Canceling actions involves a race between basal ganglia pathways
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The results support race models of action cancellation, with stopping requiring Stop-cue information to be transmitted from STN to SNr before increased striatal input creates a point of no return.Abstract:
Salient cues can prompt the rapid interruption of planned actions. It has been proposed that fast, reactive behavioral inhibition involves specific basal ganglia pathways, and we tested this by comparing activity in multiple rat basal ganglia structures during performance of a stop-signal task. Subthalamic nucleus (STN) neurons exhibited low-latency responses to 'Stop' cues, irrespective of whether actions were canceled or not. By contrast, neurons downstream in the substantia nigra pars reticulata (SNr) only responded to Stop cues in trials with successful cancellation. Recordings and simulations together indicate that this sensorimotor gating arises from the relative timing of two distinct inputs to neurons in the SNr dorsolateral 'core' subregion: cue-related excitation from STN and movement-related inhibition from striatum. Our results support race models of action cancellation, with stopping requiring Stop-cue information to be transmitted from STN to SNr before increased striatal input creates a point of no return.read more
Citations
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Basal ganglia and autism - a translational perspective.
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TL;DR: There is an abundance of emerging evidence that the basal ganglia likely plays critical roles in maintaining an inhibitory balance between cortical and subcortical structures, critical for normal motor actions and cognitive functions in autism, thus impacting key pathways that affect normal cortical network activity.
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Non-selective inhibition of inappropriate motor-tendencies during response-conflict by a fronto-subthalamic mechanism.
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Ramping single unit activity in the medial prefrontal cortex and ventral striatum reflects the onset of waiting but not imminent impulsive actions
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Sensorimotor Processing in the Basal Ganglia Leads to Transient Beta Oscillations during Behavior.
Amin Mirzaei,Arvind Kumar,Daniel K. Leventhal,Nicolas Mallet,Ad Aertsen,Joshua D. Berke,Robert Schmidt +6 more
TL;DR: It is proposed that transient beta oscillations in healthy animals share the same mechanism with pathological beta oscillation in Parkinson's disease (PD), and this important result connects functional and pathological roles of betascillations in the basal ganglia.
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