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H L Atwood

Publications and source records attributed to H L Atwood.

At least 19 recordsLinked to original sources
PubMed1992

Long-term adaptation of crayfish neurons depends on the frequency and number of impulses.

Increasing the impulse activity of crustacean neurons for a few days causes long-lasting changes in transmitter release, which are termed 'long-term adaptation' (LTA) in previous studies. Both the amount of transmitter released at the beginning of a stimulus train, and synaptic fatigue during repetitive stimulation, are reduced. The present study examines the dependence of these synaptic changes on the frequency and number of impulses used to elicit LTA. Fatigue resistance develops consistently when crayfish phasic motor neurons are stimulated for 3 days with as few as 9,000 impulses per day, and occurs in response either to low frequency stimulation (0.2 or 0.5 Hz), or to stimulation in short bursts at a moderate average frequency (2.5 Hz). In contrast, the reduction in initial transmitter release does not appear consistently when the frequency and number of impulses are both low (9,000 impulses per day delivered at 0.2 Hz), but does occur at the moderate stimulus frequency (2.5 Hz) and when a larger number of impulses (18,000) are delivered at a low frequency (0.5 Hz). The data suggest that the two changes in synaptic transmission that comprise LTA have different stimulus requirements.

Action Potentials↗
PubMed1992

Synaptic plasticity in a regenerated crayfish phasic motoneuron.

Crustacean neuromuscular systems provide many advantages for the study of synaptic transmission and plasticity. The present study examines aspects of synaptic transmission in the phasic, fast closer excitor (FCE) motoneuron of regenerated crayfish claws. Excitatory postsynaptic potentials (EPSPs) fatigued rapidly and showed poor long-term facilitation (LTF) in the smallest of regenerating claws. EPSPs in larger regenerating claws fatigued less and showed pronounced facilitation. These observations were not the same as those previously made during primary development of this motoneuron (Lnenicka and Atwood, 1985a, J. Neuroscience 5:459-467). Hence, regeneration is not the recapitulation of primary development. In situ stimulation of the FCE is known to lead to long-lasting adaptation of synaptic performance. This adaptation is age dependent; it is expressed in young but not old animals. In the regenerated FCE of old animals, we observed a novel form of long-lasting adaptation to imposed activity: EPSPs showed large initial EPSPs and did not exhibit resistance to fatigue during maintained stimulation. This indicates that aged motoneurons can express adaptive changes to increased activity following axonal regeneration, but that the adaptive changes are the opposite to what is observed in nonregenerated motoneurons.

Animals↗
PubMed1992

Maintenance of long-term adaptation of synaptic transmission requires axonal transport following induction in an identified crayfish motoneuron.

Motoneurons can adapt to altered levels of electrical activity by effecting semi-permanent changes in their neuromuscular synaptic physiology. In the present study, we tested the hypothesis that maintenance of activity-dependent long-term adaptation of synaptic transmission in a crayfish abdominal extensor motoneuron (phasic axon 3) required axonal transport following induction. Intact crayfish were chronically wired for periodic in vivo stimulation of axon 3. Periodic unilateral stimulation for 3-5 consecutive days (2 h/day) induced long-term adaptation (LTA) of neuromuscular synaptic transmission in axon 3. Initial EPSP amplitudes (measured at 0.1 Hz) were significantly reduced to approximately 40% of contralateral control amplitudes over a 7-day poststimulation period. Additionally, synaptic depression during 5 Hz test stimulation of axon 3 was significantly less in chronically stimulated neurons: excitatory postsynaptic potential (EPSP) amplitudes measured after 20 min of 5 Hz test stimulation (final EPSPs) were significantly larger in conditioned neurons than in unstimulated controls. The depression of initial EPSP amplitudes persisted for 7 days postinduction, while the increased synaptic stamina persisted for 4 days but was absent at 7 days postinduction. Axotomy of axon 3 following induction of LTA had no effect on long-term maintenance of the activity-induced reduction in initial EPSP amplitudes. Initial EPSP amplitudes in conditioned, axotomized neurons were still reduced to 42% of control amplitudes over the 7-day postinduction period. In contrast, postinduction axotomy of axon 3 elicited an accelerated decay of the enhanced synaptic stamina. Following axotomy, final EPSP amplitudes were significantly larger in conditioned neurons for only 1 day poststimulation.(ABSTRACT TRUNCATED AT 250 WORDS)

Adaptation, Physiological↗
PubMed1992

Age-dependent alterations of synaptic performance and plasticity in crustacean motor systems.

