Fast Flexor Research Articles

Motor neurons in the escape response circuit of white shrimp (Litopenaeus setiferus).

Many decapod crustaceans perform escape tailflips with a neural circuit involving giant interneurons, a specialized fast flexor motor giant (MoG) neuron, populations of larger, less specialized fast flexor motor neurons, and fast extensor motor neurons. These escape-related neurons are well described in crayfish (Reptantia), but not in more basal decapod groups. To clarify the evolution of the escape circuit, I examined the fast flexor and fast extensor motor neurons of white shrimp (Litopenaeus setiferus; Dendrobranchiata) using backfilling. In crayfish, the MoGs in each abdominal ganglion are a bilateral pair of separate neurons. In L. setiferus, the MoGs have massive, possibly syncytial, cell bodies and fused axons. The non-MoG fast flexor motor neurons and fast extensor motor neurons are generally found in similar locations to where they are found in crayfish, but the number of motor neurons in both the flexor and extensor pools is smaller than in crayfish. The loss of fusion in the MoGs and increased number of fast motor neurons in reptantian decapods may be correlated with an increased reliance on non-giant mediated tailflipping.

Time course of IL-15 expression after acute resistance exercise in trained rats: effect of diabetes and skeletal muscle phenotype.

Type 1 diabetes is associated with skeletal muscle atrophy. Skeletal muscle is an endocrine organ producing myokines such as interleukin-15 (IL-15) and interleukin-6 (IL-6) in response to contraction. These factors may mediate the effects of exercise on skeletal muscle metabolism and anabolic pathways. Lack of correlation between muscle IL-15 mRNA and protein levels after exercise training has been observed, while regulatory effects of IL-6 on IL-15 expression have also been suggested. This study determined post-exercise changes in muscle IL-15 and IL-6 mRNA expression and IL-15 protein levels in healthy and streptozotocin-induced diabetic rats in both the fast flexor hallucis longus (FHL) and slow soleus muscles. Resistance training preserved FHL muscle weight in diabetic rats and increased IL-15 protein levels in both the soleus and FHL muscles. However, the temporal pattern of this response was distinct in normal and diabetic rats. Moreover, discordance between post-exercise muscle IL-15 mRNA and protein expression was observed in our study, and diabetes suppressed post-exercise increases in FHL muscle IL-6 mRNA expression. Our study indicates that training, skeletal muscle phenotype, and metabolic status all influence the temporal pattern of post-exercise changes in IL-15 expression. Muscle IL-15 protein levels increase following training, suggesting this may be an adaptation contributing to increased capacity for secretion of this myokine that is not depressed by the diabetic state.

Expression of interleukin-15 and inflammatory cytokines in skeletal muscles of STZ-induced diabetic rats: effect of resistance exercise training

Skeletal muscle atrophy is associated with type-1 diabetes. Skeletal muscle is the source of pro- and anti-inflammatory cytokines that can mediate muscle hypertrophy and atrophy, while resistance exercise can modulate both muscle mass and muscle cytokine expression. This study determined the effects of a 5-week resistance exercise training regimen on the expression of muscle cytokines in healthy and streptozotocin-induced diabetic rats, with special emphasis on interleukin-15 (IL-15), a muscle-derived cytokine proposed to be involved in muscle hypertrophy or responses to stress. Induction of diabetes reduced muscle weight in both the fast flexor hallucis longus (FHL) and slow soleus muscles, while resistance training preserved FHL muscle weight in diabetic rats. IL-15 protein content was increased by training in both FHL and soleus muscles, as well as serum, in normal and diabetic rats. With regard to proinflammatory cytokines, muscle IL-6 levels were increased in diabetic rats, while training decreased muscle IL-6 levels in diabetic rats; training had no effect on FHL muscle IL-6 levels in healthy rats. Also, tumor necrosis factor-alpha (TNF-α) and IL-1β levels were increased by diabetes, but not changed by training. In conclusion, we found that in diabetic rats, resistance training increased muscle and serum IL-15 levels, decreased muscle IL-6 levels, and preserved FHL muscle mass.

