 |
Previous Article | Next Article 
Volume 17, Number 19,
Issue of October 1, 1997
pp. 7237-7244
Copyright ©1997 Society for Neuroscience
Modulation of a cAMP/Protein Kinase A Cascade by Protein Kinase C
in Sensory Neurons of Aplysia
Received June 30, 1997; accepted July 14, 1997.
Shuzo Sugita,
Douglas A. Baxter, and
John H. Byrne
Department of Neurobiology and Anatomy, The University of Texas
Medical School at Houston, Houston, Texas 77225
The synaptic connections between the sensory neurons of
Aplysia and their follower neurons have been used as a
model system for examining the cellular mechanisms contributing to
neuronal and synaptic plasticity. Recent studies suggest that at least two protein kinases, protein kinase A (PKA) and protein kinase C (PKC),
contribute to serotonin (5-HT)-induced short-term facilitation. The
interaction between these two kinase cascades has not been examined,
however. Using electrophysiological and biochemical approaches, we
examined possible interactions between PKA and PKC cascades. The
results indicated that prolonged activation of PKC by preincubation
with phorbol esters attenuated PKA-mediated actions of 5-HT, including
increases in sensory neuron excitability and spike broadening in the
presence of tetraethylammonium (TEA) and nifedipine. Although phorbol
esters also attenuated increases in excitability by an analog of cAMP
and small cardioactive peptide B (SCPB), the degree
of attenuation was smaller. In addition, phorbol esters did not
attenuate broadening of TEA spikes by the cAMP analog and
SCPB. Thus, phorbol esters appeared specifically to
attenuate aspects of the 5-HT activation of the cAMP/PKA cascade. Measurements of cAMP levels with radioimmunoassays revealed that phorbol esters did not attenuate 5-HT-induced cAMP synthesis, however.
Finally, the results indicated that phorbol esters themselves induced a
small but significant increase in excitability as well as an increase
in the level of cAMP. Our results suggest that there is crosstalk
between the PKC and PKA cascades. The mechanisms by which phorbol
esters specifically attenuate 5-HT-induced activation of the cAMP/PKA
cascade are not known, however.
Key words:
Aplysia californica;
protein kinase A;
protein
kinase C;
cyclic AMP;
crosstalk;
synaptic facilitation;
modulation;
serotonin;
sensory neurons;
learning and memory
This article has been cited by other articles:

|
 |

|
 |
 
C. A. Farah, D. Weatherill, T. W. Dunn, and W. S. Sossin
PKC Differentially Translocates during Spaced and Massed Training in Aplysia
J. Neurosci.,
August 19, 2009;
29(33):
10281 - 10286.
[Abstract]
[Full Text]
[PDF]
|
 |
|

|
 |

|
 |
 
J.-Y. Hu, Y. Chen, and S. Schacher
Protein Kinase C Regulates Local Synthesis and Secretion of a Neuropeptide Required for Activity-Dependent Long-Term Synaptic Plasticity
J. Neurosci.,
August 15, 2007;
27(33):
8927 - 8939.
[Abstract]
[Full Text]
[PDF]
|
 |
|

|
 |

|
 |
 
N. Alessandri-Haber, O. A. Dina, E. K. Joseph, D. Reichling, and J. D. Levine
A transient receptor potential vanilloid 4-dependent mechanism of hyperalgesia is engaged by concerted action of inflammatory mediators.
J. Neurosci.,
April 5, 2006;
26(14):
3864 - 3874.
[Abstract]
[Full Text]
[PDF]
|
 |
|

|
 |

|
 |
 
B. Dumitriu, J. E. Cohen, Q. Wan, A. M. Negroiu, and T. W. Abrams
Serotonin Receptor Antagonists Discriminate Between PKA- and PKC-Mediated Plasticity in Aplysia Sensory Neurons
J Neurophysiol,
April 1, 2006;
95(4):
2713 - 2720.
[Abstract]
[Full Text]
[PDF]
|
 |
|

