Synaptic tagging during synapse-specific long-term facilitation of Aplysia sensory-motor neurons.
Like memory, long-lasting forms of synaptic plasticity have been shown to require mRNA and protein synthesis. Since each neuron has a single nucleus, but can form thousands of synaptic connections, the requirement for transcription raises the question of whether long-lasting forms of plasticity can occur in a synapse-specific manner and, if so, how the products of gene expression can be targeted to alter synaptic strength at some but not all synapses made by a given neuron. One hypothesis that has been put forth to address this question is the synaptic tagging hypothesis, which proposes that the products of gene expression are delivered throughout the cell, but function to increase synaptic strength only at synapses that have been "tagged" by previous synaptic activity. In this review, I describe our studies of synapse-specific, transcription-dependent facilitation of cultured Aplysia sensory-motor synapse in the context of the synaptic tagging hypothesis.
Martin
Kelsey C
KC
Department of Psychiatry and Biobehavioral Sciences, Brain Research Institute, Mental Retardation Research Center, University of Caliornia at Los Angeles, 90095-1761, USA. kcmartin@mednet.ucla.edu
D000818:Animals; D000906:Antibodies / Q000276:immunology; D001048:Aplysia; D017362:Cyclic AMP Response Element-Binding Protein / Q000276:immunology / Q000378:metabolism; D019706:Excitatory Postsynaptic Potentials / Q000187:drug effects*; D009046:Motor Neurons / Q000378:metabolism*; D009473:Neuronal Plasticity / Q000187:drug effects; D009475:Neurons, Afferent / Q000378:metabolism*; D012333:RNA, Messenger / Q000378:metabolism; D012701:Serotonin / Q000493:pharmacokinetics; D013995:Time; D015533:Transcriptional Activation / Q000187:drug effects
D000906:Antibodies; D017362:Cyclic AMP Response Element-Binding Protein; D012333:RNA, Messenger; D012701:Serotonin