Effects of fetal exposure to lipopolysaccharide, perinatal anoxia and sensorimotor restriction on motor skills and musculoskeletal tissue: Implications for an animal model of cerebral palsy

Cerebral palsy (CP) is a disorder of locomotion, posture and movement that can be caused by prenatal, perinatal or postnatal insults during brain development. An increased incidence of CP has been correlated to perinatal asphyxia and maternal infections during gestation. The effects of maternal exposure to low doses of bacterial endotoxin (lipopolysaccharide, LPS) on motor behavior and hind leg muscle morphology were examined in young adult rats. Prenatal exposure to LPS was also studied in association with perinatal anoxia (PA) and/or combined with subsequent sensorimotor restriction (SR) and all possible combinations of the three conditions. Rats exposed to LPS, PA and SR alone or combined (LPS + PA, LPS + SR, PA + SR, and LPS + PA + SR) showed deficits in balance and coordination when tested on the Rotarod. The SR groups, with or without other insults, (SR, LPS + SR, PA + SR, and LPS + PA + SR) exhibited the greatest motor deficits, characterized by the reduced ability to perform the horizontal ladder and suspended bar tests on postnatal day 29 (P29) and P45. Histological assessment revealed substantial morphological alterations in the slow ankle extensor soleus muscle of all SR rats. Soleus myofibers presented a reduction in cross-sectional area (CSA), an increase in sarcomere length and a decrease in sarcomere density. The CSA of the fast flexor tibialis anterior muscle was only decreased by the association of all treatments (LPS, PA, SR), but no differences were found in sarcomere length and density when compared to control. A slow-to-fast fiber type transition was only observed in the soleus and tibialis anterior muscles in the SR groups. These results suggest that exposure to LPS during the prenatal period, PA, SR alone or in combination has various degrees of consequences on motor behavior and muscle morphology. These data corroborate the concept that early experience-dependent movements play the most important role in shaping motor behavior and that reduced or anomalous sensorimotor experience can contribute to the development of aberrant motor behavior and muscle morphology.

α‐Adrenergic signalling activates protein kinase D and causes nuclear efflux of the transcriptional repressor HDAC5 in cultured adult mouse soleus skeletal muscle fibres

The protein kinase PKD1 has recently been linked to slow fibre-type gene expression in fast skeletal muscle through phosphorylation of class II histone deacetylase (HDAC) molecules, resulting in nuclear efflux of HDAC and consequent activation of the transcription factor MEF2. However, possible upstream activators of PKD, and the time course and signalling pathway of downstream effectors have not been determined in skeletal muscle. Using fluorescent fusion proteins HDAC5-green fluorescent protein (GFP) and PKD1-mPlum expressed in fibres isolated from predominantly slow soleus muscle and maintained for 4 days in culture, we now show that alpha-adrenergic receptor activation by phenylephrine causes a transient, PKD-dependent HDAC5-GFP nuclear efflux. Concurrent to this response, PKD1-mPlum transiently redistributes from cytoplasm to plasma membrane and nuclei, and back, during 2 h exposure to phenylephrine. The recovery may reflect alpha-receptor desensitization. In contrast, the phorbol ester PMA (phorbol-12-myristate-13-acetate, a pharmacological mimic of the downstream mediator diacylglycerol in alpha-adrenergic signalling), caused continuous PKD-dependent HDAC5-GFP nuclear efflux and maintained PKD1-mPlum redistribution. In the absence of expressed HDAC, PMA increased histone H3 acetylation and increased MEF2 reporter activity in a PKD-dependent manner, consistent with PKD phosphorylation of endogenous HDAC(s) and reduced nuclear HDAC activity due to HDAC nuclear efflux. HDAC5-GFP did not respond to PMA in fibres from predominantly fast flexor digitorum brevis (FDB) muscle, but did in FDB fibres expressing exogenous PKD1. Our results demonstrate that a PKD-mediated signalling pathway for HDAC nuclear efflux is activated in slow skeletal muscle through adrenergic input, which is typically active in parallel with motor neurone input during muscular activity.

