Induction of long-term facilitation in Aplysia sensory neurons by local application of serotonin to remote synapses

Long-term synaptic facilitation at the connections of Aplysia sensory neurons onto their target cells involves alterations in gene expression. How then are the relevant cellular signals for the induction and expression of long-term synaptic changes conveyed between the nucleus and remote synaptic terminals? We have explored this question using a set of remote, peripheral terminals of siphon sensory cells, which are approximately 3 cm from the sensory cell body in the abdominal ganglion. We found that these remote synapses, like the proximal synapses previously studied in dissociated cell culture, can exhibit long-term facilitation 24 hr after cell-wide serotonin application. Furthermore, serotonin applications restricted to the remote synaptic terminals nevertheless produced long-term facilitation, indicating that signals generated in synaptic regions can trigger the long-term process, perhaps via retrograde signals to the nucleus to modify gene expression, followed by anterograde signals back to the terminal. Serotonin applications restricted to the cell body and proximal synapses of the sensory neuron also produced long-term facilitation at remote synapses, although to a lesser extent, suggesting that long-term facilitation is expressed cell-wide, but that superimposed on this cell-wide facilitation there appears to be a component that is synapse-specific.

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Inducible NO synthase: role in cellular signalling

Journal of Experimental Biology ◽

10.1242/jeb.202.6.645 ◽

1999 ◽

Vol 202 (6) ◽

pp. 645-653 ◽

Cited By ~ 1

Author(s):

K.F. Beck ◽

W. Eberhardt ◽

S. Frank ◽

A. Huwiler ◽

U.K. Messmer ◽

...

Keyword(s):

Gene Expression ◽

No Synthase ◽

Signalling Pathways ◽

Target Cells ◽

Activated Macrophages ◽

The Past ◽

Relaxing Factor ◽

Endothelium Derived Relaxing Factor ◽

Intercellular Messenger

The discovery of endothelium-derived relaxing factor and its identification as nitric oxide (NO) was one of the most exciting discoveries of biomedical research in the 1980s. Besides its potent vasodilatory effects, NO was found under certain circumstances to be responsible for the killing of microorganisms and tumour cells by activated macrophages and to act as a novel, unconventional type of neurotransmitter. In 1992, Science picked NO as the ‘Molecule of the Year’, and over the past years NO has become established as a universal intercellular messenger that acutely affects important signalling pathways and, on a more long-term scale, modulates gene expression in target cells. These actions will form the focus of the present review.

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Protein synthesis at synapse versus cell body: Enhanced but transient expression of long-term facilitation at isolated synapses

Journal of Neurobiology ◽

10.1002/neu.10242 ◽

2003 ◽

Vol 56 (3) ◽

pp. 275-286 ◽

Cited By ~ 34

Author(s):

Ke Liu ◽

Jiang-Yuan Hu ◽

Denong Wang ◽

Samuel Schacher

Keyword(s):

Protein Synthesis ◽

Transient Expression ◽

Cell Body ◽

Long Term Facilitation

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ApTrkl, a Trk-like Receptor, Mediates Serotonin- Dependent ERK Activation and Long-Term Facilitation in Aplysia Sensory Neurons

Neuron ◽

10.1016/j.neuron.2004.11.001 ◽

2004 ◽

Vol 44 (4) ◽

pp. 715-728 ◽

Cited By ~ 36

Author(s):

Jake Ormond ◽

Jonathan Hislop ◽

Yali Zhao ◽

Neil Webb ◽

Francois Vaillaincourt ◽

...

Keyword(s):

Sensory Neurons ◽

Erk Activation ◽

Long Term Facilitation

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Persistent and transcriptionally-dependent increase in protein phosphorylation in long-term facilitation ofAplysia sensory neurons

Nature ◽

10.1038/339051a0 ◽

1989 ◽

Vol 339 (6219) ◽

pp. 51-54 ◽

Cited By ~ 81

Author(s):

J. David Sweatt ◽

Eric R. Kandel

Keyword(s):

Protein Phosphorylation ◽

Sensory Neurons ◽

Long Term Facilitation

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TGF-β1 in Aplysia: Role in Long-Term Changes in the Excitability of Sensory Neurons and Distribution of TβR-II-Like Immunoreactivity

