Dopamine critically modulates prefrontal circuits underlying cognitive control, but how D1-type (D1R) and D2-type (D2R) receptors influence abstract decision coding is unclear. We recorded single-neuron activity in two monkeys performing a number comparison task, in which abstract decisions about sequentially presented dot displays were dissociated from motor responses, while locally stimulating D1R or D2R via microiontophoresis. D1R stimulation suppressed, whereas D2R stimulation enhanced, the decision-coding strength of individual neurons, effects mirrored at the population level in decoding accuracy. Interestingly, dopamine receptors also bidirectionally modulated the temporal structure of population activity: D1R stimulation reduced the temporal generalizability of neuronal decision selectivity, suggesting more transient tuning and a shift toward a more dynamic coding regime. Conversely, D2R stimulation increased temporal generalizability of decision selectivity, implying more sustained tuning and a shift toward a more static coding regime. These findings suggest that D1- and D2-mediated mechanisms in the prefrontal cortex provide a receptor-specific substrate for balancing cognitive flexibility and stability in abstract decision-making. This pattern may reflect task-dependent deviations from classical dual-state models, in which D1 receptor activity stabilizes working memory representations whereas D2 receptor activity supports flexible coding-a relationship that appears reversed in the context of abstract decision formation.

The striatum is one of the first brain regions affected in Parkinson's disease (PD), where dopaminergic axons projecting from the substantia nigra undergo dying-back degeneration. Growing evidence shows that dopamine depletion triggers network-level remodeling in the striatum, whose pathological significance extends far beyond acute changes in neuronal excitability. Striatal parvalbumin interneurons (PVINs) have recently been recognized as unique integrators of dopaminergic, neuroinflammatory and electrical network signals and as the principal striatal source of glial-cell-line-derived neurotrophic factor (GDNF). This integrative capacity renders PVINs early targets of parkinsonian injury, yet also allows them to orchestrate compensatory plasticity that shapes subsequent disease progression. Here we review how PVINs, via receptor-specific signaling, drive network reorganization in response to dopaminergic degeneration. We propose that these cells follow a compensatory-to-degenerative trajectory that canalizes abnormal synaptic plasticity and thereby exerts a maladaptive influence on PD pathogenesis. Finally, we discuss the therapeutic potential of interventions targeting these adaptive mechanisms.

Rhythmic neural network activity has been broadly linked to behavior. However, it is unclear how membrane potentials of individual neurons track behavioral rhythms, even though many neurons exhibit pace-making properties in isolated brain circuits. To examine whether single-cell voltage rhythmicity is coupled to behavioral rhythms, we focused on delta-frequencies (1-4 Hz) that are known to occur at both the neural network and behavioral levels. We performed membrane voltage imaging of individual striatal neurons simultaneously with network-level local field potential recordings in mice during voluntary movement. We report sustained delta oscillations in the membrane potentials of many striatal neurons, particularly cholinergic interneurons, which organize spikes and network oscillations at beta-frequencies (20-40 Hz) associated with locomotion. Furthermore, the delta-frequency patterned cellular dynamics are coupled to animals' stepping cycles. Thus, delta-rhythmic cellular dynamics in cholinergic interneurons, known for their autonomous pace-making capabilities, play an important role in regulating network rhythmicity and movement patterning.

Basal Ganglia Advances is a collection highlighting research on the structure, function, and disorders of the basal ganglia. It features studies spanning neuroscience, clinical insights, and computational models, serving as a hub for advances in movement, cognition, and behavior.

Recent advances in the field of Voltage Imaging, with a special focus on new constructs and novel implementations.

Work related to place tuning, spatial navigation, orientation and direction. Mainly includes articles on connectivity in the hippocampus, retrosplenial cortex, and related areas.

Somatostatin-expressing low-threshold spiking interneurons (SOM-INs) constitute a key inhibitory population in the dorsal striatum, yet their contribution to parkinsonian states and L-DOPA-induced dyskinesia (LID) remains poorly understood. Here, we combined in vivo behavioral assays, chemogenetics, and ex vivo electrophysiology to examine how nigrostriatal dopamine loss and dopaminergic therapy shape SOM-INs' activity and function. During LID, SOM-INs displayed increased c-Fos expression, revealing their recruitment during dyskinetic states. Patch-clamp recordings showed that SOM-INs in control mice fire tonically with characteristic abrupt pauses. While their firing patterns are preserved after dopamine depletion and L-DOPA therapy, dopamine depletion shifted their interspike interval distribution toward longer intervals, indicating reduced intrinsic activity. This deficit was partially reversed by chronic L-DOPA. Consistent with their expression of Drd1/Drd5 transcripts, SOM-INs were excited by the D1/D5 receptor agonist SKF81297 across groups. Chemogenetic inhibition experiments revealed a functional role for SOM-INs in early rotarod learning, demonstrating their contribution to motor skill acquisition, but did not affect baseline motor output in sham or parkinsonian mice. Moreover, SOM-IN inhibition during chronic L-DOPA treatment modestly but consistently exacerbated LID expression selectively during the wearing-off phase, without altering parkinsonian symptoms or the therapeutic efficacy of L-DOPA. Notably, SOM-IN inhibition did not modify the long-duration antiparkinsonian response that persisted after discontinuing L-DOPA. Together, these findings identify SOM-INs as an intrinsically active striatal interneuron population whose excitability is shaped by dopamine depletion and dopamine receptor stimulation, and whose activity restrains dyskinetic responses to dopaminergic overstimulation. Their selective influence on dyskinesia, but not on the therapeutic actions of L-DOPA, highlights SOM-INs as a potential target for circuit-level interventions aimed at improving the motor side-effect profile of dopaminergic therapies.

How the brain signals prediction errors for non-rewarding, yet significant, sensory events remains a central question. Although the cortical mismatch negativity provides a well-known signature for deviance detection, the contribution of subcortical dopamine remains unclear. This study tested the hypothesis that phasic dopamine in the nucleus accumbens encodes the salience associated with the violation of an ongoing statistical regularity. Using fiber photometry in freely moving rats, we contrasted an auditory oddball paradigm with a many-standards control. Deviant stimuli elicited a significantly amplified dopamine response compared with standard stimuli. Crucially, this dopamine response enhancement was absent in the control condition, demonstrating that the nucleus accumbens dopamine responds specifically to rule violation rather than mere stimulus rarity. The long latency of this signal (~500 ms) relative to the cortical mismatch negativity argues against a direct role in the initial detection of deviance. Instead, our findings support a model in which subcortical dopamine acts as a distinct salience signal, operating in parallel with cortical deviance detection, to evaluate unexpected events and guide subsequent behavioral adjustments.

Making appropriate decisions relies on the brain's capacity to evaluate the expected outcomes of available options and select the most rewarding action. The ventral striatum and midbrain dopamine neurons have been implicated in the option valuation process, consistent with the brain's reinforcement learning theory in which these brain structures encode and update value representations of expected outcomes. Extending beyond this framework, we found that the dopamine-ventral striatum system plays a more proactive role in action selection. We recorded single-unit activity from ventral striatum neurons in macaque monkeys as they sequentially evaluated an option, decided whether to perform an action to choose it, and expressed that motor action. The activity of these neurons initially reflected the value of the option but gradually shifted to reflect monkey's action selection, as if the ventral striatum translates the value information into the action. Moreover, optogenetic facilitation of dopamine input to the ventral striatum as well as electrical stimulation of this region altered monkey's action selection. Our findings reveal a previously unappreciated function of the ventral striatum as a neural hub that bridges option valuation and action selection, and demonstrate the contribution of dopamine in the process leading to action selection within this region.