Front leg movements and tibial motoneurons underlying auditory steering in the cricket (Gryllus bimaculatusdeGeer)

Front leg movements in the cricket (Gryllus bimaculatus) were measured during phonotactic steering on a trackball together with electromyogram recordings of the tibial extensor and flexor muscles. Up-down leg movements clearly indicated the step cycle and were independent of auditory stimulation. By contrast, left-right movements of the front leg were dependent on sound direction, with crickets performing rapid steering leg movements towards the active speaker. Steering movements were dependent on the phase of sound relative to the step cycle, and were greatest for sounds occurring during the swing phase. During phonotaxis the slow extensor tibiae motoneuron responded to ipsilateral sounds with a latency of 35-40 ms, whereas the fast flexor tibiae motoneurons were excited by contralateral sound. We made intracellular recordings of two tibial extensor and at least eight flexor motoneurons. The fast extensor tibiae, the slow extensor tibiae and one fast flexor tibiae motoneurons were individually identifiable, but a group of at least four fast flexor tibiae as well as at least three slow flexor tibiae motoneurons of highly similar morphology could not be distinguished. Motoneurons received descending inputs from cephalic ganglia and from local prothoracic networks. There was no overlap between the dendritic fields of the tibial motoneurons and the auditory neuropile. They did not respond to auditory stimulation at rest. Neither extracellular stimulation of descending pathways nor pharmacological activation of prothoracic motor networks changed the auditory responsiveness. Therefore, any auditory input to tibial motoneurons is likely to be indirect, possibly via the brain.

Is spinal cord isolation a good model of muscle disuse?

The patterns of normal daily activity that are required to maintain normal skeletal muscle properties remain unknown. The present study was designed to determine whether spinal cord isolation can be used as a reliable experimental model of neuromuscular inactivity, that is, as a baseline for the absence of activity. Electromyograms (EMGs) were recorded from selected hindlimb muscles of unanesthetized rats over 24-hour periods before and 7, 30, 60, and 90 days after surgical isolation of the lumbar spinal cord. Our data indicate that some rat slow muscle fibers pre-surgery were activated for less than 3 hours per day. Spinal cord isolation (SI) reduced the mean daily integrated EMG (IEMG) and daily EMG duration in the primary slow extensor muscle (soleus) to <1% of control, and in the primary fast extensor muscles [medial gastrocnemius (MG) and vastus lateralis (VL)] to <2% of control. These parameters were decreased to <8% and 3% of control, respectively, in a primary fast flexor muscle, the tibialis anterior (TA). From 30 to 90 days post-SI, the mean amplitudes of the spontaneous EMG bursts were relatively normal in the soleus, increased approximately 2-fold in the MG and VL, and increased approximately 4-fold in the TA. Some evidence of the normal antagonistic flexor-extensor relationship was apparent in the brief periods of recorded activity post-SI. These results indicate that SI eliminates nearly all of the normal EMG activity in the hindlimb muscles in the presence of relatively normal muscle innervation and functional intraspinal neural circuitry.

Loss of Escape-Related Giant Neurons in a Spiny Lobster,Panulirus argus

When attacked, many decapod crustaceans perform tailflips, which are triggered by a neural circuit that includes lateral giant interneurons, medial giant interneurons, and fast flexor motor giant neurons (MoGs). Slipper lobsters (Scyllaridae) lack these giant neurons, and it has been hypothesized that behavioral (e.g., digging) and morphological (e.g., flattening and armor) specializations in this group caused the loss of escape-related giant neurons. To test this hypothesis, we examined a species of spiny lobster, Panulirus argus. Spiny lobsters belong to the sister taxon of the scyllarids, but they have a more crayfish-like morphology than scyllarids and were predicted to have escape-related giant neurons. Ventral nerve cords of P. argus were examined using paraffin-embedded sections and cobalt backfills. We found no escape-related giant neurons and no large axon profiles in the dorsal region of the nerve cord of P. argus. Cobalt backfills showed one fewer fast flexor motor neuron than in species with MoGs and none of the fast flexor motor neurons show any of the anatomical specializations of MoGs. This suggests that all palinuran species lack this giant escape circuit, and that the loss of rapid escape behavior preceded, and may have driven, alternative predator avoidance and anti-predator strategies in palinurans.

