FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W4387472654> ?p ?o ?g. }

• W4387472654 abstract "Animals must learn to ignore stimuli that are irrelevant to survival and attend to ones that enhance survival. When a stimulus regularly fails to be associated with an important consequence, subsequent excitatory learning about that stimulus can be delayed, which is a form of nonassociative conditioning called 'latent inhibition'. Honey bees show latent inhibition toward an odor they have experienced without association with food reinforcement. Moreover, individual honey bees from the same colony differ in the degree to which they show latent inhibition, and these individual differences have a genetic basis. To investigate the mechanisms that underly individual differences in latent inhibition, we selected two honey bee lines for high and low latent inhibition, respectively. We crossed those lines and mapped a Quantitative Trait Locus for latent inhibition to a region of the genome that contains the tyramine receptor gene Amtyr1 [We use Amtyr1 to denote the gene and AmTYR1 the receptor throughout the text.]. We then show that disruption of Amtyr1 signaling either pharmacologically or through RNAi qualitatively changes the expression of latent inhibition but has little or slight effects on appetitive conditioning, and these results suggest that AmTYR1 modulates inhibitory processing in the CNS. Electrophysiological recordings from the brain during pharmacological blockade are consistent with a model that AmTYR1 indirectly regulates at inhibitory synapses in the CNS. Our results therefore identify a distinct Amtyr1-based modulatory pathway for this type of nonassociative learning, and we propose a model for how Amtyr1 acts as a gain control to modulate hebbian plasticity at defined synapses in the CNS. We have shown elsewhere how this modulation also underlies potentially adaptive intracolonial learning differences among individuals that benefit colony survival. Finally, our neural model suggests a mechanism for the broad pleiotropy this gene has on several different behaviors.To efficiently navigate their environment, animals must pay attention to cues associated with events important for survival while also dismissing meaningless signals. The difference between relevant and irrelevant stimuli is learned through a range of complex mechanisms that includes latent inhibition. This process allows animals to ignore irrelevant stimuli, which makes it more difficult for them to associate a cue and a reward if that cue has been unrewarded before. For example, bees will take longer to ‘learn’ that a certain floral odor signals a feeding opportunity if they first repeatedly encountered the smell when food was absent. Such a mechanism allows organisms to devote more attention to other stimuli which have the potential to be important for survival. The strength of latent inhibition – as revealed by how quickly and easily an individual can learn to associate a reward with a previously unrewarded stimulus – can differ between individuals. For instance, this is the case in honey bee colonies, where workers have the same mother but may come from different fathers. Such genetic variation can be beneficial for the hive, with high latent inhibition workers being better suited for paying attention to and harvesting known resources, and their low latent inhibition peers for discovering new ones. However, the underlying genetic and neural mechanisms underpinning latent inhibition variability between individuals remained unclear. To investigate this question, Latshaw et al. cross-bred bees from high and low latent inhibition genetic lines. The resulting progeny underwent behavioral tests, and the genome of low and high latent inhibition individuals was screened. These analyses revealed a candidate gene, Amtyr1, which was associated with individual variations in the learning mechanism. Further experiments showed that blocking or disrupting the production the AMTYR1 protein led to altered latent inhibition behavior as well as dampened attention-related processing in recordings from the central nervous system. Based on these findings, a model was proposed detailing how varying degrees of Amtyr1 activation can tune Hebbian plasticity, the brain mechanism that allows organisms to regulate associations between cues and events. Importantly, because of the way AMTYR1 acts in the nervous system, this modulatory role could go beyond latent inhibition, with the associated gene controlling the activity of a range of foraging-related behaviors. Genetic work in model organisms such as fruit flies would allow a more in-depth understanding of such network modulation." @default.
• W4387472654 created "2023-10-11" @default.
• W4387472654 creator A5001290554 @default.
• W4387472654 creator A5042856346 @default.
• W4387472654 creator A5053823603 @default.
• W4387472654 creator A5068113226 @default.
• W4387472654 creator A5074551601 @default.
• W4387472654 creator A5080721456 @default.
• W4387472654 creator A5080778283 @default.
• W4387472654 creator A5083350746 @default.
• W4387472654 creator A5083383180 @default.
• W4387472654 creator A5085585732 @default.
• W4387472654 creator A5089797160 @default.
