scholarly journals Long-term sensitization training in Aplysia leads to an increase in the expression of BiP, the major protein chaperon of the ER.

1992 ◽  
Vol 119 (5) ◽  
pp. 1069-1076 ◽  
Author(s):  
D Kuhl ◽  
T E Kennedy ◽  
A Barzilai ◽  
E R Kandel
Keyword(s):  
Protein Synthesis ◽  
Motor Neurons ◽  
Structural Changes ◽  
State Level ◽  
Long Term Memory ◽  
Major Protein ◽  
Synaptic Connections ◽  
Term Memory ◽  
Long Term Facilitation

Long-term memory for sensitization of the gill- and siphon-withdrawal reflexes in Aplysia californica requires RNA and protein synthesis. These long-term behavioral changes are accompanied by long-term facilitation of the synaptic connections between the gill and siphon sensory and motor neurons, which are similarly dependent on transcription and translation. In addition to showing an increase in over-all protein synthesis, long-term facilitation is associated with changes in the expression of specific early, intermediate, and late proteins, and with the growth of new synaptic connections between the sensory and motor neurons of the reflex. We previously focused on early proteins and have identified four proteins as members of the immunoglobulin family of cell adhesion molecules related to NCAM and fasciclin II. We have now cloned the cDNA corresponding to one of the late proteins, and identified it as the Aplysia homolog of BiP, an ER resident protein involved in the folding and assembly of secretory and membrane proteins. Behavioral training increases the steady-state level of BiP mRNA in the sensory neurons. The increase in the synthesis of BiP protein is first detected 3 h after the onset of facilitation, when the increase in overall protein synthesis reaches its peak and the formation of new synaptic terminals becomes apparent. These findings suggest that the chaperon function of BiP might serve to fold proteins and assemble protein complexes necessary for the structural changes characteristic of long-term memory.

scholarly journals Reinstatement of long-term memory following erasure of its behavioral and synaptic expression in Aplysia

eLife ◽  
2014 ◽  
Vol 3 ◽  
Author(s):  
Shanping Chen ◽  
Diancai Cai ◽  
Kaycey Pearce ◽  
Philip Y-W Sun ◽  
Adam C Roberts ◽  
...  
Keyword(s):  
Motor Neurons ◽  
Long Term Memory ◽  
Synaptic Connections ◽  
Synaptic Growth ◽  
Term Memory ◽  
Synaptic Structure ◽  
Synaptic Change ◽  
Long Term Facilitation ◽  
The Brain

Long-term memory (LTM) is believed to be stored in the brain as changes in synaptic connections. Here, we show that LTM storage and synaptic change can be dissociated. Cocultures of Aplysia sensory and motor neurons were trained with spaced pulses of serotonin, which induces long-term facilitation. Serotonin (5HT) triggered growth of new presynaptic varicosities, a synaptic mechanism of long-term sensitization. Following 5HT training, two antimnemonic treatments—reconsolidation blockade and inhibition of PKM—caused the number of presynaptic varicosities to revert to the original, pretraining value. Surprisingly, the final synaptic structure was not achieved by targeted retraction of the 5HT-induced varicosities but, rather, by an apparently arbitrary retraction of both 5HT-induced and original synapses. In addition, we find evidence that the LTM for sensitization persists covertly after its apparent elimination by the same antimnemonic treatments that erase learning-related synaptic growth. These results challenge the idea that stable synapses store long-term memories.

Structural changes and the storage of long-term memory in Aplysia

1999 ◽  
Vol 77 (9) ◽  
pp. 738-747 ◽  
Author(s):  
Craig H Bailey
Keyword(s):  
Motor Neurons ◽  
Structural Changes ◽  
Long Term Memory ◽  
Synaptic Growth ◽  
Term Memory ◽  
Molecular Logic ◽  
Dissociated Cell Culture ◽  
Synaptic Circuitry ◽  
Activity Dependent

Long-term memory for sensitization of the gill-withdrawal reflex inAplysia is associated with the growth of new synaptic connections between sensory and motor neurons. The duration of this structural change parallels the behavioral retention of the memory. Such changes can be reconstituted in dissociated cell culture by repeated presentations of the modulatory neurotransmitter serotonin (5HT) and are associated with an activity-dependent downregulation of NCAM-related cell adhesion molecules thought to contribute to cell recognition and axonal outgrowth during development. Thus, aspects of the mechanisms utilized for learning-related synaptic growth initiated by experience in the adult may eventually be understood in the context of the molecular logic that shapes synaptic circuitry during the later stages of neuronal development.Key words: learning, synapse, invertebrate, habituation, sensitization.