Differential modulation of myosin heavy chain phenotype in an inactive extensor and flexor muscle of adult rats

The effects of chronic neuromuscular inactivity on the phenotype and size of muscle fibres in a fast ankle extensor (medial gastrocnemius, MG) and a fast ankle flexor (tibialis anterior, TA) muscle of the rat hindlimb were determined. Inactivity was produced by spinal cord isolation (SI), i.e. complete spinal cord transections at a mid-thoracic and high sacral level and bilateral deafferentation between the transection sites. After 90 days of SI, the MG and TA muscle weights were 53 and 45% lower than in age-matched controls. Overall mean fibre sizes in the deep (close to the bone) and superficial (away from the bone) regions were approximately 60 and 65% smaller in the MG and approximately 40 and 50% smaller in the TA of SI than control rats, respectively. The myosin heavy chain (MHC) composition shifted towards the faster isoforms after SI: the MG showed an increase in both types IIx (20%) and IIb (23%), whereas the TA showed a marked increase in type IIx (94%) and a decrease in type IIb (18%) MHC. Both muscles in SI rats showed no type IIa and only one MG muscle had approximately 5% type I MHC. These results show that prolonged inactivity has a stronger effect on a fast extensor compared with a fast flexor in the rat hindlimb. The larger decrease in mass and fibre size in the MG than the TA most probably reflects the larger impact of chronic inactivity on the normally more highly recruited extensor than flexor muscle. The primary shift to type IIb MHC in the MG and type IIx MHC in the TA indicate a different default mode for an inactive extensor vs. flexor muscle, and may reflect differing activity-independent neural influences, i.e. neurotrophic factors, on muscle fibre phenotype in extensors vs. flexors.

Postnatal appearance of 5-HT2A receptors on fast flexor and slow extensor rat motor neurons

Motor neurons to the slowly contracting extensor soleus muscle in behaving rats begin to fire tonically in the 2nd week after birth. In the adult, tonic firing becomes predominant and appears to arise from plateau potentials under monoaminergic control. In the present work, motor neurons to slowly contracting extensor soleus and rapidly contracting extensor digitorum longus, a physiological flexor muscle, were retrogradely labeled with fluorescent dextran and examined for immunoreactivity to 5-HT 2A receptors in 1 and 2 week old and adult rats. No reactivity was detected at 1 week. At 2 weeks, reactivity was detected on 67% slowly contracting extensor soleus (16 of 24) and 19% extensor digitorum longus (11 of 57) motor neurons. In the adult, the intensity of staining was higher and the percentage of labeled motor neurons 79 for slowly contracting extensor soleus (34 of 43) and 31 for extensor digitorum longus (11 of 35). On slowly contracting extensor soleus motor neurons, labeling appeared more often on soma and dendrites than on dendrites only, whereas on extensor digitorum longus motor neurons, labeling appeared more often on dendrites only. These results are consistent with the hypothesis that serotonergic innervation contributes to the appearance and subsequent increase in tonic firing of rat slowly contracting extensor soleus motor neurons in postnatal development.

Gravitational unloading effects on muscle fiber size, phenotype and myonuclear number

The effects of gravitational unloading with or without intact neural activity and/or tension development on myosin heavy chain (MHC) composition, cross-sectional area (CSA), number of myonuclei, and myonuclear domain (cytoplasmic volume per myonucleus ratio) in single fibers of both slow and fast muscles of rat hindlimbs are reviewed briefly. The atrophic response to unloading is generally graded as follows: slow extensors > fast extensors > fast flexors. Reduction of CSA is usually greater in the most predominant fiber type of that muscle. The percentage of fibers expressing fast MHC isoforms increases in unloaded slow but not fast muscles. Myonuclear number per mm of fiber length and myonuclear domain is decreased in the fibers of the unloaded predominantly slow soleus muscle, but not in the predominantly fast plantaris. Decreases in myonuclear number and domain, however, are observed in plantaris fibers when tenotomy, denervation, or both are combined with hindlimb unloading. All of these results are consistent with the view that a major factor for fiber atrophy is an inhibition or reduction of loading of the hindlimbs. These data also indicate that predominantly slow muscles are more responsive to unloading than predominantly fast muscles.

Pattern generation for walking and searching movements of a stick insect leg. II. Control of motoneuronal activity.

In the stick insect, Cuniculina impigra, intracellular recordings from mesothoracic motoneurons that control flexion and extension of the tibia and depression and levation of the trochantero-femur were made while the leg performed walking-like movements on a treadband or stereotyped rhythmic searching movements. We were interested in how synaptic input and intrinsic properties contribute to form the activity pattern of motoneurons during rhythmic leg movements without sensory feedback from other legs. During searching and walking, motoneurons expressed a rhythmic bursting pattern that was formed by a depolarizing input followed by a hyperpolarizing input in the inter-burst interval. This basic pattern was similar in all fast, semi-fast, and slow motoneurons that were recorded. Hyperpolarizations were in synchrony with activity in the antagonistic motoneurons. De- and hyperpolarizations were associated with a decrease in input resistance. All motoneurons showed spike frequency adaptation when depolarized by current injection to a membrane potential similar to that observed during walking. In the hyperpolarizing phase of fast flexor motoneurons, the initial maximum hyperpolarization was followed by a sag in potential toward more depolarized values. Consistent with this observation, only fast flexor motoneurons developed a depolarizing sag potential when hyperpolarized by injection of constant negative current.