Age-related changes in synaptic performance and plasticity are surveyed in crustacean neuromuscular systems. These systems are functionally differentiated into phasic and tonic types, with different attributes of synaptic function and plasticity. Conversion of phasic neuromuscular junctions to a more phasic phenotype can be brought about by altering the activity of selected neurons. This type of plasticity disappears in older animals in some motor neurons, but is retained in others. Developmental programs set constraints on the age-dependent modifications of plasticity. Crustacean motor neurons are often characterized by great longevity, with progressive addition of new branches and synapses to keep up with growth of innervated muscle cells. Certain age-related compensatory mechanisms found in neuromuscular junctions of other species may not be required in crustaceans.

Aging↗
PubMed1991

Maximum likelihood estimation of non-uniform transmitter release probabilities at the crayfish neuromuscular junction.

The classical model of quantal release of neurotransmitter assumes that a fixed number of quantal units are available for release in the presynaptic terminal, and that each unit has the same probability of being released. This model also assumes that different units are released independently of one another. We consider two variations of the classical model. In the first case we assume that release is independent, but with potentially different release probabilities at different sites. In the second case we allow for dependence among the release units. A maximum likelihood procedure for the estimation of model parameters is developed, and an estimator of the number of quantal units is proposed. The performance of the method is assessed through a simulation study, and the procedures are applied to the analysis of a sequence of post-synaptic potentials recorded intracellularly at the crayfish neuromuscular junction. Goodness of fit and hypothesis test procedures reject the classical model in favor of an independent release mechanism with differing release probabilities. A more general release mechanism, allowing for dependence in the release process, also provides a good fit to the data analyzed.

Animals↗
PubMed1991

Variation in terminal morphology and presynaptic inhibition at crustacean neuromuscular junctions.

Synaptic terminals of excitatory and inhibitory neurons supplying muscle fibers in leg muscles of crabs (Pachygrapsus crassipes and Hyas areneus) were investigated with light and electron microscopy. Terminals responsible for large excitatory postsynaptic potentials (EPSPs) at low frequencies of activation had a compact configuration with clusters of terminal boutons radiating from the main axon branch. Terminals responsible for small EPSPs had a more diffuse organization, with boutons often arranged in series along thin axon branches. Inhibitory neurons, when activated, produced both presynaptic and postsynaptic inhibitory effects, with the former being more potent at low frequencies of activation. Presynaptic inhibition was variable in magnitude but was generally strong in fibers with large EPSPs. Representative terminals from regions of strong and weak presynaptic inhibition were identified by activity-dependent uptake of horseradish peroxidase, serially sectioned, and reconstructed from electron micrographs. Both regions were found to contain axo-axonal synapses from inhibitory to excitatory terminals, with a larger number in the region of strong presynaptic inhibition. In addition, axo-axonal synapses were more uniformly distributed in the latter region. The number of inhibitory presynaptic dense bars (active zones) was somewhat higher in the region of weak inhibition, but larger individual dense bars occurred in the region of strong inhibition. Possible factors contributing to the differences in strength of inhibition include: (1) morphology and electrical properties of terminals; and (2) high probability of transmission at a relatively small number of inhibitory synapses during low frequency activation in the region of strong inhibition.

Action Potentials↗
PubMed1991

Intracellular potassium and membrane potential in rat muscles during malnutrition and subsequent refeeding.

