedforward inhibition were found which prevent such disruption. The sensory input that recruits the LG also recruits powerful feedforward inhibition of the telson FF motor neurones, which reduces the probability that they will be fired by the LG. The same sensory stimulus also evokes inhibition of FFs in G5, excitation of FFs in G2 and G3, and mixed excitation and inhibition of FFs in G4. In addition, the telson FIs fire at short latency during LG-mediated tailflips. This occurs because the telson FIs are excited by sensory input. In fact, the firing threshold of the telson FIs to sensory input is lower than that of the LGs, at least for electrical stimulation of nerves. When the LGs do fire, they produce additional excitation of the FIs. The telson FIs also are excited by the LGs but not by the MGs. In contrast’ the anterior homologues of the telson FIs receive equivalent, delayed excitation from both MGs and LGs, and weaker sensory input, so that they tend to fire only after the peak of flexion (Wine & Mistick, 1977). The predicted net effect of these connections is that the telson flexor muscles should not contract during naturally elicited LG tailflips, and this is consistent with observed behaviour. The results can be interpreted as providing additional examples of potentially maladaptive central connections which are not expressed in behaviour because of feedforward inhibition.

The Telson Flexor Neuromuscular System of the Crayfish: II. Segment-Specific Differences in Connectivity Between Premotor Neurones and the Motor Giants

ABSTRACT The telson and sixth ganglion of the crayfish contain a fast flexor system that is homologous to that found in anterior segments, but doubled (Dumont & Wine, 1986a). In this paper we document differences in connections to the motor giants (MoGs) in the telson as compared to the MoGs in the anterior five abdominal segments. Unlike their homologues in anterior segments, the telson MoGs receive excitatory input via a trisynaptic pathway that is activated by the escape command axons, the lateral and medial giants (LGs and MGs), and includes the identified corollary discharge interneurones 12 and 13. For 13, at least, the connection to the MoGs is monosynaptic, electrical and rectifying, and is sufficiently strong that simultaneous activation of the two I3s alone fires the telson MoGs. The trisynaptic pathway from the LGs to the telson MoGs is inhibited by central, command-derived, postsynaptic inhibition of the telson MoGs, which typically arrives earlier than the excitation. In experimental preparations, this inhibition can be partially circumvented by stimulating the LGs anywhere anterior to the third abdominal ganglion. This is possible because the polysynaptic excitatory pathway is recruited in the third ganglion, while inhibition is recruited by the LGs locally in the sixth ganglion. Hence the site of impulse initiation in the LG affects the relative timing of excitation and inhibition of the telson MoGs. This arrangement makes it possible, in principle, for the site of impulse initiation in the LG to affect the form of the resulting tailflip. In dissected preparations, LG impulses initiated anterior to the third ganglion fired the telson MoGs in 16 out of 25 experiments, while impulses initiated posteriorly never fired the telson MoGs (nine experiments). Behavioural studies indicate that anterior stimuli which evoke LG activity do not cause activation of the telson MoGs. We suggest that in intact animals inhibition of the telson MoGs is more effective than in physiological preparations. As far as we can tell from available evidence, the 13 input to the telson MoG is never expressed, and therefore cannot be explained in functional terms. We suggest that the differences between the inputs to the MoGs of the telson and of the fourth and fifth ganglia is the incidental result of developmental constraints during evolution.

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

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.

Integrative properties of crayfish medial giant neuron: steady-state model.