Modulatory effects of nitric oxide on synaptic depression in the crayfish neuromuscular system.

A characteristic physiological property of the neuromuscular junction between giant motor neurones (MoGs) and fast flexor muscles in crayfish is synaptic depression, in which repetitive electrical stimulation of the MoG results in a progressive decrease in excitatory junction potential (EJP) amplitude in flexor muscle fibres. Previous studies have demonstrated that l-arginine (l-Arg) modulates neuromuscular transmission. Since l-Arg is a precursor of nitric oxide (NO), we examined the possibility that NO may be involved in modulating neuromuscular transmission from MoGs to abdominal fast flexor muscles. The effect of a NO-generating compound, NOC7, was similar to that of l-Arg, reversibly decreasing the EJP amplitude mediated by the MoG. While NOC7 reduced the amplitude of the EJP, it induced no significant change in synaptic depression. In contrast, a scavenger of free radical NO, carboxy-PTIO, and an inhibitor of nitric oxide synthase, l-NAME, reversibly increased the EJP amplitude mediated by MoGs. Synaptic depression mediated by repetitive stimulation of MoGs at 1 Hz was partially blocked by bath application of l-NAME. Bath application of a NO scavenger, a NOS inhibitor and NO-generating compounds had no significant effects on the depolarisation of the muscle fibres evoked by local application of l-glutamate. The opposing effects on EJP amplitude of NOC7 and of carboxy-PTIO and l-NAME suggest that endogenous NO presynaptically modulates neuromuscular transmission and that it could play a prominent role at nerve terminals in eliciting MoG-mediated synaptic depression in the crayfish Procambarus clarkii.

Modulatory effects of amino acids on neuromuscular transmission on the crayfish fast flexor muscle

The modulatory effects of amino acids on neuromuscular transmission from an identified giant motor neuron (MoG) and abdominal fast flexor muscles of the crayfish were examined using electrophysiological and pharmacological techniques. The distribution of amino acids in the cell body and axon of a single MoG was revealed using high-performance liquid chromatography with electrochemical detection. Eight different amino acids—aspartate, glutamate, glutamine, arginine, glycine, taurine, alanaine and γ-aminobutyric acid—were simultaneously detected in either the cell body or the axon of MoG. Aspartate, glutamate, alanine and arginine were present at relatively high concentration. Local pressure ejection of glutamate caused a depolarization of the abdominal fast flexor muscle fibers. On the other hand, aspartate, alanine and arginine had no clear effects on the same muscle fibers. Aspartate and arginine, however, had modulatory effects on neuromuscular transmission. Alanine had no significant effect on the neuromuscular transmission. Aspartate at a concentration of 200 μM decreased the amplitude of EJPs in the fast flexor muscle mediated by stimulation of both the MoG and non-giant fast flexor motor neurons. Arginine at a concentration of 200 μM reduced the EJP amplitude of the muscle fibers in response to MoG stimulation but enhanced the EJP amplitude of the same muscle fibers by stimulation of non-giant fast flexor motor neurons. Although rather high concentration (1 mM) were required, aspartate increased and arginine decreased the depolarization of the muscle fibers induced by local ejection of glutamate. The opposite effect of arginine on the fast flexor muscles in response to the stimulation of different motor neurons suggested its modulatory role in the different effects of these motor neurons (depression and facilitation) in the fast flexor muscles. J. Exp. Zool. 283:531–540, 1999. © 1999 Wiley-Liss, Inc.

