Frontiers in integrative neuroscience
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Front Integr Neurosci · Jan 2017
Sensory Disturbances, but Not Motor Disturbances, Induced by Sensorimotor Conflicts Are Increased in the Presence of Acute Pain.
Incongruence between our motor intention and the sensory feedback of the action (sensorimotor conflict) induces abnormalities in sensory perception in various chronic pain populations, and to a lesser extent in pain-free individuals. The aim of this study was to simultaneously investigate sensory and motor disturbances evoked by sensorimotor conflicts, as well as to assess how they are influenced by the presence of acute pain. It was hypothesized that both sensory and motor disturbances would be increased in presence of pain, which would suggest that pain makes body representations less robust. ⋯ Finally, results showed no relationship between the amount of motor and sensory disturbances evoked in a given individual. Contrary to what was hypothesized, acute pain does not appear to make people more sensitive to the conflict itself, but rather impacts on the type and amount of sensory disturbances that they experienced in response to that conflict. Moreover, the results suggest that some sensorimotor integration processes remain intact in presence of acute pain, allowing us to maintain adaptive motor behavior.
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Front Integr Neurosci · Jan 2017
Stimulation of Cortico-Subthalamic Projections Amplifies Resting Motor Circuit Activity and Leads to Increased Locomotion in Dopamine-Depleted Mice.
Deep brain stimulation (DBS) of the subthalamic nucleus (STN) improves motor function in patients with Parkinson's disease (PD). STN-DBS enables similar improved motor function, including increased movement speed (reduced bradykinesia), in the 6-OHDA dopamine-depletion mouse model of PD. Previous analyses of electrophysiological recordings from STN and motor cortex (M1) have explored signaling changes that correspond to PD and amelioration of PD symptoms. ⋯ However, in this study, stimulation of layer five cortico-subthalamic glutamatergic axons that do not directly project to dopaminergic neurons increased movement and amplified cortico-subthalamic excitatory signaling in dopamine-depleted mice. The correlation between M1-LFP amplitude and locomotion speed observed in these mice points to a role for upregulated hyperdirect pathway excitatory signaling in bradykinesia amelioration. In addition to providing insight into the elusive mechanisms of DBS, these motor circuit amplification relationships suggest that specific manipulation of NMDA, AMPA, and/or metabotropic glutamate receptors in the hyperdirect pathway may be beneficial for upregulating signaling and movement in PD.