Cyclic GMP pathway is critical for inducing long–term sensitization of nociceptive sensory neurons

10.1038/4520 ◽  
1999 ◽  
Vol 2 (1) ◽  
pp. 18-23 ◽  
Author(s):  
Matthew R. Lewin ◽  
Edgar T. Walters
Keyword(s):  
Sensory Neurons ◽  
Cyclic Gmp

Sensory Neurons With Activated Caspase-3 Survive Long-Term Experimental Diabetes

Diabetes ◽  
2003 ◽  
Vol 52 (9) ◽  
pp. 2363-2371 ◽  
Author(s):  
C. Cheng ◽  
D. W. Zochodne
Keyword(s):  
Sensory Neurons ◽  
Caspase 3 ◽  
Experimental Diabetes

Long-term sensitization in Aplysia: biophysical correlates in tail sensory neurons

Science ◽  
1987 ◽  
Vol 235 (4789) ◽  
pp. 685-687 ◽  
Author(s):  
K. Scholz ◽  
J. Byrne
Keyword(s):  
Sensory Neurons

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

1993 ◽  
Vol 90 (23) ◽  
pp. 11411-11415 ◽  
Author(s):  
G A Clark ◽  
E R Kandel
Keyword(s):  
Gene Expression ◽  
Sensory Neurons ◽  
Cell Body ◽  
Sensory Cells ◽  
Target Cells ◽  
Synaptic Terminals ◽  
Dissociated Cell Culture ◽  
Synaptic Changes ◽  
Long Term Facilitation

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.

Long-term cell culture of electrically active sensory neurons free of glial cells

1977 ◽  
Vol 5 (3-4) ◽  
pp. 153-157 ◽  
Author(s):  
Ellen Rieske ◽  
Georg W. Kreutzberg
Keyword(s):  
Cell Culture ◽  
Sensory Neurons ◽  
Glial Cells

Involvement of the nitric oxide-cyclic GMP pathway in the desensitization of bradykinin responses of cultured rat sensory neurons

Neuron ◽  
1992 ◽  
Vol 9 (2) ◽  
pp. 315-324 ◽  
Author(s):  
Daniel S. McGehee ◽  
Michael F. Goy ◽  
Gerry S. Oxford
Keyword(s):  
Nitric Oxide ◽  
Sensory Neurons ◽  
Cyclic Gmp

A regulatory subunit of the cAMP-dependent protein kinase down-regulated in aplysia sensory neurons during long-term sensitization

Neuron ◽  
1992 ◽  
Vol 8 (2) ◽  
pp. 387-397 ◽  
Author(s):  
Peter J. Bergold ◽  
Sven A. Beushausen ◽  
Todd C. Sacktor ◽  
Stephen Cheley ◽  
Hagan Bayley ◽  
...  
Keyword(s):  
Protein Kinase ◽  
Sensory Neurons ◽  
Regulatory Subunit ◽  
Dependent Protein Kinase ◽  
Camp Dependent Protein Kinase ◽  
Dependent Protein

Chemically Induced, Activity-Independent LTD Elicited by Simultaneous Activation of PKG and Inhibition of PKA

1999 ◽  
Vol 82 (3) ◽  
pp. 1577-1589 ◽  
Author(s):  
Linda Santschi ◽  
Magali Reyes-Harde ◽  
Patric K. Stanton
Keyword(s):  
Protein Kinase ◽  
Cyclic Amp ◽  
Cyclic Gmp ◽  
Long Term Potentiation ◽  
Dependent Protein Kinase ◽  
Schaffer Collateral ◽  
Chemically Induced ◽  
Bath Application ◽  
Dependent Protein

Although it is widely agreed that cyclic AMP is necessary for the full expression of long-term potentiation of synaptic strength, it is unclear whether cyclic AMP or cyclic AMP-dependent protein kinase (PKA) play roles in the induction of long-term depression (LTD). We show here that two PKA inhibitors, H-89 (10 μM) and KT5720 (1 μM), are unable to block induction of LTD at Schaffer collateral-CA1 synapses in hippocampal slices in vitro. Rather, H-89 enhanced the magnitude of LTD induced by submaximal low-frequency stimulation. Raising [cGMP] with zaprinast (20 μM), a selective type V phosphodiesterase inhibitor, reversibly depressed synaptic potentials. However, coapplication of H-89 plus zaprinast converted this to a robust LTD that depended critically on activation of cyclic GMP-dependent protein kinase (PKG). Chemically induced LTD is activity-independent because it could be induced without stimulation and in tetrodotoxin (0.5 μM). Additionally, chemical LTD did not require activation of N-methyl-d-aspartate or GABA receptors and could be reversed by LTP. Stimulus-induced LTD occluded chemical LTD, suggesting a common expression mechanism. In contrast to bath application, postsynaptic infusion of H-89 into CA1 pyramidal neurons did not enhance LTD, suggesting a presynaptic site of action. Further evidence for a presynaptic locus was supplied by experiments where H-89 applied postsynaptically along with bath application of zaprinast was unable to produce chemical LTD. Thus simultaneous presynaptic generation of cyclic GMP and inhibition of PKA is sufficient to induce LTD of synaptic transmission at Schaffer collateral-CA1 synapses.

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