• W4387472654 date "2023-10-10" @default.
• W4387472654 modified "2023-10-17" @default.
• W4387472654 title "Tyramine and its Amtyr1 receptor modulate attention in honey bees (Apis mellifera)" @default.
• W4387472654 cites W1779400460 @default.
• W4387472654 cites W1944780026 @default.
• W4387472654 cites W1972444757 @default.
• W4387472654 cites W1976575629 @default.
• W4387472654 cites W1979933953 @default.
• W4387472654 cites W1980083097 @default.
• W4387472654 cites W1990614364 @default.
• W4387472654 cites W1997178639 @default.
• W4387472654 cites W1999352179 @default.
• W4387472654 cites W2001213757 @default.
• W4387472654 cites W2005018941 @default.
• W4387472654 cites W2005811042 @default.
• W4387472654 cites W2011077323 @default.
• W4387472654 cites W2014043898 @default.
• W4387472654 cites W2018698699 @default.
• W4387472654 cites W2022104690 @default.
• W4387472654 cites W2026329327 @default.
• W4387472654 cites W2029124091 @default.
• W4387472654 cites W2032382791 @default.
• W4387472654 cites W2034116837 @default.
• W4387472654 cites W2037824587 @default.
• W4387472654 cites W2041163137 @default.
• W4387472654 cites W2045755339 @default.
• W4387472654 cites W2048134531 @default.
• W4387472654 cites W2052917504 @default.
• W4387472654 cites W2052955184 @default.
• W4387472654 cites W2055099335 @default.
• W4387472654 cites W2058357158 @default.
• W4387472654 cites W2059437434 @default.
• W4387472654 cites W2081662677 @default.
• W4387472654 cites W2082056860 @default.
• W4387472654 cites W2096798307 @default.
• W4387472654 cites W2097237250 @default.
• W4387472654 cites W2098550830 @default.
• W4387472654 cites W2099878675 @default.
• W4387472654 cites W2102617823 @default.
• W4387472654 cites W2103441770 @default.
• W4387472654 cites W2104508398 @default.
• W4387472654 cites W2107565452 @default.
• W4387472654 cites W2108234281 @default.
• W4387472654 cites W2114145948 @default.
• W4387472654 cites W2131534671 @default.
• W4387472654 cites W2133760341 @default.
• W4387472654 cites W2135781772 @default.
• W4387472654 cites W2136784736 @default.
• W4387472654 cites W2137040250 @default.
• W4387472654 cites W2138206619 @default.
• W4387472654 cites W2144653642 @default.
• W4387472654 cites W2150802969 @default.
• W4387472654 cites W2154432392 @default.
• W4387472654 cites W2158959107 @default.
• W4387472654 cites W2159271282 @default.
• W4387472654 cites W2162291628 @default.
• W4387472654 cites W2165022931 @default.
• W4387472654 cites W2165820447 @default.
• W4387472654 cites W2168335606 @default.
• W4387472654 cites W2414866293 @default.
• W4387472654 cites W2473863911 @default.
• W4387472654 cites W2560763733 @default.
• W4387472654 cites W2586641343 @default.
• W4387472654 cites W2602041554 @default.
• W4387472654 cites W2608234654 @default.
• W4387472654 cites W2612459977 @default.
• W4387472654 cites W2762949903 @default.
• W4387472654 cites W2766619371 @default.
• W4387472654 cites W2895684610 @default.
• W4387472654 cites W2898306222 @default.
• W4387472654 cites W2914312676 @default.
• W4387472654 cites W3005314022 @default.
• W4387472654 cites W3023069762 @default.
• W4387472654 cites W3043460073 @default.
• W4387472654 cites W3047388478 @default.
• W4387472654 cites W3111630222 @default.
• W4387472654 cites W3118847578 @default.
• W4387472654 cites W3205439447 @default.
• W4387472654 cites W3207323893 @default.
• W4387472654 cites W4224994191 @default.
• W4387472654 cites W4225619479 @default.
• W4387472654 cites W4246854168 @default.
• W4387472654 cites W4301795335 @default.
• W4387472654 cites W4387472654 @default.
• W4387472654 doi "https://doi.org/10.7554/elife.83348" @default.
• W4387472654 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/37814951" @default.
• W4387472654 hasPublicationYear "2023" @default.

• next