Presynaptic Morphological Changes Associated with Long-Term Synaptic Facilitation Are Triggered by Actin Polymerization at Preexisting Varicositis

Hatada, Yohko; Wu, Fang; Sun, Zhongyi; Schacher, Samuel; Goldberg, Daniel J.

doi:10.1523/jneurosci.20-13-j0001.2000

Cited by 79 publications

(65 citation statements)

References 35 publications

(59 reference statements)

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“…Indeed, the upregulation of the proteasome subunit P31 after fear conditioning training suggests the activation of these processes. Recent studies have further emphasized the importance of actin-mediated cytoskeletal rearrangements for pre-and postsynaptic plasticity (Hatada et al 2000;Matus 2000). The differential expression of two actin transcripts after fear conditioning supports this idea.…”

mentioning

confidence: 84%

Identification of Genes Expressed in the Amygdala During the Formation of Fear Memory

Stork

Stork²,

Pape³

et al. 2001

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In this study we describe changes of gene expression that occur in the basolateral complex of the mouse amygdala (BLA) during the formation of fear memory. Through the combination of a behavioral training scheme with polymerase chain reaction-based expression analysis (subtractive hybridization and virtual Northern analysis) we were able to identify various gene products that are increased in expression after Pavlovian fear conditioning and are of potential significance for neural plasticity and information storage in the amygdala. In particular, a key enzyme of monoamine metabolism, aldehyde reductase, and the protein sorting and ubiquitination factor Praja1, showed pronounced and learning-specific induction six hours after fear conditioning training. Aldehyde reductase and Praja1, including a novel alternatively spliced isoform termed Praja1a, were induced in the BLA depending on the emotional stimulus presented and showed different expression levels in response to associative conditioning, training stress, and experience of conditioned fear. Stress and fear were further found to induce various signal transduction factors (transthyretin, phosphodiesterase1, protein kinase inhibitor-␣) and structural reorganization factors (e.g., E2-ubiquitin conjugating enzyme, neuroligin1, actin, UDP-galactose transporter) during training. Our results show that the formation of Pavlovian fear memory is associated with changes of gene expression in the BLA, which may contribute to neural plasticity and the processing of information about both conditioned and unconditioned fear stimuli.[The Praja1a sequence has been deposited in GenBank data base under accession no. AF335250.]

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mentioning

confidence: 84%

Identification of Genes Expressed in the Amygdala During the Formation of Fear Memory

Stork

Stork²,

Pape³

et al. 2001

Learn. Mem.

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“…One of the critical steps involved in synaptic remodeling is thought to be the reorganization of actin cytoskeleton. Actin polymerization inhibitors block 5-HTinduced LTF and the LTF-associated morphological changes in the sensory neurons of Aplysia (Hatada et al, 2000;Udo et al, 2005) and selectively block L-LTP in hippocampus (Krucker et al, 2000;Fukazawa et al, 2003;. Does L-LTP induced by 5-HT in neurons of the BL depend on the regulation of actin cytoskeleton?…”

Section: -Ht-induced L-ltp In Amygdala Requires New Protein Synthesimentioning

confidence: 99%

5-Hydroxytryptamine Induces a Protein Kinase A/Mitogen-Activated Protein Kinase-Mediated and Macromolecular Synthesis-Dependent Late Phase of Long-Term Potentiation in the Amygdala

Huang¹,

Kandel²

2007

J. Neurosci.

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The amygdala is a critical site for the acquisition of learned fear memory in mammals, and the formation and long-term maintenance of fear memories are thought to be associated with changes of synaptic strength in the amygdala. Here we report that serotonin (5-hydroxytryptamine; 5-HT), a modulatory neurotransmitter known to be linked to learned fearful and emotional behavior, has dual effects on excitatory synaptic transmission in the basolateral amygdala. There is an early depression of synaptic transmission lasting 30 -50 min, mediated by 5-HT 1A , and a late, long-lasting facilitation lasting Ͼ5 h in slice recordings, mediated by the 5-HT 4 receptor. 5-HT late phase long-term potentiation (L-LTP) is blocked by inhibitors of either protein kinase

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“…The other substrate, synapsin, tethers synaptic vesicles to the cytoskeleton, providing a constraint for vesicle exocytosis that is relieved by phosphorylation (Hay et al, 2001;Ferreira and Rapoport, 2002). During the development of long-term facilitation, new connections form primarily by the growth of new branches and synapses (Hatada et al, 2000). PKA activity has been shown to be crucial for this neurite outgrowth (Schacher et al, 1993;Wu et al, 1995;Yao et al, 2000;Kao et al, 2002), as well as for the formation and maintenance of the new synapses (Wu et al, 1995).…”

Section: Rii-akap Binding and The Compartmentalization Of The Camp-pkmentioning

confidence: 99%

The Two Regulatory Subunits ofAplysiacAMP-Dependent Protein Kinase Mediate Distinct Functions in Producing Synaptic Plasticity

Liu¹,

Hu²,

Schacher³

et al. 2004

J. Neurosci.

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Activation of the cAMP-dependent protein kinase (PKA) is critical for both short-and long-term facilitation in Aplysia sensory neurons. There are two types of the kinase, I and II, differing in their regulatory (R) subunits. We cloned Aplysia RII; RI was cloned previously. Type I PKA is mostly soluble in the cell body whereas type II is enriched at nerve endings where it is bound to two prominent A kinaseanchoring-proteins (AKAPs). Disruption of the binding of RII to AKAPs by Ht31, an inhibitory peptide derived from a human thyroid AKAP, prevents both the short-and the long-term facilitation produced by serotonin (5-HT). During long-term facilitation, RII is transcriptionally upregulated; in contrast, the amount of RI subunits decreases, and previous studies have indicated that the decrease is through ubiquitin-proteosome-mediated proteolysis. Experiments with antisense oligonucleotides injected into the sensory neuron cell body show that the increase in RII protein is essential for the production of long-term facilitation. Using synaptosomes, we found that 5-HT treatment causes RII protein to increase at nerve endings. In addition, using reverse transcription-PCR, we found that RII mRNA is transported from the cell body to nerve terminals. Our results suggest that type I operates in the nucleus to maintain cAMP response element-binding protein-dependent gene expression, and type II PKA acts at sensory neuron synapses phosphorylating proteins to enhance release of neurotransmitter. Thus, the two types of the kinase have distinct but complementary functions in the production of facilitation at synapses of an identified neuron.

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Presynaptic Morphological Changes Associated with Long-Term Synaptic Facilitation Are Triggered by Actin Polymerization at Preexisting Varicositis

Cited by 79 publications

References 35 publications

Identification of Genes Expressed in the Amygdala During the Formation of Fear Memory

Identification of Genes Expressed in the Amygdala During the Formation of Fear Memory

5-Hydroxytryptamine Induces a Protein Kinase A/Mitogen-Activated Protein Kinase-Mediated and Macromolecular Synthesis-Dependent Late Phase of Long-Term Potentiation in the Amygdala

The Two Regulatory Subunits ofAplysiacAMP-Dependent Protein Kinase Mediate Distinct Functions in Producing Synaptic Plasticity

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