A quantitative morphological description of the crayfish medial giant (MG) neuron was obtained on the basis of 14 individual cells filled with lucifer yellow. The cable parameters of seven MGs were measured in the axon with two or three microelectrodes. The length constant is 4.3 +/- 0.8 mm, the membrane time constant is 3.1 +/- 0.8 ms, the input resistance is 3.6 +/- 0.2 (X10(4) alpha, the mean axon diameter is 208 +/- 34 microns. The specific membrane resistance (Rm) is 2,000 +/- 204 alpha x cm2. The specific axoplasmic resistance (Ri) is 60 +/- 29 alpha x cm and the membrane capacitance is 1.6 +/- microF/cm2. The MG is electrotonically coupled to its symmetrical homolog. The coupling coefficient is 0.46 for both steady-state signals and spike transmission. A steady-state cable model of the MG was calculated on the basis of the axonal Rm and Ri values, the electrotonic coupling coefficient to the MG symmetrical homolog, and the mean dimensions of the 14 MG neurites. The model successfully predicts geometrically determined variations in input resistance and steady-state signal attenuation. A salient feature of the MG steady-state model is the extent to which dendritic input conductance and the attenuation of steady-state voltages is determined by the large input conductance of the axon. Because of the large diameter of the MG neurites, electrotonic distances between dendrite terminals and the integrating segment are short (0.3-0.74 lambda) and the principal basis of excitatory postsynaptic potential (EPSP) attenuation is variation is local input resistance. The time integral of the electrotonic coupling potential between the MGs is diminished by 9.5-21.4% during a monosynaptic sensory EPSP. The magnitude of the inferred synaptic conductance seen at the decussation is inversely related to the electrotonic distance between the decussation and the active dendritic branch. The modest change in input resistance near the electrotonic junction is consistent with the morphological and electrotonic separation of the electrotonic junction and the sites of synaptic action on the dendrites. When the reversal potentials of monosynaptic EPSPs are measured at the integrating segment, the measurements vary systematically with the input pathway selected and overestimate the dendritic reversal potentials by up to 60%.(ABSTRACT TRUNCATED AT 400 WORDS)

Inhibition of mechanosensory interneurons in the crayfish. I. Presynaptic inhibition from giant fibers.

1. Sucrose-gap and intracellular recordings were used to study the primary afferent depolarization (PAD) produced in mechanosensory afferents by impulses in lateral and medial giant axons, which are the command cells for the tail flip escape response in the crayfish. 2. The lateral and medial giant axons produce PAD through a polysynaptic interneuronal pathway. The response has a relatively long intraganglionic latency (7--11 ms), and command-evoked PAD can be recorded in ganglia from which the giant axons have been experimentally disconnected. 3. The final neurons of the pathway that delivers inhibition are few in number and extensive in distribution; most appear to be common to lateral and medial giant pathways. 4. At least some of the inhibitory interneurons have axons in the interganglionic connectives and probably produce both presynaptic and postsynaptic inhibition. 5. Stimulation of the lateral, but not the medial, giant axons causes a small, short-latency deplorization that is stable at high repetition rates. This small potential can be accounted for by transmission across known electrical synapses between mechanosensory afferents and the lateral giants in each abdominal ganglion. 6. Repetitive stimulation of the lateral giant axons causes substantial augmentation of PAD, apparently through recruitment of additional interneurons. PAD evoked by a single medial giant (MG) stimulus is generally much larger than that elicited by a single lateral giant (LG) spike. However, MG-PAD summates little and so the maximum PAD deltaV reached during repetitive firing is equivalent for the two types of giant axons. 7. Iontophoresis of gamma-aminobutyric acid (GABA) into the ganglionic neuropil depolarizes the primary afferents and blocks activity in neurons that have axons in the interganglionic connective. 8. The extrapolated PAD reversal potential and pharmacological studies suggest that a GABA-mediated chloride conductance increase is involved in the production of PAD.

Biochemical studies of trophic dependencies in crayfish giant axons

Data from previous histological studies28 indicate that long-term survival of crayfish medial giant axons might be due in part to trophic support from cells of the surrounding glial sheath which often hypertrophy in response to transection of the medial giants.The biochemical studies reported herein show that segments from transected ventral nerve cords (VNC) always incorporate more [3H]leucine into protein than do corresponding segments from intact VNCs. Furthermore, the relative amount of [3H]leucine incorporation in severed segments seems to be influenced by distance and direction from the lesion site as well as time after lesioning. Similar spatiotemporal parameters were previously shown to be correlated with extent of glial hypertrophy around severed medial giant axons28.Quantitative autoradiography of medial giant axons after incubation in [3H]-leucine revealed that the grain density of label in glial sheaths surrounding severed medial giants was over two-fold greater than in sheaths around corresponding control axons. Moreover, the grain density in the axoplasm of severed medial giants was nearly four-fold greater than the grain density in the axoplasm of control axons. Data from experiments using short or long labeling intervals suggests that labeling in the medial giant axoplasm may be due more to transfer from glial sheat cells than from inherent axonal synthetic mechanisms. In light of this and other data, we conclude that long-term survival of severed medial giant axons is probably due to the direct transfer of trophic substances from cells of the glial sheath into the axon.