Hippocampal long term memory: Effect of the cholinergic system on local protein synthesis

2013 ◽  
Vol 106 ◽  
pp. 246-257 ◽  
Author(s):  
Daniele Lana ◽  
Francesca Cerbai ◽  
Jacopo Di Russo ◽  
Francesca Boscaro ◽  
Ambra Giannetti ◽  
...  
Keyword(s):  
Protein Synthesis ◽  
Memory Effect ◽  
Cholinergic System ◽  
Long Term Memory ◽  
Term Memory ◽  
Local Protein Synthesis ◽  
Local Protein

scholarly journals Protein synthesis required for long-term memory is induced by PKC activation on days before associative learning

2005 ◽  
Vol 102 (45) ◽  
pp. 16432-16437 ◽  
Author(s):  
D. L. Alkon ◽  
H. Epstein ◽  
A. Kuzirian ◽  
M. C. Bennett ◽  
T. J. Nelson
Keyword(s):  
Protein Synthesis ◽  
Associative Learning ◽  
Long Term Memory ◽  
Term Memory ◽  
Pkc Activation

scholarly journals Long-term memory requires sequential protein synthesis in three subsets of mushroom body output neurons in Drosophila

2017 ◽  
Vol 7 (1) ◽  
Author(s):  
Jie-Kai Wu ◽  
Chu-Yi Tai ◽  
Kuan-Lin Feng ◽  
Shiu-Ling Chen ◽  
Chun-Chao Chen ◽  
...  
Keyword(s):  
Protein Synthesis ◽  
Mushroom Body ◽  
Long Term Memory ◽  
Term Memory ◽  
Output Neurons

scholarly journals The amnestic agent anisomycin disrupts intrinsic membrane properties of hippocampal neurons via a loss of cellular energetics

2019 ◽  
Vol 122 (3) ◽  
pp. 1123-1135 ◽  
Author(s):  
C. J. Scavuzzo ◽  
M. J. LeBlancq ◽  
F. Nargang ◽  
H. Lemieux ◽  
T. J. Hamilton ◽  
...  
Keyword(s):  
Protein Synthesis ◽  
Mitochondrial Function ◽  
Neural Activity ◽  
Memory Consolidation ◽  
Hippocampal Neurons ◽  
Membrane Properties ◽  
Long Term Memory ◽  
Term Memory ◽  
Cellular Energetics

The nearly axiomatic idea that de novo protein synthesis is necessary for long-term memory consolidation is based heavily on behavioral studies using translational inhibitors such as anisomycin. Although inhibiting protein synthesis has been shown to disrupt the expression of memory, translational inhibitors also have been found to profoundly disrupt basic neurobiological functions, including the suppression of ongoing neural activity in vivo. In the present study, using transverse hippocampal brain slices, we monitored the passive and active membrane properties of hippocampal CA1 pyramidal neurons using intracellular whole cell recordings during a brief ~30-min exposure to fast-bath-perfused anisomycin. Anisomycin suppressed protein synthesis to 46% of control levels as measured using incorporation of radiolabeled amino acids and autoradiography. During its application, anisomycin caused a significant depolarization of the membrane potential, without any changes in apparent input resistance or membrane time constant. Anisomycin-treated neurons also showed significant decreases in firing frequencies and spike amplitudes, and showed increases in spike width across spike trains, without changes in spike threshold. Because these changes indicated a loss of cellular energetics contributing to maintenance of ionic gradients across the membrane, we confirmed that anisomycin impaired mitochondrial function by reduced staining with 2,3,5-triphenyltetrazolium chloride and also impaired cytochrome c oxidase (complex IV) activity as indicated through high-resolution respirometry. These findings emphasize that anisomycin-induced alterations in neural activity and metabolism are a likely consequence of cell-wide translational inhibition. Critical reevaluation of studies using translational inhibitors to promote the protein synthesis dependent idea of long-term memory is absolutely necessary. NEW & NOTEWORTHY Memory consolidation is thought to be dependent on the synthesis of new proteins because translational inhibitors produce amnesia when administered just after learning. However, these agents also disrupt basic neurobiological functions. We show that blocking protein synthesis disrupts basic membrane properties of hippocampal neurons that correspond to induced disruptions of mitochondrial function. It is likely that translational inhibitors cause amnesia through their disruption of neural activity as a result of dysfunction of intracellular energetics.

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