Sensitizing stimuli cause translocation of protein kinase C in Aplysia sensory neurons.
about
Protein synthesis during acquisition of long-term facilitation is needed for the persistent loss of regulatory subunits of the Aplysia cAMP-dependent protein kinase.Evolutionary conservation of the signaling proteins upstream of cyclic AMP-dependent kinase and protein kinase C in gastropod mollusks.Characterization of small RNAs in Aplysia reveals a role for miR-124 in constraining synaptic plasticity through CREB.Calcium-activated proteases are critical for refilling depleted vesicle stores in cultured sensory-motor synapses of Aplysia.PKA and PKC are required for long-term but not short-term in vivo operant memory in Aplysia.The fickle mutation of a cytoplasmic tyrosine kinase effects sensitization but not dishabituation in Drosophila melanogaster.Multiple serotonergic mechanisms contributing to sensitization in aplysia: evidence of diverse serotonin receptor subtypes.Neural and molecular bases of nonassociative and associative learning in Aplysia.Physiological role for phosphatidic acid in the translocation of the novel protein kinase C Apl II in Aplysia neurons.Reversal of synaptic depression by serotonin at Aplysia sensory neuron synapses involves activation of adenylyl cyclase.Second messengers involved in the two processes of presynaptic facilitation that contribute to sensitization and dishabituation in Aplysia sensory neurons.Mapping molecular memory: navigating the cellular pathways of learning.A molecular switch for the consolidation of long-term memory: cAMP-inducible gene expression.Regulation of eukaryotic initiation factor 4E phosphorylation in the nervous system of Aplysia californica.Antagonistic modulation of a hyperpolarization-activated Cl(-) current in Aplysia sensory neurons by SCP(B) and FMRFamide.Long-term effects of axotomy on excitability and growth of isolated Aplysia sensory neurons in cell culture: potential role of cAMP.Ubiquitous molecular substrates for associative learning and activity-dependent neuronal facilitation.Regulatory properties of p105: a novel PKC isoenzyme in mantle tissue from marine mussels.Rapid development of synaptic connections and plasticity between sensory neurons and motor neurons of Aplysia in cell culture: implications for learning and regulation of synaptic strength.Activation and degradation of the transcription factor C/EBP during long-term facilitation in Aplysia.Long-term changes in excitability induced by protein kinase C activation in Aplysia sensory neurons.Computational model of the serotonergic modulation of sensory neurons in Aplysia.
P2860
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P2860
Sensitizing stimuli cause translocation of protein kinase C in Aplysia sensory neurons.
description
article científic
@ca
article scientifique
@fr
articolo scientifico
@it
artigo científico
@pt
bilimsel makale
@tr
scientific article published on March 1990
@en
vedecký článok
@sk
vetenskaplig artikel
@sv
videnskabelig artikel
@da
vědecký článek
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name
Sensitizing stimuli cause translocation of protein kinase C in Aplysia sensory neurons.
@en
Sensitizing stimuli cause translocation of protein kinase C in Aplysia sensory neurons.
@nl
type
label
Sensitizing stimuli cause translocation of protein kinase C in Aplysia sensory neurons.
@en
Sensitizing stimuli cause translocation of protein kinase C in Aplysia sensory neurons.
@nl
prefLabel
Sensitizing stimuli cause translocation of protein kinase C in Aplysia sensory neurons.
@en
Sensitizing stimuli cause translocation of protein kinase C in Aplysia sensory neurons.
@nl
P2860
P356
P1476
Sensitizing stimuli cause translocation of protein kinase C in Aplysia sensory neurons.
@en
P2093
Sacktor TC
Schwartz JH
P2860
P304
P356
10.1073/PNAS.87.5.2036
P407
P577
1990-03-01T00:00:00Z