|
 |

|
 |
 
R.-Q. Sun, Y.-J. Tu, N. B. Lawand, J.-Y. Yan, Q. Lin, and W. D. Willis
Calcitonin Gene-Related Peptide Receptor Activation Produces PKA- and PKC-Dependent Mechanical Hyperalgesia and Central Sensitization
J Neurophysiol,
November 1, 2004;
92(5):
2859 - 2866.
[Abstract]
[Full Text]
[PDF]
|
 |
|

|
 |

|
 |
 
D. Barbas, L. DesGroseillers, V. F. Castellucci, T. J. Carew, and S. Marinesco
Multiple Serotonergic Mechanisms Contributing to Sensitization in Aplysia: Evidence of Diverse Serotonin Receptor Subtypes
Learn. Mem.,
September 1, 2003;
10(5):
373 - 386.
[Abstract]
[Full Text]
[PDF]
|
 |
|

|
 |

|
 |
 
H. Kubota, S. Katsurabayashi, A. J Moorhouse, N. Murakami, H. Koga, and N. Akaike
GABAB receptor transduction mechanisms, and cross-talk between protein kinases A and C, in GABAergic terminals synapsing onto neurons of the rat nucleus basalis of Meynert
J. Physiol.,
August 15, 2003;
551(1):
263 - 276.
[Abstract]
[Full Text]
[PDF]
|
 |
|

|
 |

|
 |
 
J. E. Cohen, C. U. Onyike, V. L. McElroy, A. H. Lin, and T. W. Abrams
Pharmacological Characterization of an Adenylyl Cyclase-Coupled 5-HT Receptor in Aplysia: Comparison With Mammalian 5-HT Receptors
J Neurophysiol,
March 1, 2003;
89(3):
1440 - 1455.
[Abstract]
[Full Text]
[PDF]
|
 |
|

|
 |

|
 |
 
L. E. Fox and P. E. Lloyd
Mechanisms Involved in Persistent Facilitation of Neuromuscular Synapses in Aplysia
J Neurophysiol,
April 1, 2002;
87(4):
2018 - 2030.
[Abstract]
[Full Text]
[PDF]
|
 |
|

|
 |

|
 |
 
F. Manseau, X. Fan, T. Hueftlein, W. S. Sossin, and V. F. Castellucci
Ca2+-Independent Protein Kinase C Apl II Mediates the Serotonin-Induced Facilitation at Depressed Aplysia Sensorimotor Synapses
J. Neurosci.,
February 15, 2001;
21(4):
1247 - 1256.
[Abstract]
[Full Text]
[PDF]
|
 |
|

|
 |

|
 |
 
L. E. Fox and P. E. Lloyd
Role of cAMP in the Short-Term Modulation of a Neuromuscular System in Aplysia
J Neurophysiol,
March 1, 2000;
83(3):
1567 - 1579.
[Abstract]
[Full Text]
[PDF]
|
 |
|

|
 |

|
 |
 
D. A. Baxter, C. C. Canavier, J. W. Clark Jr., and J. H. Byrne
Computational Model of the Serotonergic Modulation of Sensory Neurons in Aplysia
J Neurophysiol,
December 1, 1999;
82(6):
2914 - 2935.
[Abstract]
[Full Text]
[PDF]
|
 |
|

|
 |

|
 |
 
K. M. Braas and V. May
Pituitary Adenylate Cyclase-activating Polypeptides Directly Stimulate Sympathetic Neuron Neuropeptide Y Release through PAC1 Receptor Isoform Activation of Specific Intracellular Signaling Pathways
J. Biol. Chem.,
September 24, 1999;
274(39):
27702 - 27710.
[Abstract]
[Full Text]
[PDF]
|
 |
|

|
 |

|
 |
 
M. Farr, J. Mathews, D.-F. Zhu, and R. T. Ambron
Inflammation Causes a Long-Term Hyperexcitability in the Nociceptive Sensory Neurons of Aplysia
Learn. Mem.,
May 1, 1999;
6(3):
331 - 340.
[Abstract]
[Full Text]
|
 |
|

|
 |

|
 |
 
A. M. Pepio and W. S. Sossin
Membrane Translocation of Novel Protein Kinase Cs Is Regulated by Phosphorylation of the C2 Domain
J. Biol. Chem.,
February 2, 2001;
276(6):
3846 - 3855.
[Abstract]
[Full Text]
[PDF]
|
 |
|
|

|