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32 The neural architecture of loops connecting the cortex and basal ganglia allow rapid inhibition and release of motor programs via the direct, indirect, and hyperdirect pathways.
Dopamine deficiency impairs phasic activation of the cortico-striato-EPN direct pathway and release of motor actions, and would be involved in the bradykinesia seen in PD.
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Its reduction shows a faster and more efficacy release of posturographic motor commands.
The release of the motor programme by SAS does not require the combination of two stimuli, and, therefore, it does not seem to involve reinforcement of afferent input but rather a timely occurrence in the preparation phase of movement execution.
In the process of preparation for task execution, whether self-generated or in the context of a reaction time task, structures and circuits along the motor pathway from cortex to alpha motoneurons that are involved in the execution of the required task have to reach a critical level of excitability enhancement just preceding the release of the motor programme.
It is known that, in reaction time task experiments, a SAS delivered at the same time as the imperative signal causes a rapid release of the motor programme, which may be executed by passing the normal cortical execution pathways [ 21, 22].
If one admits that a decrease of activity in orbito-frontal cortex mimics, although to a different extent, the effect of a lesion one may account for the motor activation in response to ugly stimuli as a covert release of an appropriate motor behavior.
The scanning systems present a challenge to efforts by state and federal governments to limit the amount of information that can be released by departments of motor vehicles.
It has been proposed that unwanted movements may arise because of a release of the primary motor cortex (M1) from conscious control by intentional planning systems [8].
Finally, hsc70 is important for the release of the molecular motor kinesin from its vesicular cargo permitting its precise localization [53].
It was shown that magnesium antagonizes calcium-dependent release of acetylcholine at motor endplates [ 6].
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