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Query: UMLS:C0598853 (
forgetting
)
3,232
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
Forgetting
memories is important for animals to properly respond to continuously changing environments. To elucidate the mechanisms of
forgetting
, we used one of the behavioral plasticities of
Caenorhabditis elegans
hermaphrodite, olfactory adaptation to an attractive odorant, diacetyl, as a simple model of learning. In
C. elegans,
the TIR-1/JNK-1 pathway accelerates
forgetting
of olfactory adaptation by facilitating neural secretion from AWC sensory neurons. In this study, to identify the downstream effectors of the TIR-1/JNK-1 pathway, we conducted a genetic screen for suppressors of the gain-of-function mutant of
tir-1
(
ok1052
), which shows excessive
forgetting
. Our screening showed that three proteins-a membrane protein, MACO-1; a
receptor tyrosine kinase
, SCD-2; and its putative ligand, HEN-1-regulated
forgetting
downstream of the TIR-1/JNK-1 pathway. We further demonstrated that MACO-1 and SCD-2/HEN-1 functioned in parallel genetic pathways, and only MACO-1 regulated
forgetting
of olfactory adaptation to isoamyl alcohol, which is an attractive odorant sensed by different types of sensory neurons. In olfactory adaptation, odor-evoked Ca
2+
responses in olfactory neurons are attenuated by conditioning and recovered thereafter. A Ca
2+
imaging study revealed that this attenuation is sustained longer in
maco-1
and
scd-2
mutant animals than in wild-type animals like the TIR-1/JNK-1 pathway mutants. Furthermore, temporal silencing by histamine-gated chloride channels revealed that the neuronal activity of AWC neurons after conditioning is important for proper
forgetting
. We propose that distinct signaling pathways, each of which has a specific function, may coordinately and temporally regulate
forgetting
by controlling sensory responses.
SIGNIFICANCE STATEMENT
Active
forgetting
is an important process to understand the whole mechanisms of memories. Recent papers have reported that the noncell autonomous regulations are required for proper
forgetting
in invertebrates. We found that in
Caenorhabditis elegans
hermaphrodite, the noncell autonomous regulations of
forgetting
of olfactory adaptation is regulated by three conserved proteins: a membrane protein, MACO-1; a
receptor tyrosine kinase
, SCD-2: and its ligand, HEN-1. MACO-1 and SCD-2/HEN-1, working in coordination, accelerate
forgetting
by controlling sensory responses in parallel. Furthermore, temporal regulation of neuronal activity is important for proper
forgetting
. We suggest that multiple pathways may coordinately and temporally regulate
forgetting
through control of sensory responses. This study should lead to a better understanding of
forgetting
in higher organisms.
...
PMID:Multiple Signaling Pathways Coordinately Regulate Forgetting of Olfactory Adaptation through Control of Sensory Responses in
Caenorhabditis elegans
. 2892 7
Social isolation in adolescence leads to lasting deficits, including emotional and cognitive dysregulation. It remains unclear, however, how social isolation affects certain processes of memory and what molecular mechanisms are involved. In this study, we found that social isolation during the post-weaning period resulted in
forgetting
of the long-term fear memory, which was attributable to the downregulation of synaptic function in the hippocampal CA1 region mediated by EphB2, a
receptor tyrosine kinase
which involves in the glutamate receptor multiprotein complex. Viral-mediated EphB2 knockdown in CA1 mimicked the memory defects in group-housed mice, whereas restoration of EphB2 by either viral overexpression or resocialization reversed the memory decline in isolated mice. Taken together, our finding indicates that social isolation gives rise to memory
forgetting
by disrupting EphB2-mediated synaptic plasticity, which may provide a potential target for preventing memory loss caused by social isolation or loneliness.
...
PMID:EphB2 mediates social isolation-induced memory forgetting. 3316
