Cellular analysis of long-term habituation of the gill-withdrawal reflex of Aplysia californica

Science ◽  
1978 ◽  
Vol 202 (4374) ◽  
pp. 1306-1308 ◽  
Author(s):  
V. Castellucci ◽  
T. Carew ◽  
E. Kandel
2018 ◽  
Author(s):  
Robert Calin-Jageman ◽  
Irina Calin-Jageman

This is a pre-print of a paper now published in Neurobiology of Learning and Memory: https://doi.org/10.1016/j.nlm.2018.09.007 Most long-term memories are forgotten, becoming progressively less likely to be recalled. Still, some memory fragments may persist beyond forgetting, as savings memory (easier relearning) can persist long after recall has become impossible. What happens to a memory trace during forgetting that makes it inaccessible for recall and yet still effective to spark easier re-learning? We are addressing this question by tracking the transcriptional changes that accompany learning and then forgetting of a long-term sensitization memory in the tail-elicited siphon withdrawal reflex of Aplysia californica. First, we tracked savings memory. We found that even though recall of sensitization fades completely within 1 week of training, savings memory is still robustly expressed at 2 weeks post training. Next, we tracked the time-course of regulation of 11 transcripts we previously identified as potentially being regulated beyond the decay of recall. Remarkably, 3 transcripts still show strong regulation of expression 2 weeks after training and an additional 4 are regulated for at least 1 week. These long-lasting changes in gene expression always began early in the memory process, within 1 day of training. We present a synthesis of our results tracking gene expression changes accompanying sensitization and provide a testable model of how sensitization memory is forgotten.


2020 ◽  
Author(s):  
Robert Calin-Jageman ◽  
Irina Calin-Jageman ◽  
Tania Rosiles ◽  
Melissa Nguyen ◽  
Annette Garcia ◽  
...  

[[This is a Stage 2 Registered Report manuscript now accepted for publication at eNeuro. The accepted Stage 1 manuscript is posted here: https://psyarxiv.com/s7dft, and the pre-registration for the project is available here (https://osf.io/fqh8j, 9/11/2019). A link to the final Stage 2 manuscript will be posted after peer review and publication.]] There is fundamental debate about the nature of forgetting: some have argued that it represents the decay of the memory trace, others that the memory trace persists but becomes inaccessible due to retrieval failure. These different accounts of forgetting lead to different predictions about savings memory, the rapid re-learning of seemingly forgotten information. If forgetting is due to decay, then savings requires re-encoding and should thus involve the same mechanisms as initial learning. If forgetting is due to retrieval failure, then savings should be mechanistically distinct from encoding. In this registered report we conducted a pre-registered and rigorous test between these accounts of forgetting. Specifically, we used microarray to characterize the transcriptional correlates of a new memory (1 day after training), a forgotten memory (8 days after training), and a savings memory (8 days after training but with a reminder on day 7 to evoke a long-term savings memory) for sensitization in Aplysia californica (n = 8 samples/group). We found that the re-activation of sensitization during savings does not involve a substantial transcriptional response. Thus, savings is transcriptionally distinct relative to a newer (1-day old) memory, with no co-regulated transcripts, negligible similarity in regulation-ranked ordering of transcripts, and a negligible correlation in training-induced changes in gene expression (r = .04 95% CI [-.12, .20]). Overall, our results suggest that forgetting of sensitization memory represents retrieval failure.


2020 ◽  
Author(s):  
Robert Calin-Jageman ◽  
Irina Calin-Jageman ◽  
Tania Rosiles ◽  
Melissa Nguyen ◽  
Annette Garcia ◽  
...  

[[This is a Stage 1 Registered Report manuscript. The project was submitted for review to eNeuro. Upon revision and acceptance, this version of the manuscript was pre-registered on the OSF (9/11/2019, https://osf.io/fqh8j) (but due to an oversight not posted as a preprint until July 2020). A Stage 2 manuscript is now posted as a pre-print (https://psyarxiv.com/h59jv) and is under review at eNeuro. A link to the final Stage 2 manuscript will be added when available.]]There is fundamental debate about the nature of forgetting: some have argued that it represents the decay of the memory trace, others that the memory trace persists but becomes inaccessible due to retrieval failure. These different accounts of forgetting make different predictions about savings memory, the rapid re-learning of seemingly forgotten information. If forgetting is due to decay then savings requires re-encoding and should thus involve the same mechanisms as initial learning. If forgetting is due to retrieval-failure then savings should be mechanistically distinct from encoding. In this registered report we conducted a pre-registered and rigorous test between these accounts of forgetting. Specifically, we used microarray to characterize the transcriptional correlates of a new memory (1 day from training), a forgotten memory (8 days from training), and a savings memory (8 days from training but with a reminder on day 7 to evoke a long-term savings memory) for sensitization in Aplysia californica (n = 8 samples/group). We find that the transcriptional correlates of savings are [highly similar / somewhat similar / unique] relative to new (1-day-old) memories. Specifically, savings memory and a new memory share [X] of [Y] regulated transcripts, show [strong / moderate / weak] similarity in sets of regulated transcripts, and show [r] correlation in regulated gene expression, which is [substantially / somewhat / not at all] stronger than at forgetting. Overall, our results suggest that forgetting represents [decay / retrieval-failure / mixed mechanisms].