Nutrition alters total body potassium (TBK) and muscle potassium but little is known about in vivo intracellular K+. We measured free intracellular potassium-ion activity (aKi+), membrane potential (Em), and total potassium (Kt) and calculated intracellular potassium concentration [K+]i in predominantly slow- (soleus) and fast- (extensor digitorum longus) twitch muscles in rats undergoing underfeeding and subsequent refeeding. After underfeeding, aKi+ and Em decreased (P less than 0.025 and P less than 0.006, respectively) only in soleus muscle with restoration after refeeding, whereas [K+]i decreased in both muscles (P less than 0.005) and remained low after refeeding. K+ supplementation did not significantly change these indices or the ratio of free to total intracellular potassium (gamma Ki+). The data show that aKi+ behaves differently from [K+]i during malnutrition and that changes in aKi+ occur especially in slow-twitch fibers, suggesting that previously observed changes in TBK and muscle function are the result of fundamental alterations in muscle-cell energetics and membrane functions, not just mass.

Animals↗
PubMed1991

Activity-dependent recruitment of silent synapses.

At the crayfish neuromuscular junction, a long-lasting enhancement of synaptic transmission can be induced by tetanic stimulation of 10-20 Hz for several minutes. The long-lasting enhancement is presynaptic in origin, because quantal content increases but not quantal size, and is not dependent upon broadening or enlargement of the presynaptic action potential. The enhancement can be selectively blocked by presynaptic injection of agents that inhibit adenylate cyclase or the cyclic AMP-dependent protein kinase. Entry of calcium may not be sufficient in itself to produce the enhancement. Analyses of quantal events using both a simple binomial statistical method, and a more refined method that takes into account the possibility of unequal probabilities of responding units, have shown that the number of responding units increases during the long-lasting enhancement. In addition, there is an increase in the probability of transmitter release at preexisting units. In contrast, during short-term facilitation accompanying repetitive stimulation, response probability increases greatly whereas the number of responding units increases only moderately with frequencies of activation up to 20 Hz, which increase quantal output severalfold. These results indicate that responding units, hypothesized to be transmitting synapses, can be recruited to active transmission from an unresponsive pool by tetanic activity, and that protein phosphorylation is required for long-lasting changes to occur. The existence of an excess of synapses on crustacean nerve terminals is indicated by ultrastructural studies, which invariably show many synapses on the terminals. The number of morphologically defined synapses is always greater than the number of responding units seen in statistical analyses of quantal release for the same recording location.

Animals↗
PubMed1991

Synaptic transmission in decentralized axons of rock lobster.

Axons of the lobster deep abdominal extensor muscles were cut, and the resulting effects on their synaptic properties were observed. Decentralized axons continued to conduct action potentials and to release transmitter for at least a year after the cut. In controls, the single quanta were brief, and their decay phase could be fit by a single exponent, with a time constant of about 2 msec. Quanta of "cut axons" were slower, and their decay phase could not be fit by a single exponent. At midamplitude, the duration of the cut-axon quanta varied between 1.6 and 5.8 msec, as opposed to 0.6-2.8 msec in controls. Synaptic delay histograms were taken as a measure of time course of evoked release. In controls, evoked release lasted less than 10 msec at 14 degrees C. In cut axons, release lasted up to 10 times longer. The duration of release was not affected by tetrodotoxin, membrane depolarization, or hyperpolarization. It appears that the basic mechanism that controls the time course of evoked release is altered in degenerating terminals.

Action Potentials↗
PubMed1990

Axotomy-induced temporal dissociation of long-term adaptive changes at neuromuscular synapses of a crayfish phasic motoneuron.

Periodic in situ stimulation of an identified crayfish phasic extensor motoneuron for 3 consecutive days (2 h/day) at 2.5 Hz leads to long-term adaptation (LTA) of its neuromuscular synapses. LTA is characterized by reductions in both initial excitatory postsynaptic potential (EPSP) amplitudes and synaptic depression during repeated stimulation. These adaptive changes were evident 1 day following periodic stimulation. Axotomy of the motoneuron before or after the first day of stimulation of its distal surviving axon abolished both adaptive changes. Axotomy between the second and third stimulation periods abolished only the resistance to synaptic depression. Both adaptive changes were expressed following axotomy after the third day of stimulation. Axotomy alone did not affect neuromuscular transmission in control, unstimulated animals. These results show that axonal continuity between the phasic extensor motoneuron's cell body and its neuromuscular synapses is required at specific times during periodic stimulation for the expression of each of these long-term adaptive changes in neuromuscular transmission. Furthermore, the two adaptive changes in transmission are temporally separable, with the resistance to depression requiring more periodic stimulation to emerge than the reduction in initial EPSP amplitudes. The results also suggest that the molecular components responsible for the expression of these adaptive changes are synthesized in the soma and transported down the axon in response to periodic stimulation of the phasic axon.

