Journal of neurophysiology
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Clinical Trial
Subthalamic stimulation and neuronal activity in the substantia nigra in Parkinson's disease.
High-frequency stimulation of the subthalamic nucleus (STN) is an effective treatment for severe forms of Parkinson's disease (PD). To study the effects of high-frequency STN stimulation on one of the main output pathways of the basal ganglia, single-unit recordings of the neuronal activity of the substantia nigra pars reticulata (SNr) were performed before, during, and after the application of STN electrical stimulation in eight PD patients. ⋯ The SNr residual neuronal activity during 140-Hz STN stimulation was driven by the STN stimulation. How the decrease in rate and modification of firing pattern of SNr-evoked neural activity, during high-frequency STN stimulation, contribute to the improvement of parkinsonian motor disability remains to be elucidated.
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This study examines motor cortical representation of hand position and its relationship to the representation of hand velocity during reaching movements. In all, 978 motor cortical neurons were recorded from the proximal arm area of rostral motor cortex. The results demonstrate that position and velocity are simultaneously encoded by single motor cortical neurons in an additive fashion and that the relative weights of the position and velocity signals change dynamically during reaching. ⋯ A new reaching task (standard reaching) is introduced to minimize these correlations. Likewise, a new decoding method (indirect OLE) was developed to analyze the data by simultaneously decoding both three-dimensional (3D) hand position and 3D hand velocity from correlated neural activity. This method shows that, on average, the reconstructed velocity led the actual hand velocity by 122 ms, whereas the reconstructed position signal led the actual hand position by 81 ms.
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The pedunculopontine tegmental (PPT) GABAergic system plays a crucial role in the regulation of rapid eye movement (REM) sleep. I recently reported that the activation of PPT GABA(B) receptors suppressed REM sleep by inhibiting REM-on cells. One of the important mechanisms for GABA(B) receptor activation-mediated physiological action is the inhibition of the intracellular cAMP-dependent protein kinase A (cAMP-PKA) signaling pathway. ⋯ On the contrary, microinjection of baclofen (1.5 nmol) suppressed REM sleep by delaying its appearance for approximately 183 min; however, the suppression of REM sleep by baclofen was prevented by a subsequent microinjection of SpCAMPS. These results provide evidence that the activation of cAMP-PKA within the PPT can successfully block the GABA(B) receptor activation-mediated REM sleep suppression effect. These findings suggest that the PPT GABA(B) receptor activation-mediated REM sleep regulating mechanism involves inactivation of cAMP-PKA signaling in the freely moving rat.
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As a hormone in the hypothalamic-pituitary-adrenocortical (HPA) axis corticotropin-releasing factor (CRF) mediates stress responses. CRF can also act as a neuromodulator of synaptic transmission outside the HPA axis. A major site of extrahypothalamic expression of CRF and its G-protein-coupled receptors is the amygdala, a key player in affect-related disorders such as anxiety. ⋯ A selective CRF1 receptor antagonist (NBI27914; 1-100 microM, concentration in microdialysis probe; 15 min) inhibited evoked responses and background activity in arthritis (n = 9) but had no effect under normal conditions before arthritis (n = 9). In contrast, a selective CRF2 receptor antagonist (Astressin-2B; 1-100 microM, 15 min) had no effect in arthritis (n = 7) but increased the neurons' responses under normal conditions (n = 8). These data suggest that CRF1 receptors in the amygdala contribute to pain-related sensitization, whereas the normally inhibitory function of CRF2 receptors is lost in the arthritis pain model.