1989 ◽  
Vol 103 (3) ◽  
pp. 585-604 ◽  
Author(s):  
Janet L. Leonard ◽  
John Edstrom ◽  
Ken Lukowiak

Author(s):  
Kathrin I. Thiede ◽  
Jan Born ◽  
Albrecht P. A. Vorster

Sleep is essential for memory consolidation after learning as shown in mammals and invertebrates such as bees and flies. Aplysia californica displays sleep and sleep in this mollusk was also found to support memory for an operant conditioning task. Here, we investigated whether sleep in Aplysia is also required for memory consolidation in a simpler type of learning, i.e., the conditioning of the siphon withdrawal reflex. Two groups of animals (Wake, Sleep, each n=11) were conditioned on the siphon withdrawal reflex with the training following a classical conditioning procedure where an electrical tail shock served as unconditioned stimulus (US) and a tactile stimulus to the siphon as conditioned stimulus (CS). Responses to the CS were tested before (Pre-test), 24 and 48 hours after training. While Wake animals remained awake for 6 hours after training, Sleep animals had undisturbed sleep. The 24h-test in both groups was combined with extinction training, i.e., the extended presentation of the CS alone over two blocks. At the 24h-test, siphon withdrawal durations to the CS were distinctly enhanced in both Sleep and Wake groups with no significant difference between groups, consistent with the view that consolidation of a simple conditioned reflex response does not require post-training sleep. Surprisingly, extinction training did not reverse the enhancement of responses to the CS. On the contrary, at the 48h-test, withdrawal durations to the CS were even further enhanced across both groups. This suggests that processes of sensitization, an even simpler non-associative type of learning, contributed to the withdrawal responses. Our study provides evidence for the hypothesis that sleep preferentially benefits consolidation of more complex learning paradigms than conditioning of simple reflexes.


2019 ◽  
Vol 320 ◽  
pp. 44-49 ◽  
Author(s):  
Christopher Herm ◽  
Vera Silbereisen ◽  
Bernhard M. Graf ◽  
Christoph L. Lassen

2005 ◽  
Vol 94 (3) ◽  
pp. 2218-2230 ◽  
Author(s):  
Xavier Gasull ◽  
Xiaogang Liao ◽  
Michael F. Dulin ◽  
Cynthia Phelps ◽  
Edgar T. Walters

Peripheral axotomy induces long-term hyperexcitability (LTH) of centrally located sensory neuron (SN) somata in diverse species. In mammals this LTH can promote spontaneous activity of pain-related SNs, and such activity may contribute to neuropathic pain and hyperalgesia. However, few axotomized SN somata begin to fire spontaneously in any species, and why so many SNs display soma LTH after axotomy remains a mystery. Is soma LTH a side effect of injury with pathological but no adaptive consequences, or was this response selected during evolution for particular functions? A hypothesis for one function of soma LTH in nociceptive SNs in Aplysia californica is proposed: after peripheral injury that produces partial axotomy of some SNs, compensation for sensory deficits and protective sensitization are achieved by facilitating afterdischarge near the soma, which amplifies sensory input from injured peripheral fields. Four predictions of this hypothesis were confirmed in SNs that innervate the tail. First, LTH of SN somata was induced by a relatively natural axotomizing event—a small cut across part of the tail in the absence of anesthesia. Second, soma LTH was selectively expressed in SNs having axons in cut or crushed nerves rather than nearby, uninjured nerves. Third, after several weeks soma LTH began to reverse when functional recovery of the interrupted afferent pathway was shown by reestablishment of a centrally mediated siphon reflex. Fourth, axotomized SNs developed central afterdischarge that amplified sensory discharge coming from the periphery, and the afterdepolarization underlying this afterdischarge was enhanced by previous axotomy.


1992 ◽  
Vol 70 (2) ◽  
pp. 259-267 ◽  
Author(s):  
Manuel Martínez-Padrón ◽  
William R. Gray ◽  
Ken Lukowiak

Superfusion of an invertebrate vasopressin structural analogue, conopressin G, over the abdominal ganglion of an in vitro preparation of Aplysia californica has significant neurophysiological and behavioral effects. Both the amplitude of the siphon-evoked gill withdrawal reflex and concomitant activity in gill motor neurons are reduced in the presence of conopressin G. Moreover, the frequency of spontaneous gill movements and their neural correlate, interneuron II activity, are increased. These behavioral modifications strongly resemble those that occur during the food-aroused behavioral state in intact Aplysia. In addition, conopressin G superfusion reduces both the excitability of gill motor neurons and the strength of gill contractions in response to gill motor neuron discharges elicited by direct depolarizing current. A role for conopressin G or a similar peptide in the modulation of gill behaviors associated with the food-aroused state is suggested.Key words: Aplysia californica, conopressin G, gill withdrawal reflex, spontaneous gill movements.


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