title: Initiating morphological changes associated with long-term facilitation in Aplysia is independent of transcription or translation in the cell body.
abstract: 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.
authors.affiliation: Department of Pharmacology, Columbia University, New York, New York 10032, USA. pwg@columbia.edu
authors.forename: Peter W
authors.initials: PW
authors.lastname: Grabham
authors.forename: Fang
authors.initials: F
authors.lastname: Wu
authors.forename: Samuel
authors.initials: S
authors.lastname: Schacher
authors.forename: Daniel J
authors.initials: DJ
authors.lastname: Goldberg
mesh_terms: D000704:Analysis of Variance; D000818:Animals; D000841:Anisomycin / Q000494:pharmacology; D001048:Aplysia; D022081:Cell Surface Extensions / Q000187:drug effects / Q000502:physiology*; D002478:Cells, Cultured; D003609:Dactinomycin / Q000494:pharmacology; D003911:Dextrans / Q000378:metabolism; D004347:Drug Interactions; D004558:Electric Stimulation / Q000379:methods; D019706:Excitatory Postsynaptic Potentials / Q000187:drug effects / Q000502:physiology; D005455:Fluorescent Antibody Technique / Q000379:methods; D017952:Ganglia, Invertebrate / Q000166:cytology; D017774:Long-Term Potentiation / Q000187:drug effects / Q000502:physiology*; D009475:Neurons, Afferent / Q000187:drug effects / Q000502:physiology*; D014176:Protein Biosynthesis / Q000187:drug effects / Q000502:physiology*; D011500:Protein Synthesis Inhibitors / Q000494:pharmacology; D012701:Serotonin / Q000494:pharmacology; D013569:Synapses / Q000187:drug effects / Q000502:physiology; D013997:Time Factors; D014158:Transcription, Genetic / Q000187:drug effects / Q000502:physiology*
chemical_list: D003911:Dextrans; D011500:Protein Synthesis Inhibitors; D003609:Dactinomycin; D012701:Serotonin; D000841:Anisomycin