The basal ganglia: focused selection and inhibition of competing motor programs.by: JW Mink
Prog Neurobiol, Vol. 50, No. 4. (November 1996), pp. 381-425.
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- extensive review of basal ganglia anatomy, electrophysiology, and clinical deficits
- proposes a focused selection/inhibition of competing motor program hypothesis for basal ganglia function: cortical motor signals drive a fast inhibitory signal via STN-GPI to broadly inhibit thalamocortical and brainstem motor pathways, and a slower excitation via striatum-GPI that selectively disinhibits the chosen motor action pathway
- argues against alternative models for basal ganglia function, including initiation of movement, direct-indirect scaling of movement, and movement sequencing
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AbstractThe basal ganglia comprise several nuclei in the forebrain, diencephalon, and midbrain thought to play a significant role in the control of posture and movement. It is well recognized that people with degenerative diseases of the basal ganglia suffer from rigidly held abnormal body postures, slowing of movement, involuntary movements, or a combination of these a abnormalities. However, it has not been agreed just what the basal ganglia contribute to normal movement. Recent advances in knowledge of the basal ganglia circuitry, activity of basal ganglia neurons during movement, and the effect of basal ganglia lesions have led to a new hypothesis of basal ganglia function. The hypothesis states that the basal ganglia do not generate movements. Instead, when voluntary movement is generated by cerebral cortical and cerebellar mechanisms, the basal ganglia act broadly to inhibit competing motor mechanisms that would otherwise interfere with the desired movement. Simultaneously, inhibition is removed focally from the desired motor mechanisms to allow that movement to proceed. Inability to inhibit competing motor programs results in slow movements, abnormal postures and involuntary muscle activity.
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