Using an invertebrate model to investigate the mechanisms of short-term memory deficits induced by food deprivation.
Excitability
Feeding suppression
Food deprivation
Memory
Short-term sensitization
Journal
Behavioural brain research
ISSN: 1872-7549
Titre abrégé: Behav Brain Res
Pays: Netherlands
ID NLM: 8004872
Informations de publication
Date de publication:
10 02 2022
10 02 2022
Historique:
received:
04
06
2021
revised:
29
09
2021
accepted:
26
10
2021
pubmed:
11
11
2021
medline:
15
3
2022
entrez:
10
11
2021
Statut:
ppublish
Résumé
Although prolonged food deprivation is known to cause memory deficits, the underlying mechanisms are only partially understood. In this study, we began to investigate the cellular substrates of food deprivation-induced memory impairments in the invertebrate Aplysia. Following a single trial of noxious stimuli, Aplysia concurrently express short-term sensitization (an elementary form of learning in which withdrawal reflexes are enhanced) and short-term feeding suppression for at least 15 min. Cellular correlates of sensitization and feeding suppression include increased excitability of the tail sensory neurons (TSNs) controlling the withdrawal reflexes, and decreased excitability of feeding decision-making neuron B51, respectively. Recently, 14 days of food deprivation (14DFD) was reported to break the co-expression of sensitization and feeding suppression in Aplysia without health deterioration. Specifically, under 14DFD, sensitization was completely prevented while feeding suppression was present albeit attenuated. This study explored the cellular mechanisms underlying the absent sensitization and reduced feeding suppression under 14DFD. A reduced preparation was used to evaluate the short-term cellular modifications induced by delivering an aversive training protocol in vitro. TSN excitability failed to increase following in vitro training under 14DFD, suggesting that the lack of sensitization may be a consequence of the fact that TSN excitability failed to increase. B51 excitability also failed to decrease following in vitro training, indicating that additional neurons may contribute to the conserved albeit reduced feeding suppression in 14DFD animals. This study lays the foundations for the future use of the Aplysia model system to investigate the mechanisms underlying the memory impairments induced by prolonged food deprivation.
Identifiants
pubmed: 34757110
pii: S0166-4328(21)00534-9
doi: 10.1016/j.bbr.2021.113646
pmc: PMC8671320
mid: NIHMS1756162
pii:
doi:
Types de publication
Journal Article
Research Support, N.I.H., Extramural
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
113646Subventions
Organisme : NIGMS NIH HHS
ID : SC3 GM111188
Pays : United States
Informations de copyright
Copyright © 2021 Elsevier B.V. All rights reserved.
Références
Behav Biol. 1974 Jan;10(1):1-26
pubmed: 4815142
J Neurosci. 1998 Aug 1;18(15):5988-98
pubmed: 9671684
Behav Brain Res. 2019 Mar 15;360:341-353
pubmed: 30528940
Learn Mem. 2017 Jul 17;24(8):331-340
pubmed: 28716953
J Comp Neurol. 2004 Mar 29;471(2):219-40
pubmed: 14986314
Nat Neurosci. 2016 May;19(5):734-741
pubmed: 27019015
Neuron. 2008 Sep 11;59(5):815-28
pubmed: 18786364
Front Neurosci. 2012 Jul 26;6:113
pubmed: 22855670
Cold Spring Harb Perspect Biol. 2015 Feb 26;7(5):
pubmed: 25722464
J Neurosci. 2010 Aug 18;30(33):11028-31
pubmed: 20720109
J Neurophysiol. 1990 Mar;63(3):539-58
pubmed: 2329360
Learn Mem. 2012 Mar 14;19(4):159-63
pubmed: 22419814
J Neurosci. 1989 Dec;9(12):4200-13
pubmed: 2592997
Learn Mem. 2012 Dec 14;20(1):1-5
pubmed: 23242417
Behav Brain Res. 2018 Sep 3;349:177-185
pubmed: 29704600
J Physiol. 1974 Oct;242(1):61-76
pubmed: 4548090
J Neurosci. 1999 Mar 15;19(6):2247-60
pubmed: 10066276
J Neurophysiol. 2011 Apr;105(4):1642-50
pubmed: 21273320
Science. 2013 Jan 25;339(6118):440-2
pubmed: 23349289
Neuroscience. 2008 Jun 2;153(4):929-34
pubmed: 18434026
Behav Brain Res. 2020 Apr 6;383:112504
pubmed: 31981653
J Comp Neurol. 1991 Sep 15;311(3):425-33
pubmed: 1955588
Neuroscience. 1987 Nov;23(2):721-9
pubmed: 3437986
J Neurosci. 2011 Oct 12;31(41):14789-93
pubmed: 21994395