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Humans can rapidly convert instructions about a rule into functional neural structures used to apply the rule. The early stages of this encoding process are poorly understood. We designed a stimulus-response (SR) task in which participants were first shown a SR rule on a screen for 200 ms, and then had to apply it to a test stimulus T, which either matched the S in the rule (SR trial) or not (catch trial). To investigate the early stages of rule encoding, the delay between the end of rule display and the onset of the test stimulus was manipulated and chosen between values of 50 ms to 1300 ms. Participants conducted three sessions of 288 trials each, separated by a median of 9 h. Random sequences of 20 rules were used. We then analysed the reaction times and the types of errors made by participants in the different conditions. The analysis of practice effects in session 1 suggests that the neural networks that process SR and catch trials are at least partially distinct, and improve separately during the practice of respectively SR and catch trials. The rule-encoding process, however, is common to both tasks and improves with the number of trials, irrespective of the trial type. Rule encoding shows interesting dynamic properties that last for 500 ms after the end of the stimulus presentation. The encoding process increases the response time in a non-stochastic way, simply adding a reaction time cost to all responses. The rule-retrieval system is functional before the encoding has stabilized, as early as 50 ms after the end of SR rule presentation, with low response errors. It is sensitive to masking however, producing errors with brief (100 ms) test stimulus presentations. Once encoding has stabilized, the sensitivity to masking disappears. It is suggested that participants do encode rules as a parametrized function, using the same neural encoding structure for each trial, rather than reconfiguring their brain anew for each new SR rule. This structure would have been implemented from instructions received prior to the experiment, by using a library of neural functions available in the brain. The observed errors are consistent with this view.
This article was published in the following journal.
Name: Bio Systems
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The interval between two successive CELL DIVISIONS during which the CHROMOSOMES are not individually distinguishable. It is composed of the G phases (G1 PHASE; G0 PHASE; G2 PHASE) and S PHASE (when DNA replication occurs).
Functionalization of exogenous substances to prepare them for conjugation in PHASE II DETOXIFICATION. Phase I enzymes include CYTOCHROME P450 enzymes and some OXIDOREDUCTASES. Excess induction of phase I over phase II detoxification leads to higher levels of FREE RADICALS that can induce CANCER and other cell damage. Induction or antagonism of phase I detoxication is the basis of a number of DRUG INTERACTIONS.
The period of the CELL CYCLE following DNA synthesis (S PHASE) and preceding M PHASE (cell division phase). The CHROMOSOMES are tetraploid in this point.
Genes that show rapid and transient expression in the absence of de novo protein synthesis. The term was originally used exclusively for viral genes where immediate-early referred to transcription immediately following virus integration into the host cell. It is also used to describe cellular genes which are expressed immediately after resting cells are stimulated by extracellular signals such as growth factors and neurotransmitters.
Involuntary movements of the eye that are divided into two types, jerk and pendular. Jerk nystagmus has a slow phase in one direction followed by a corrective fast phase in the opposite direction, and is usually caused by central or peripheral vestibular dysfunction. Pendular nystagmus features oscillations that are of equal velocity in both directions and this condition is often associated with visual loss early in life. (Adams et al., Principles of Neurology, 6th ed, p272)
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