Nucleus accumbens D1-receptors regulate and focus transitions to reward-seeking action.

It is well established that dopamine transmission is integral in mediating the influence of reward expectations on reward-seeking actions. However, the precise causal role of dopamine transmission in moment-to-moment reward-motivated behavioral control remains contentious, particularly in contexts where it is necessary to refrain from responding to achieve a beneficial outcome. To examine this, we manipulated dopamine transmission pharmacologically as rats performed a Go/No-Go task that required them to either make or withhold action to gain either a small or large reward.

Subthalamic beta-targeted neurofeedback speeds up movement initiation but increases tremor in Parkinsonian patients.

Previous studies have explored neurofeedback training for Parkinsonian patients to suppress beta oscillations in the subthalamic nucleus (STN). However, its impacts on movements and Parkinsonian tremor are unclear. We developed a neurofeedback paradigm targeting STN beta bursts and investigated whether neurofeedback training could improve motor initiation in Parkinson's disease compared to passive observation.

Beta Oscillation-Targeted Neurofeedback Training Based on Subthalamic LFPs in Parkinsonian Patients.

Increased oscillatory activities in the beta frequency band (13-30 Hz) in the subthalamic nucleus (STN), and in particular prolonged episodes of increased synchrony in this frequency band, have been associated with motor symptoms such as bradykinesia and rigidity in Parkinson's disease (PD). Numerous studies have investigated sensorimotor cortical beta oscillations either as a control signal for Brain Computer Interfaces (BCI) or as target signal for neurofeedback training (NFB). However, it still remains unknown whether patients with PD can gain control of the pathological oscillations recorded from a subcortical site - the STN - with neurofeedback training.

Representation of spontaneous movement by dopaminergic neurons is cell-type selective and disrupted in parkinsonism.

Midbrain dopaminergic neurons are essential for appropriate voluntary movement, as epitomized by the cardinal motor impairments arising in Parkinson's disease. Understanding the basis of such motor control requires understanding how the firing of different types of dopaminergic neuron relates to movement and how this activity is deciphered in target structures such as the striatum. By recording and labeling individual neurons in behaving mice, we show that the representation of brief spontaneous movements in the firing of identified midbrain dopaminergic neurons is cell-type selective.

Action initiation shapes mesolimbic dopamine encoding of future rewards.

It is widely held that dopamine signaling encodes predictions of future rewards and such predictions are regularly used to drive behavior, but the relationship between these two is poorly defined. We found in rats that nucleus accumbens dopamine following a reward-predicting cue was attenuated unless movement was correctly initiated. Our results indicate that dopamine release in this region is contingent on correct action initiation and not just reward prediction.

Effect of sensory stimulation in rat barrel cortex, dorsolateral striatum and on corticostriatal functional connectivity.

The striatum integrates sensory information to enable action selection and behavioural reinforcement. In the rat, a large topographical projection from the rat barrel cortex to widely distributed areas of the striatum is assumed to be an important structural component supporting these processes. The striatal sensory response is, however, not comprehensively understood at a network level.

A modified MPTP treatment regime produces reproducible partial nigrostriatal lesions in common marmosets.

Standard MPTP treatment regimens in primates result in > 85% destruction of nigral dopaminergic neurons and the onset of marked motor deficits that respond to known symptomatic treatments for Parkinson's disease (PD). The extent of nigral degeneration reflects the late stages of PD rather than events occurring at its onset. We report on a modified MPTP treatment regimen that causes nigral dopaminergic degeneration in common marmosets equivalent to that occurring at the time of initiation of motor symptoms in man.