Modulatory effects of amino acids on neuromuscular transmission on the crayfish fast flexor muscle

The modulatory effects of amino acids on neuromuscular transmission from an identified giant motor neuron (MoG) and abdominal fast flexor muscles of the crayfish were exam- ined using electrophysiological and pharmacological techniques. The distribution of amino acids in the cell body and axon of a single MoG was revealed using high-performance liquid chromatogra- phy with electrochemical detection. Eight different amino acids—aspartate, glutamate, glutamine, arginine, glycine, taurine, alanaine and γ-aminobutyric acid—were simultaneously detected in ei- ther the cell body or the axon of MoG. Aspartate, glutamate, alanine and arginine were present at relatively high concentration. Local pressure ejection of glutamate caused a depolarization of the abdominal fast flexor muscle fibers. On the other hand, aspartate, alanine and arginine had no clear effects on the same muscle fibers. Aspartate and arginine, however, had modulatory effects on neuromuscular transmission. Alanine had no significant effect on the neuromuscular transmission. Aspartate at a concentration of 200 μM decreased the amplitude of EJPs in the fast flexor muscle mediated by stimulation of both the MoG and non-giant fast flexor motor neurons. Arginine at a concentration of 200 μM reduced the EJP amplitude of the muscle fibers in response to MoG stimulation but enhanced the EJP amplitude of the same muscle fibers by stimulation of non-giant fast flexor motor neurons. Although rather high concentration (1 mM) were required, aspartate increased and arginine de- creased the depolarization of the muscle fibers induced by local ejection of glutamate. The oppo- site effect of arginine on the fast flexor muscles in response to the stimulation of different motor neurons suggested its modulatory role in the different effects of these motor neurons (depression and facilitation) in the fast flexor muscles. J. Exp. Zool. 283:531n540, 1999. © 1999 Wiley-Liss, Inc.

Differential response of fast hindlimb extensor and flexor muscles to exercise in adult spinalized cats

Differential response of fast hindlimb extensor and flexor muscles to exercise in adult spinalized cats

L-glutamate as an Excitatory Transmitter of Motor Giant Neurons in the Crayfish Procambarus Clarkii

Motor giant neurons (MoGs) of the crayfish are identifiable motor neurons that innervate abdominal fast flexor muscles. The role of L-glutamate as a neurotransmitter at the neuromuscular junction between MoG and the abdominal fast flexor muscles was investigated using electrophysiological and pharmacological techniques. Local application of L-glutamate to a fast flexor muscle induced a depolarization of the muscle fibers. This glutamatergic depolarization was dose-dependent and was associated with a conductance increase. Bath application of L-glutamate caused a reversible reduction in the amplitude of the excitatory junctional potentials (EJPs) of the fast flexor muscles evoked by MoG stimulation. Twenty micromole L-glutamate was sufficient to reduce the amplitude of MoG-evoked EJP. The effect of depression was dose-dependent and MoG stimulation elicited almost no response in flexor muscle fibers under 1 mM L-glutamate application. Joro spider toxin, an L-glutamate antagonist, reduced the amplitude of EJPs elicited by MoG stimulation at a concentration of 0.1 tAM. The response of the flexor muscle to MoG stimulation did not recover completely after washing. When 5 jAM Joro spider toxin was applied, the EJP evoked by MoG was completely blocked and no recovery was observed after washing. These results strongly suggest that L-glutamate is the neurotransmitter at the neuromuscular junction between MoG and the abdominal fast flexor muscle in the crayfish.