Adaptation, Physiological↗
PubMed1990

Pericardial peptides enhance synaptic transmission and tension in phasic extensor muscles of crayfish.

Two identified peptides, which are structurally related to FMRF-NH2 and are known to be associated with lobster pericardial organs, increase nerve-evoked tension and excitatory postsynaptic potentials (EPSPs) recorded from crayfish deep abdominal extensor muscles. At low stimulus frequencies, which produce marked depression of muscle twitches with successive stimuli, the peptides quickly and reversibly restore tension. Increased quantal content of transmitter release, rather than changes in postsynaptic input resistance, accounted for most of the increase in EPSP amplitude. The results support earlier suggestions that these two peptides may act as circulating neurohormones and provide the first evidence for peptidergic modulation of a phasic neuromuscular system in a crustacean.

Animals↗
PubMed1990

Characterization and partial purification of different factors with contraction-potentiating activities from neurohaemal organs of the locust.

Phe-Met-Arg-Phe (FMRF-NH2) and structurally related peptides enhance neuromuscular transmission and contraction of the M. extensor tibiae preparations of the locusts Locusta migratoria and Schistocerca gregaria (Walther et al.: Neurosci. Lett. 45:99-104, '84). Similar effects could also be obtained with extracts of locust ganglia (Walther and Schiebe: Neurosci. Lett. 77:209-214, '87). By using two HPLC systems, we have partially purified extracts of the unpaired median nerves (including their neurohaemal organs) of different locust ganglia. The biological activity of the extracts served as an estimate for the degree of purification. Six different bioactive fractions were identified migrating at and close to retention times of known -RFamide peptides with similar bioactivity. No fraction coeluted with authentic FMRF-NH2 or FLRF-NH2. We demonstrate that extensor tibiae muscle contractions were potentiated by HPLC fractions from raw material with -RF-NH2 immunoreactivity, but also by HPLC fractions from raw material without such immunoreactivity.

Animals↗
PubMed1990

Long-term adaptation in lobster motor neurons and compensation of transmitter release by synergistic inputs.

Earlier studies with crayfish have shown that chronic increases in neural activity, by electrical stimulation, cause a long-lasting reduction in the amount of transmitter released at low stimulus frequencies or at the beginning of a stimulus train. When such chronic stimulation is applied to phasic extensor motor neurons of the lobster abdomen, a similar change in transmitter release is apparent, as indicated by a decrease in excitatory postsynaptic potential (EPSP) size at 0.1 Hz. However, the EPSPs from unstimulated axons which innervate the same target muscle from a different nerve increase in size. Thus, activity-dependent reduction in transmitter release at one set of synapses appears to be compensated for by increased synaptic efficacy from less active synergistic inputs. The mechanism of such compensation is not known.

Action Potentials↗
PubMed1990

Expression of long-term adaptation of synaptic transmission requires a critical period of protein synthesis.

