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Controlling instabilities in manipulation requires specific cortical-striatal-cerebellar networks.

ABSTRACT: Dexterous manipulation requires both strength, the ability to produce fingertip forces of a specific magnitude, and dexterity, the ability to dynamically regulate the magnitude and direction of fingertip force vectors and finger motions. Although cortical activity in fronto-parietal networks has been established for stable grip and pinch forces, the cortical regulation in the dexterous control of unstable objects remains unknown. We used functional magnetic resonance imaging (fMRI) to interrogate cortical networks engaged in the control of four objects with increasing instabilities but requiring constant strength. In addition to expected activity in fronto-parietal networks we find that dexterous manipulation of increasingly unstable objects is associated with a linear increase in the amplitude of the BOLD signal in the basal ganglia (P = 0.007 and P = 0.023 for 2 compression tasks). A computational regression (connectivity) model identified independent subsets of cortical networks whose connection strengths were mutable and associated with object instability (P < 0.001). Our results suggest that in the presence of object instability, the basal ganglia may modulate the activity of premotor areas and subsequent motor output. This work, therefore, provides new evidence for the selectable cortical representation and execution of dynamic multifinger manipulation for grasp stability.

SUBMITTER: Mosier K

PROVIDER: S-EPMC3074419 | biostudies-literature | 2011 Mar

REPOSITORIES: biostudies-literature

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Controlling instabilities in manipulation requires specific cortical-striatal-cerebellar networks.

Mosier Kristine K Lau Chad C Wang Yang Y Venkadesan Madhusudhan M Valero-Cuevas Francisco J FJ

Journal of neurophysiology 20110112 3

Dexterous manipulation requires both strength, the ability to produce fingertip forces of a specific magnitude, and dexterity, the ability to dynamically regulate the magnitude and direction of fingertip force vectors and finger motions. Although cortical activity in fronto-parietal networks has been established for stable grip and pinch forces, the cortical regulation in the dexterous control of unstable objects remains unknown. We used functional magnetic resonance imaging (fMRI) to interrogat ...[more]

PMID: 21228301

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Project description:In contrast to the prenatal topographic development of sensory cortices, striatal circuit organization is slow and requires the functional maturation of cortical and thalamic excitatory inputs throughout the first postnatal month. While mechanisms regulating synapse development and plasticity are quite well described at excitatory synapses of glutamatergic neurons in the neocortex, comparatively little is known of how this translates to glutamate synapses onto GABAergic neurons in the striatum. Here we investigate excitatory striatal synapse plasticity in an in vitro system, where glutamate can be studied in isolation from dopamine and other neuromodulators. We examined pre-and post-synaptic structural and functional plasticity in GABAergic striatal spiny projection neurons (SPNs), co-cultured with glutamatergic cortical neurons. After synapse formation, medium-term (24 h) TTX silencing increased the density of filopodia, and modestly decreased dendritic spine density, when assayed at 21 days in vitro (DIV). Spine reductions appeared to require residual spontaneous activation of ionotropic glutamate receptors. Conversely, chronic (14 days) TTX silencing markedly reduced spine density without any observed increase in filopodia density. Time-dependent, biphasic changes to the presynaptic marker Synapsin-1 were also observed, independent of residual spontaneous activity. Acute silencing (3 h) did not affect presynaptic markers or postsynaptic structures. To induce rapid, activity-dependent plasticity in striatal neurons, a chemical NMDA receptor-dependent "long-term potentiation (LTP)" paradigm was employed. Within 30 min, this increased spine and GluA1 cluster densities, and the percentage of spines containing GluA1 clusters, without altering the presynaptic signal. The results demonstrate that the growth and pruning of dendritic protrusions is an active process, requiring glutamate receptor activity in striatal projection neurons. Furthermore, NMDA receptor activation is sufficient to drive glutamatergic structural plasticity in SPNs, in the absence of dopamine or other neuromodulators.

Dataset Information

Controlling instabilities in manipulation requires specific cortical-striatal-cerebellar networks.

Publications

Controlling instabilities in manipulation requires specific cortical-striatal-cerebellar networks.

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