Response of the Neuromuscular Unit to Spaceflight

Despite the inherent limitations placed on spaceflight investigations, much has been learned about the adaptations of the neuromuscular system to weightlessness from studies of rats flown for relatively short periods (approximately 4-22 days). Below is a summary of the major effects of spaceflight observed in muscles of rats that are not in their rapid growth stage: 1. Skeletal muscles atrophy rapidly during spaceflight; significant atrophy is observed as early as after 4 days of flight. 2. The atrophic response appears to be related to the primary function of the muscle. In the hindlimb, the relative amount of atrophy can be characterized as slow extensors > fast extensors > fast flexors. This pattern of relative atrophy does not appear to be occurring in the forelimb; however, not enough data are available to draw any definitive conclusions at this time. 3. Both slow and fast fibers atrophy during spaceflight, with the largest fibers within an individual muscle generally showing the greatest atrophic response. Interestingly, the amount of fiber atrophy appears to reach a plateau after about 14 days of flight. 4. Adaptations have been observed in the concentration and content of all muscle proteins pools, with the protein pools in slow muscles the most affected. 5. Some slow and fast fibers in predominantly slow and fast muscles show shifts in their histochemical and biochemical properties, toward those observed in a "faster" phenotype. 6. Some fibers, presumably expressing slow MHC isoforms before flight, begin to express fast MHC isoforms during flight. 7. The oxidative capacity of the muscles or fibers is relatively unaffected by spaceflight, particularly in the slow muscles. Any change in whole-body fatigability associated with spaceflight most likely reflects the loss in muscle and fiber mass. 8. The glycolytic capacity of the muscles and muscle fibers is enhanced after spaceflight. This metabolic adaptation seems to be related to the shift in the contractile proteins towards "faster" isoforms. 9. The vascularity of muscles appears to be maintained after flight, based, at least, on histological observations of capillarity. 10. The force capabilities of the muscles and fibers appear to decrease in parallel with the decreases in size, i.e., the specific tension is not significantly affected after flight. 11. Changes in the speed-related properties of the slow muscles are consistent with the adaptations in the myosin molecule, i.e., the slow muscles and some fibers in the slow muscles become "faster." 12. Some muscle fiber and neuromuscular junction damage has been observed after flight, particularly in the slow muscles. The extent of damage may be related to the amount of time that the muscles are allowed to reload before removal, i.e., in general, shorter intervals result in less fiber damage. 13. Adaptations in the motor (ventral horn) and sensory (spinal ganglia) neurons have been quite variable, but this may be related to the amount of time that the muscles are allowed to reload before removal. Morphological adaptations after relatively short periods of reloading may reflect a decrease in the activation of the neural elements during flight.

Long-lasting potentiation of a direct central connection between identified motor neurons in the locust.

The plasticity of the direct central connection between the fast extensor and the posterior fast flexor tibiae motor neurons in the locust (Schistocerca gregaria) metathoracic ganglion was studied. An action potential in the fast extensor results in a monosynaptic excitatory postsynaptic potential (EPSP) in the flexor motor neuron. Antidromic stimulation of the fast extensor at 100 Hz for 3.5 s resulted in a long-lasting potentiation of the EPSP amplitude. The potentiation was not dependent on feedback caused by movement of the tibia, and was associated with an increase in the input resistance of the flexor motor neuron. The potentiation was heterosynaptic, and was not affected by bath application of the N-methyl-D-aspartate receptor antagonist 2-amino-5-phosphonovaleric acid. The potentiation was voltage dependent, as hyperpolarizing the flexor motor neuron during the stimulation blocked the development of the potentiation whereas depolarizing the flexor in the absence of presynaptic activity caused potentiation of subsequent fast extensor-evoked EPSPs. The depolarization-induced potentiation was calcium dependent. Antidromic stimulation of the fast extensor at 100 Hz for 3.5 s also caused modulation of the presynaptic action potential. The spike duration was increased and the amplitude of the afterhyperpolarization reduced. These effects were dependent on movement of the tibia. Bath application of the 5-hydroxytryptamine (5-HT) receptor antagonist ketanserin blocked the changes in the presynaptic spike. The modulation was probably due to the release of 5-HT from proprioceptive afferents that monitor movement of the tibia about the femur. The modulation of the presynaptic action potential increases transmitter release onto the flexor motor neurons, and this acts in synergy with the postsynaptic modulation to potentiate the connection.

Intrinsic Differences in Axonal Growth from Crayfish Fast and Slow Motoneurons

The motoneurons innervating the fast and slow flexor muscles in the abdomen of crayfish form morphologically distinct motor terminals. Axons of the fast flexor (FF) motoneurons, which innervate the large (fast) flexor muscle, produce extensive motor terminal arbors with many branches. Axons of the slow flexor (SF) motoneurons, which innervate the thin (slow) flexor muscle, produce small terminal arbors with many fewer branches. To determine whether intrinsic factors contribute to these differences in terminal arbors, we compared regenerating axonal arbors from these two populations of motoneurons. We used an explant of the crayfish nerve cord in which axons from the FF and SF motoneurons regenerate on a homogeneous substrate. We found that regardless of the substrate, FF motor axons produced arbors with a greater total length and a greater number and density of branches than SF motor axons. These differences in regenerated arbors persisted in defined medium and in the absence of impulse activity, indicating that they result from intrinsic, neuron-specific factors. The greater branching of the FF motor axons may be related to differences in growth cones: growth cones of FF axons were significantly larger with more filopodia than growth cones of SF axons.