The European journal of neuroscience
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Chronic pain is a major complaint for up to 85% of Parkinson's disease patients; however, it often not identified as a symptom of Parkinson's disease. Adequate treatment of motor symptoms often provides analgesic effects in Parkinson's patients but how this occurs remains unclear. Studies have shown both Parkinson's patients and 6-hydroxydopamine-lesioned rats exhibit decreased sensory thresholds. ⋯ Interestingly, during von Frey testing, low-frequency stimulation provided a more robust improvement in some 6OHDA lesioned rats, while in others, the magnitude of improvement on high-frequency stimulation was greater. This study shows that subthalamic deep brain stimulation improves mechanical allodynia and thermal hyperalgesia in 6-hydroxydopamine-lesioned animals at both high and low frequencies. Furthermore, we suggest considering using low-frequency stimulation when treating Parkinson's patients where pain remains the predominant complaint.
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Dexmedetomidine (an alpha-2 adrenergic agonist) sedation is commonly used during subthalamic nucleus (STN) deep-brain stimulation (DBS). Its effects on the electrophysiological characteristics of human STN neurons are largely unknown. We hypothesised that dexmedetomidine modulates the firing rates and bursting of human STN neurons. ⋯ Dexmedetomidine was associated with a slight increase in firing rate (41.1 ± 9.9 vs. 34.5 ± 10.6 Hz, P = 0.02) but a significant decrease in burstiness (number of bursts, P = 0.02; burst index, P < 0.001; percentage of spikes in burst, P = 0.002) of dorsal but not ventral STN neurons. This was not associated with modulation of beta oscillations in the spike-oscillations analysis(beta peak, P = 0.4; signal-to-noise ratio in the beta range for spikes and bursts, P = 0.3 and P = 0.5, respectively) and LFP analysis (Beta power, P = 0.17). As bursting pattern is often used to identify STN and guide electrode placement, we recommend that high-dose dexmedetomidine should be avoided during DBS surgery.
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Glucose is the sole neural fuel for the brain and is essential for cognitive function. Abnormalities in glucose tolerance may be associated with impairments in cognitive function. Experimental obese model mice can be generated by an intraperitoneal injection of monosodium glutamate (MSG; 2 mg/g) once a day for 5 days from 1 day after birth. ⋯ The protein levels of vesicular glutamate transporter 1 and GluA1 glutamate receptor subunits decreased in the CA1 region of MSG-treated mice. These results suggest that deficits in glutamatergic presynapses as well as postsynapses lead to impaired synaptic plasticity in MSG-treated mice during the development of glucose intolerance, though it remains unknown whether impaired LTP is due to altered inhibitory transmission. It may be important to examine changes in glucose tolerance in order to prevent cognitive malfunctions associated with diabetes.
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The ability to understand competitive games is closely connected to the mirror neuron system (MNS). This network is activated not only when an action is performed, but also when it is observed. Apart from allowing the understanding of actions performed by others, the MNS has been implicated in predicting subsequent actions. ⋯ In some videos (congruents) the prediction was satisfied, but in the rest of the videos (incongruents) the prediction was not satisfied. When the result was shown, higher activity in the MNS was observed in the congruent videos than in the incongruent ones. Therefore, the observation of a simple manual game leads to a significant activation of the MNS, and this activity seems to be modulated by the final outcome of a prediction, and when predictions are satisfied the activity is higher.
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Opioids are well known for their robust analgesic effects. Chronic activation of mu opioid receptors (MOPs) is, however, accompanied by various unwanted effects such as analgesic tolerance. Among other mechanisms, interactions between MOPs and delta opioid receptors (DOPs) are thought to play an important role in morphine-induced behavioral adaptations. ⋯ As opposed to NTI, 7-benzylidenenaltrexone and naltriben were reported to be selective DOP subtype 1 and DOP subtype 2 antagonists, respectively. Interestingly, naltriben but not 7-benzylidenenaltrexone was able to attenuate the development of morphine analgesic tolerance in inflamed rats. Altogether, our results suggest that targeting of DOP subtype 2 with antagonists provides a valuable strategy to attenuate the analgesic tolerance that develops after repeated morphine administration in the setting of chronic inflammatory pain.