Biomedical subjects

Craig H Bailey

Publications and source records attributed to Craig H Bailey.

5 recordsLinked to original sources

PubMed2006

Common molecular mechanisms in explicit and implicit memory.

Cellular and molecular studies of both implicit and explicit memory suggest that experience-dependent modulation of synaptic strength and structure is a fundamental mechanism by which these memories are encoded and stored within the brain. In this review, we focus on recent advances in our understanding of two types of memory storage: (i) sensitization in Aplysia, a simple form of implicit memory, and (ii) formation of explicit spatial memories in the mouse hippocampus. These two processes share common molecular mechanisms that have been highly conserved through evolution.

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PubMed2006

Molecular mechanisms of memory storage in Aplysia.

Cellular studies of implicit and explicit memory suggest that experience-dependent modulation of synaptic strength and structure is a fundamental mechanism by which these memories are encoded, processed, and stored within the brain. In this review, we focus on recent advances in our understanding of the molecular mechanisms that underlie short-term, intermediate-term, and long-term forms of implicit memory in the marine invertebrate Aplysia californica, and consider how the conservation of common elements in each form may contribute to the different temporal phases of memory storage.

Animals↗

PubMed2005

Serotonin-induced regulation of the actin network for learning-related synaptic growth requires Cdc42, N-WASP, and PAK in Aplysia sensory neurons.

Application of Clostridium difficile toxin B, an inhibitor of the Rho family of GTPases, at the Aplysia sensory to motor neuron synapse blocks long-term facilitation and the associated growth of new sensory neuron varicosities induced by repeated pulses of serotonin (5-HT). We have isolated cDNAs encoding Aplysia Rho, Rac, and Cdc42 and found that Rho and Rac had no effect but that overexpression in sensory neurons of a dominant-negative mutant of ApCdc42 or the CRIB domains of its downstream effectors PAK and N-WASP selectively reduces the long-term changes in synaptic strength and structure. FRET analysis indicates that 5-HT activates ApCdc42 in a subset of varicosities contacting the postsynaptic motor neuron and that this activation is dependent on the PI3K and PLC signaling pathways. The 5-HT-induced activation of ApCdc42 initiates reorganization of the presynaptic actin network leading to the outgrowth of filopodia, some of which are morphological precursors for the learning-related formation of new sensory neuron varicosities.

Actin Cytoskeleton↗

PubMed2004

The persistence of long-term memory: a molecular approach to self-sustaining changes in learning-induced synaptic growth.

Recent cellular and molecular studies of both implicit and explicit memory storage suggest that experience-dependent modulation of synaptic strength and structure is a fundamental mechanism by which these diverse forms of memory are encoded and stored. For both forms of memory storage, some type of synaptic growth is thought to represent the stable cellular change that maintains the long-term process. In this review, we discuss recent findings on the molecular events that underlie learning-related synaptic growth in Aplysia and discuss the possibility that an active, prion-based mechanism is important for the maintenance of the structural change and for the persistence of long-term memory.

Animals↗

PubMed2003

Presynaptic activation of silent synapses and growth of new synapses contribute to intermediate and long-term facilitation in Aplysia.

The time course and functional significance of the structural changes associated with long-term facilitation of Aplysia sensory to motor neuron synaptic connections in culture were examined by time-lapse confocal imaging of individual sensory neuron varicosities labeled with three different fluorescent markers: the whole-cell marker Alexa-594 and two presynaptic marker proteins-synaptophysin-eGFP to monitor changes in synaptic vesicle distribution and synapto-PHluorin to monitor active transmitter release sites. Repeated pulses of serotonin induce two temporally, morphologically, and molecularly distinct presynaptic changes: (1) a rapid activation of silent presynaptic terminals by filling of preexisting empty varicosities with synaptic vesicles, which parallels intermediate-term facilitation, is completed within 3-6 hr and requires translation but not transcription and (2) a slower generation of new functional varicosities which occurs between 12-18 hr and requires transcription and translation. Enrichment of empty varicosities with synaptophysin accounts for 32% of the newly activated synapses at 24 hr, whereas newly formed varicosities account for 68%.

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