Learning & Memory ◽

10.1101/lm.6.3.317 ◽

1999 ◽

Vol 6 (3) ◽

pp. 317-330

Author(s):

Jeannie Chin ◽

Annie Angers ◽

Leonard J. Cleary ◽

Arnold Eskin ◽

John H. Byrne

Keyword(s):

Synaptic Plasticity ◽

Sensory Neurons ◽

Motor Neurons ◽

Transforming Growth Factor ◽

Transforming Growth Factor Β ◽

Tissue Extracts ◽

The Central Nervous System ◽

Long Term Facilitation ◽

Tgf Β1

Exogenous recombinant human transforming growth factor β-1 (TGF-β1) induced long-term facilitation ofAplysia sensory-motor synapses. In addition, 5-HT-induced facilitation was blocked by application of a soluble fragment of the extracellular portion of the TGF-β1 type II receptor (TβR-II), which presumably acted by scavenging an endogenous TGF-β1-like molecule. Because TβR-II is essential for transmembrane signaling by TGF-β, we sought to determine whether Aplysia tissues contained TβR-II and specifically, whether neurons expressed the receptor. Western blot analysis of Aplysia tissue extracts demonstrated the presence of a TβR-II-immunoreactive protein in several tissue types. The expression and distribution of TβR-II-immunoreactive proteins in the central nervous system was examined by immunohistochemistry to elucidate sites that may be responsive to TGF-β1 and thus may play a role in synaptic plasticity. Sensory neurons in the ventral–caudal cluster of the pleural ganglion were immunoreactive for TβR-II, as well as many neurons in the pedal, abdominal, buccal, and cerebral ganglia. Sensory neurons cultured in isolation and cocultured sensory and motor neurons were also immunoreactive. TGF-β1 affected the biophysical properties of cultured sensory neurons, inducing an increase of excitability that persisted for at least 48 hr. Furthermore, exposure to TGF-β1 resulted in a reduction in the firing threshold of sensory neurons. These results provide further support for the hypothesis that TGF-β1 plays a role in long-term synaptic plasticity in Aplysia.

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Neural analogue of long-term sensitization training produces long-term (24 and 48 h) facilitation of the sensory-to-motor neuron connection in Aplysia

Journal of Neurophysiology ◽

10.1152/jn.1994.72.2.778 ◽

1994 ◽

Vol 72 (2) ◽

pp. 778-784 ◽

Cited By ~ 10

Author(s):

F. Zhang ◽

J. R. Goldsmith ◽

J. H. Byrne

Keyword(s):

Sensory Neurons ◽

Motor Neurons ◽

Peripheral Nerves ◽

Time Course ◽

Membrane Properties ◽

Four Blocks ◽

Long Term Facilitation ◽

Stimulation Of Nerve ◽

Stimulation Of

1. An in vitro analogue of long-term sensitization training was used to gain insights into the mechanisms and time course of the memory for long-term sensitization in Aplysia. The analogue, consisting of four blocks of shocks, was delivered to peripheral nerves of the isolated pleural-pedal ganglia, which contain the sensory neurons and motor neurons that mediate the tail withdrawal reflex. 2. Long-term facilitation of the connections between the sensory neurons and motor neurons was produced by the conjoint stimulation of two peripheral nerves, P8 and P9. Long-term facilitation, however, was not observed after conjoint stimulation of three nerves, P7, P8, and P9. 3. The preparation was viable and stable (no changes in the amplitudes of excitatory postsynaptic potentials (EPSPs) and membrane properties in controls) for at least 48 h. Moreover, the long-term facilitation persisted for at least 48 h. 4. We observed no significant long-term changes in the resting membrane potentials of the sensory and motor neurons or in the input resistance of the motor neurons 24 and 48 h after the conjoint stimulation of nerves P8 and P9. Thus changes in these biophysical properties do not appear to contribute to the expression of long-term facilitation. 5. The finding that conjoint stimulation of three nerves, P7, P8, and P9, produced no long-term facilitation raised the possibility that stimulation of nerve P7 alone might produce long-term inhibition that opposes the facilitatory effects induced by conjoint stimulation of nerves P8 and P9. Stimulation of nerve P7 alone, however, had no long-term inhibitory effect on the EPSPs.(ABSTRACT TRUNCATED AT 250 WORDS)

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