Histological studies of trophic dependencies in crayfish giant axons

Medial giant (MGA) and lateral giant (LGA) axons of crayfish were doubly cut in order to selectively isolate axonal segments from perikaryal and transsynaptic sources of trophic input. Isolated MGA segments remained morphologically intact for over 43 days, whereas isolated LGA segments usually degenerated within one week. The glial sheaths around isolated MGA segments had significantly increased in thickness within one week, but severed LGA segments showed no increase in sheath thickness at any time after lesioning. These data suggest that cells of the surrounding glial sheath can provide trophic support to isolated MGA segments but not to isolated LGA segments. Extent of glial hypertrophy seems dependent upon specific spatiotemporal parameters.The diameters of isolated MGA segments decreased more rapidly than the diameters of singly cut MGA segments. These data suggest that the MGA also receives some trophic support from pre- or postsynaptic sources. Conversely, some singly cut LGA segments completely degenerated within one week, whereas other singly cut LGA segments remained intact for at least 43 days after lesioning. Such results suggest that the LGA receives a significant trophic input from pre- or postsynaptic structures.

Synaptic connections between medial giant neurons in lobsters

1. 1. Synaptic connections between the pair of medial giant (MG) interneurons were found in the supraesophageal ganglion (brain) of the lobster. Transmission at this connection appears to be mediated via a two-way electrical synapse. 2. 2. A posterior connection between the MGs, in one or more abdominal ganglia, was also observed. Conduction at the posterior synapse was usually observed after blocking of the anterior synapse. 3. 3. In some cases, transmission at the posterior connection was one-way. This resulted in a “reverberating circuit” with an action potential traveling around the nervous system for several circuits in the MGs. 4. 4. Mode of transmission in this posterior synapse is unknown but may occur through neural elements which receive common input from the MGs.

Inhibition of an abdominal proprioceptive reflex in crayfish

Stimulation of the tonic muscle receptor organs inProcambarus clarkii results in reflex activation of the superficial extensors. This pathway is inhibited by activity in the lateral giant fibers and both medial giants. A labile synapse in the same pathway works synergistically with the giant fiber-mediated inhibition to prevent maladaptive activation of the superficial extensors during escape behavior. Evidence did not support the notion of giant fiber-mediated peripheral inhibition (via the accessory nerve) of MRO activity.

The different connections and motor outputs of lateral and medial giant fibres in the crayfish.

ABSTRACT High-speed cinematography was used to analyse the abdominal movements of crayfish in response to separate stimulation of medial and lateral giant axons. These films showed that the medial giant fibres command complete abdominal flexions with little flaring of the tail appendages. The lateral giants, in contrast, evoked a relatively weak flexion of the middle abdominal segments, accompanied by promotion of the exopodites of the uropods. An examination of the muscles activated by the two types of giant fibres shows that differences in the connexions between the giant fibres and specific motor neurones can account for the behavioural differences observed. The output of the giant fibres was determined in the sixth abdominal ganglion, where their differential effects are most pronounced. The medial giants activate motor neurones whose axons emerge from root 6 of the sixth ganglion. The lateral giants activate motor neurones whose axons emerge via roots 2 and 3, as well as those emerging via root 6. The larger motor neurones associated with the giant axons in the sixth root of the sixth ganglion have been mapped by Procion Yellow injection, and the terminations of the central giant axons in the sixth ganglion have also been determined. The connexions revealed by this technique are consistent with the physiological findings. The evidence suggests that root 6 of the sixth ganglion is homologous with root 3 of the more anterior ganglia. However, the giant motor neurone of the sixth ganglion has not been identified. The medial and lateral giant fibres, and perhaps other specific ‘command’ interneurones, can thus drive specific ensembles of phasic motor neurones to provide a range of stereotyped quick movements. In this respect the organization of the phasic system of interneurones and motor neurones resembles that in the tonic system.