The crayfish claw closer muscle is innervated by 2 distinct excitatory motoneurons, one tonic and the other phasic. The phasic motoneuron is relatively inactive and generates large EPSPs that normally depress rapidly with repetitive stimulation at moderate frequencies. Stimulation of the phasic motoneuron in vivo for 3 d at 5 Hz (2 hr/d) produced a marked adaptive shift in the neuromuscular synaptic response properties of the motoneuron: average initial EPSPs and depression of EPSPs were significantly reduced. We tested the hypothesis that neuronal protein synthesis is required for full expression of long-term adaptation (LTA). A reversible inhibitor of neuronal protein synthesis, cycloheximide (CHX), was injected into intact crayfish at various times prior to, during, or after each stimulation period. At a dosage of 5 micrograms/gm body weight, CHX inhibited the incorporation of [35S]-methionine into abdominal nerve cord protein for approximately 2 hr after administration (greater than 80% inhibition). Full expression of LTA was selectively blocked when CHX was administered 6 hr or 2 hr prior to each stimulation period. Both the reduction in initial EPSP amplitude and the resistance to synaptic depression were significantly attenuated. CHX administered at the onset of or at the end of each stimulation period did not affect the expression of LTA. Control experiments using unstimulated animals showed that neither chronic nor acute administration of CHX adversely affected the phasic axon's synaptic response properties. Our results suggest that full expression of neuronal LTA requires the presence of a pool of preexisting, short-lived (or rapidly utilized) protein(s). Depletion of such a pool prior to each stimulation period appears to interfere with subsequent induction of LTA.

Adaptation, Physiological↗
PubMed1989

Long-term survival of decentralized axons and incorporation of satellite cells in motor neurons of rock lobsters.

Previous electrophysiological experiments have shown that in the abdominal extensor muscles of rock lobsters, axons which were cut in surviving animals do not degenerate peripherally for several months, but conduct action potentials and release transmitter quanta on stimulation closely distal to the scar. Electron micrographs from the axon distal to the scar (in a reliably conducting region) show invasion of the axoplasmic space by nucleated cells, probably glia. After several months, the cell membranes of the invaders have vanished and apparently functional multiple nuclei remain. We suggest that decentralized axons may survive for months with the help of 'donated' nuclei.

Action Potentials↗
PubMed1989

Rapid introduction of long-lasting synaptic changes at crustacean neuromuscular junctions.

In this review we present recent evidence implicating second-messenger systems in two forms of long-lasting synaptic change seen at crustacean neuromuscular junctions. Crustacean motor axons are endowed with numerous terminals, each possessing many individual synapses. Some synapses appear to be quiescent or impotent, but can be recruited in response to imposed functional demands. Supernormal impulse activity leads to long-term facilitation (LTF) which persists for many hours. During the persistent phase, additional synapses are physiologically effective, and morphological changes in synapses are seen at the ultrastructural level. Pulsatile application of serotonin, a neuromodulator, also enhances synaptic transmission, but this enhancement declines more rapidly than LTF. Elevation of intraterminal Ca2+ is neither necessary nor sufficient for long-lasting enhancement of transmission, but activation of A-kinase is necessary. LTF is set in motion by an unknown depolarization-dependent mechanism leading to A-kinase activation, whereas serotonin facilitation depends for its initiation on the phosphatidylinositol system. The initial phase of serotonin facilitation may be accounted for by production of inositol triphosphate, whereas the secondary long-lasting phase appears to require participation of both C kinase and A kinase. Neither LTF nor serotonin facilitation requires an intact neuron; both are presynaptic phenomena expressed by the nerve terminals. Brief comparison is made with long-lasting synaptic changes in other systems.

Animals↗
PubMed1989

Synaptic restructuring during long-term facilitation at the crayfish neuromuscular junction.

Long-term facilitation was induced by 20-Hz stimulation of the motor axon innervating the opener muscle of the crayfish, Procambarus clarkii. Excitatory postsynaptic potentials remained potentiated for several hours after stimulation. Structural correlates of potentiation were sought. Nerve terminals of the motor axon were fixed for electron microscopy in unstimulated preparations (controls), and during and after 20-Hz stimulation. Synapses were reconstructed from micrographs obtained from serial sections. Synaptic contact area and the number of vesicles at the presynaptic membrane did not change after 20-Hz stimulation, but the latter decreased during stimulation. Presynaptic dense bars ("active zones") decreased in number during and increased after stimulation, while perforated synapses increased after stimulation. Modification of presynaptic structures occurs rapidly and may be linked to long-lasting changes in quantal content of transmission.

Animals↗