Rapid introduction of long‐lasting synaptic changes at crustacean neuromuscular junctions

Atwood, Harold L.; Dixon, D.; Wojtowicz, J. Martin

doi:10.1002/neu.480200509

Cited by 25 publications

(15 citation statements)

References 31 publications

(32 reference statements)

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“…Inhibition of protein kinase A or protein kinase C accelerates LFD cAMP-dependent protein kinases A (PKA) and protein kinase C (PKC) were shown to be involved in LTF at crayfish neuromuscular junction (Atwood et al, 1989;Dixon and Atwood, 1989a) and in neuropeptide-induced potentiation (Friedrich et al, 1998). To examine the role of PKA, we applied the inhibitor Rp-cAMPS (300 M), which binds to the regulatory subunit of PKA (Dostmann et al, 1990) 10 min before 0.2 Hz stimulation.…”

Section: Kinase Inhibitor Accelerates Phase II Of Lfdmentioning

confidence: 99%

Phosphorylation-Dependent Low-Frequency Depression at Phasic Synapses of a Crayfish Motoneuron

Silverman‐Gavrila¹,

Orth²,

Charlton³

2005

J. Neurosci.

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Extremes in presynaptic differentiation can be studied at the crayfish leg extensor muscle where, on the same muscle fiber, one motoneuron makes "phasic" depressing synapses that have a high probability of neurotransmitter release and another motoneuron makes "tonic," low-probability, facilitating synapses. The large motor axons permit intracellular access to presynaptic sites. We examined the role of phosphorylation during low-frequency depression ( This study shows that phosphorylation-dependent mechanisms are involved in LFD and suggests that exocytosis is controlled by conditions that shift the balance between phosphorylated and unphosphorylated substrates. The shift can occur by alteration in the relative activities of protein kinases and phosphatases.

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Section: Kinase Inhibitor Accelerates Phase II Of Lfdmentioning

confidence: 99%

Phosphorylation-Dependent Low-Frequency Depression at Phasic Synapses of a Crayfish Motoneuron

Silverman‐Gavrila¹,

Orth²,

Charlton³

2005

J. Neurosci.

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“…[Key words: augmentation, facilitation, posftetanic pofentiafion, crayfish neuromuscular junction, furaActivity-dependent or frequency-dependent synaptic enhancement is a fundamental property of a diversity of central and peripheral vertebrate and invertebrate synapses (Zengel et al, 1980;Atwood and Wojtowicz, 1986;Magleby, 1987;Atwood et al, 1989;Zucker 1989). It results from an increase in evoked and spontaneous transmitter release that builds up during a train of presynaptic action potentials and decays following train termination.…”

mentioning

confidence: 99%

“…In the crayfish preparation, the recovery of synaptic enhancement after high-frequency trains, as well as its buildup during trains, is kinetically complex, requiring up to five time constants for a complete description Atwood et al, 1989). During trains of action potentials [Ca*+], rises in crayfish neuromuscular nerve terminals, eventually reaching a plateau when the rate of influx is equal to the rate of efflux .…”

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confidence: 99%

A quantitative measurement of the dependence of short-term synaptic enhancement on presynaptic residual calcium

1994

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We simultaneously measured presynaptic free calcium ion concentration ([Ca2+]i) and synaptic strength at the crayfish claw opener neuromuscular junction (nmj) under a variety of experimental conditions. Our experiments were designed both to test the hypothesis that elevated [Ca2+]i is necessary and sufficient for the induction of a form of synaptic enhancement that persists for several seconds after tetanic stimulation--augmentation--and to determine the quantitative relationship between elevated [Ca2+]i and this enhancement. Action potential trains increased [Ca2+]i and enhanced transmission. During the decay phase of synaptic enhancement known as augmentation (time constant of decay approximately 7 sec at 20 degrees C with < 200 microM fura-2 in terminals), [Ca2+]i was elevated 700 nM or less above rest and an essentially linear relationship between [Ca2+]i and enhancement was observed. Introduction of exogenous Ca2+ buffers into the presynaptic terminal slowed the buildup and recovery kinetics of both [Ca2+]i and the component of synaptic enhancement corresponding to augmentation. The slope of the relationship relating delta [Ca2+]i to augmentation was not changed. The time course of augmentation and recovery of [Ca2+]i remained correlated as the temperature of the preparation was changed from about 10 degrees C to 20 degrees C, but the quantitative relationship of enhancement to [Ca2+]i was increased more than two- to threefold. During moderate frequency trains of action potentials, a slowly developing component of the total synaptic enhancement was approximately linearly related to residual [Ca2+]i measured with fura-2. The quantitative relationship between [Ca2+]i and this component of synaptic enhancement during trains was the same as that during synaptic augmentation after trains.(ABSTRACT TRUNCATED AT 250 WORDS)

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“…Increases in synaptic transmission lasting hours have been shown to occur when transcription is blocked (Sutton et al, 2001) and even when the cell body is detached from the axonal tree (Liu et al, 2003). Similarly, studies of the crayfish neuromuscular junction showed that LTF and rapid morphological changes do not require an intact neuron (Atwood et al, 1989).…”

Section: Discussionmentioning

confidence: 96%

Initiating morphological changes associated with long‐term facilitation in Aplysia is independent of transcription or translation in the cell body

Grabham

Schacher

et al. 2005

J. Neurobiol.

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In Aplysia, the growth of axonal arbor and the formation of new presynaptic varicosities are thought to contribute to long-term facilitation (LTF) produced by serotonin (5-HT). While it is known that there is a requirement for both transcription and translation in LTF and in the accompanying morphological changes, the mechanisms mediating the initiation and maintenance of these changes are poorly understood. We used long-term labeling of the presynaptic sensory neuron to carry out repeated imaging of axonal morphology, coupled with electrophysiology, to further elucidate the macromolecular requirements of this process. Robust synaptic facilitation, axonal growth, and the formation of axonal varicosities were elicited by 5-HT even when transcription was blocked with actinomycin. Increases in synaptic efficacy and varicosity number were detected 12 h after exposure to 5-HT but did not persist to 24 h. Even when sensory neuron cell bodies were removed, eliminating the contributions of both somal transcription and translation, 5-HT elicited these transient morphological and electrophysiological responses. New sensory varicosities contacting the postsynaptic neuron were filled with the neuropeptide sensorin. Under all conditions, global inhibition of protein synthesis completely blocked the formation of new axonal branches and varicosities. These results demonstrate that neither transcription nor somal translation is required to initiate the axonal growth that often accompanies long-term synaptic plasticity-protein synthesis in the axon is sufficient. Macromolecular synthesis in the cell body is, however, required to maintain the enlarged arbor.

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Rapid introduction of long‐lasting synaptic changes at crustacean neuromuscular junctions

Cited by 25 publications

References 31 publications

Phosphorylation-Dependent Low-Frequency Depression at Phasic Synapses of a Crayfish Motoneuron

Phosphorylation-Dependent Low-Frequency Depression at Phasic Synapses of a Crayfish Motoneuron

A quantitative measurement of the dependence of short-term synaptic enhancement on presynaptic residual calcium

Initiating morphological changes associated with long‐term facilitation in Aplysia is independent of transcription or translation in the cell body

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