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Expression of magi-1 in RIA neurons also rescued the learning defect in the salt chemotaxis learning paradigm (Fig. 3b).
As a next step, we wondered if the observed associative learning defect was specific to volatile chemo-attractants or reflected a more general learning deficit.
In contrast, a deletion mutant of MAGI-1 lacking PDZ1-3 wableble to interact with HMP-2 β-catenin (Fig. 6a), but was not sufficient to rescue the associative learning defect of magi-1 lf) magi-1 lfFig. 6b).
We state that these differences are due to a learning defect and are not a consequence of an inability to perform the task correctly.
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Mice born with extra copies of a human gene develop learning defects that may resemble those in Down syndrome.
Those learning defects are specific since no differences were observed in swimming speed or in the motivational/motor aspects in the cued session.
As reported by a number of studies, neuroligins and neurexins have a role in memory and learning defects that result in documented neurological disorders such as autism.
In the olfactory learning paradigm, Pglr-3 or Pglr-6-driven magi-1 gfp magi-1 gfp learescuedefectheof magi-1(learningnts, while no rescue was observedefectsPglr-1-driven magi-1::gfp (Fig 3a,d).
Defective suppression mechanisms would thus lead to the dominance of certain prepotent behaviors (e.g., the optomotor response) and possibly learning defects when these prevent proper acquisition (or retrieval) of relevant events.
Although we did not test visual learning in the Gal4 networks described in this work, a recent publication using aversive phototaxic suppression (APS) found that wild-type dunce expression in c309 cells rescued dunce learning defects in that visual paradigm [7].
Ifnb –/– mice had age-associated motor learning defects, neuromuscular deficiencies, and cognitive impairment.
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