A neuropeptide signal confers ethanol state dependency during olfactory learning in Caenorhabditis elegans.
A neuropeptide signal confers ethanol state dependency during olfactory learning in Caenorhabditis elegans.
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DOI：
10.1073/pnas.2210462119
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发表时间：
2022-11-16
影响因子：
11.1
通讯作者：
中科院分区：
文献类型：
--
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An altered internal state experienced during learning can enhance the specificity of learned information and promote situation-specific recall. Intoxication during training can confer state dependency so that recall requires the same intoxication state. Olfactory learning (OL) in Caenorhabditis elegans can become state dependent during ethanol intoxication. A neuropeptide originating outside of the OL circuit activates a receptor tyrosine kinase within the circuit to signal intoxication during learning to confer state dependency. Surprisingly, intoxication is encoded using a distinct mechanism during recall. State information can be added to existing OL but cannot be removed from state-dependent OL. These observations provide insight into the modulation of learning by alcohol and demonstrate that the effects of intoxication on learning and memory are distinct. Alcohol intoxication can impact learning and this may contribute to the development of problematic alcohol use. In alcohol (ethanol)-induced state-dependent learning (SDL), information learned while an animal is intoxicated is recalled more effectively when the subject is tested while similarly intoxicated than if tested while not intoxicated. When Caenorhabditis elegans undergoes olfactory learning (OL) while intoxicated, the learning becomes state dependent such that recall of OL is only apparent if the animals are tested while intoxicated. We found that two genes known to be required for signal integration, the secreted peptide HEN-1 and its receptor tyrosine kinase, SCD-2, are required for SDL. Expression of hen-1 in the ASER neuron and scd-2 in the AIA neurons was sufficient for their functions in SDL. Optogenetic activation of ASER in the absence of ethanol during learning could confer ethanol state dependency, indicating that ASER activation is sufficient to signal ethanol intoxication to the OL circuit. To our surprise, ASER activation during testing did not substitute for ethanol intoxication, demonstrating that the effects of ethanol on learning and recall rely on distinct signals. Additionally, intoxication-state information could be added to already established OL, but state-dependent OL did not lose state information when the intoxication signal was removed. Finally, dopamine is required for state-dependent OL, and we found that the activation of ASER cannot bypass this requirement. Our findings provide a window into the modulation of learning by ethanol and suggest that ethanol acts to modify learning using mechanisms distinct from those used during memory access.
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影响因子：
64.5
作者：
BARGMANN, CI;HARTWIEG, E;HORVITZ, HR
通讯作者：
HORVITZ, HR
DOI：
10.1037/adb0000747
发表时间：
2021-08
期刊：
Psychology of addictive behaviors : journal of the Society of Psychologists in Addictive Behaviors
影响因子：
--
作者：
Merrill JE;Carpenter RW;Boyle HK;Haikalis M;Jackson KM;Miranda R;Carey KB;Piasecki TM
通讯作者：
Piasecki TM
DOI：
10.1523/jneurosci.2246-11.2011
发表时间：
2011-07-27
期刊：
The Journal of neuroscience : the official journal of the Society for Neuroscience
影响因子：
--
作者：
Adamantidis AR;Tsai HC;Boutrel B;Zhang F;Stuber GD;Budygin EA;Touriño C;Bonci A;Deisseroth K;de Lecea L
通讯作者：
de Lecea L
影响因子：
6
作者：
Crawford, Zachary;San-Miguel, Adriana
通讯作者：
San-Miguel, Adriana
DOI：
10.1037/h0035025
发表时间：
1973-01-01
期刊：
JOURNAL OF COMPARATIVE AND PHYSIOLOGICAL PSYCHOLOGY
影响因子：
--
作者：
BLISS, DK
通讯作者：
BLISS, DK