Dopamine is essential for striatal function and learning. Striatal dopamine release can be triggered by dopamine cell firing, but also by coordinated cholinergic interneuron activity, which stimulates dopamine release via presynaptic nicotinic acetylcholine receptors on dopamine axons. While acetylcholine-dependent dopamine release is well-documented ex vivo and under artificial optogenetic stimulation in vivo, its role during natural behavior has remained unclear. One possible endogenous driver of acetylcholine-dependent dopamine release is thalamic input, which provides strong excitatory drive to cholinergic interneurons. To examine whether thalamic input provokes acetylcholine-dependent dopamine release during behavior, we performed simultaneous fiber photometry recordings of striatal dopamine (GRAB-rDA3m) and thalamic axon activity (gCaMP8m) in the dorsomedial (DMS) and dorsolateral striatum (DLS) of mice learning the accelerating rotarod, a striatal-dependent task that demands precise and effortful motor control. Recordings were obtained on- and off-task and across days of training to capture the full arc of learning. Dopamine transients in DMS, but not DLS, were frequently coupled to peaks in thalamic axon activity via an acetylcholine-dependent mechanism. The occurrence of these thalamic-evoked DMS dopamine transients depended on learning, task engagement, and the recent history of dopamine activity, but did not contribute to motor error signals. Together, these findings establish thalamic input as a physiological driver of acetylcholine-dependent dopamine release in DMS. Moreover, they reveal that striatal sensitivity to this local release mechanism is dynamically gated by dopaminergic history, providing a compelling framework for understanding how local and soma-triggered dopamine signals are coordinated to support learning.

High-resolution extracellular electrophysiology is the gold standard for recording spikes from distributed neural populations and is especially powerful when combined with optogenetics for manipulation of specific cell types with high temporal resolution. We integrated these approaches into prototype Neuropixels Opto probes, which combine electronic and photonic circuits. These devices pack 960 electrical recording sites and two sets of 14 light emitters onto a 70-μm-wide, 1-cm-long shank, allowing spatially addressable optogenetic stimulation with blue and red light. In mouse cortex, Neuropixels Opto probes delivered high-quality recordings together with spatially addressable optogenetics, differentially activating or silencing neurons at distinct cortical depths. In the mouse striatum and other deep structures, Neuropixels Opto probes delivered efficient optotagging, facilitating the identification of two cell types in parallel. Neuropixels Opto probes represent a promising tool for recording, identifying and manipulating neuronal populations.

Although learning in response to extrinsic reinforcement is theorized to be driven by dopamine signals that encode the difference between expected and experienced rewards, skills that enable verbal or musical expression can be learned without extrinsic reinforcement. Instead, spontaneous execution of these skills is thought to be intrinsically reinforcing. Whether dopamine signals similarly guide learning of these intrinsically reinforced behaviours is unknown. In juvenile zebra finches learning from an adult tutor, dopamine signalling in a song-specialized basal ganglia region is required for successful song copying, a spontaneous, intrinsically reinforced process. Here we show that dopamine dynamics in the song basal ganglia faithfully track the learned quality of juvenile song performance on a rendition-by-rendition basis. Furthermore, dopamine release in the basal ganglia is driven not only by inputs from midbrain dopamine neurons classically associated with reinforcement learning but also by song premotor inputs, which act by means of local cholinergic signalling to elevate dopamine during singing. Although both cholinergic and dopaminergic signalling are necessary for juvenile song learning, only dopamine tracks the learned quality of song performance. Therefore, dopamine dynamics in the basal ganglia encode performance quality during self-directed, long-term learning of natural behaviours.

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.

Premature ventricular contractions (PVCs) are common arrhythmia encountered in patients with and without structural heart disease. Although often benign and asymptomatic, they may also cause palpitations, exercise intolerance, presyncope, and reduced quality of life, and in some patients can contribute to PVC-induced cardiomyopathy or trigger malignant ventricular arrhythmias. Their clinical significance depends on symptom burden, PVC frequency, ventricular function, and the presence of underlying myocardial disease. Diagnostic evaluation includes electrocardiography, ambulatory rhythm monitoring, echocardiography, exercise testing, and cardiac magnetic resonance imaging for tissue characterization and risk stratification. Management ranges from reassurance and lifestyle modification to pharmacologic therapy and catheter ablation. Beta-blockers and nondihydropyridine calcium channel blockers remain common first-line options, whereas antiarrhythmic drugs may be considered in carefully selected patients. Catheter ablation is an effective treatment for symptomatic PVCs, high PVC burden, and PVC-induced cardiomyopathy, with high procedural success rates and favorable effects on arrhythmic burden and ventricular function. Novel approaches, including electrocardiographic imaging-guided planning, pulsed field ablation, stereotactic radioablation, neuromodulation, and renal denervation, may further expand future therapeutic options. This review summarizes the pathophysiology, clinical implications, diagnostic evaluation, and contemporary management of PVCs, with emphasis on medical therapy, catheter ablation, and emerging treatments.

Cardiac arrhythmias are traditionally attributed to structural and electrophysiological abnormalities; however, increasing evidence highlights the critical role of systemic inflammation and autonomic dysregulation in arrhythmogenesis. The neuroimmune-cardiac axis represents a bidirectional communication network between the autonomic nervous system and immune signaling pathways that collectively modulate cardiac electrical stability. Pro-inflammatory cytokines and immune mediators influence central autonomic regulatory centers, leading to sympathetic overactivation and parasympathetic withdrawal, reflected by reduced heart rate variability and increased arrhythmic susceptibility. Conversely, autonomic dysfunction further amplifies inflammatory signaling, establishing a self-perpetuating feed-forward loop that promotes electrical instability and adverse cardiac remodeling. Key neuroanatomical structures, including circumventricular organs and the stellate ganglion, serve as critical interfaces linking systemic inflammation to autonomic cardiac control. Inflammatory mediators such as interleukin (IL)-17A and metabolic adipokines like leptin contribute to stellate ganglion remodeling, enhanced sympathetic discharge, and increased vulnerability to ventricular arrhythmias. At the molecular level, activation of the NLRP3 inflammasome plays a central role in integrating inflammatory and electrical signaling pathways by promoting IL-1β and IL-18 release, oxidative stress, calcium handling abnormalities, and gap junction disruption, thereby establishing a proarrhythmic substrate. Importantly, sustained arrhythmias may further potentiate inflammasome activation, reinforcing the vicious cycle between inflammation and electrical instability. Anti-inflammatory and immunomodulatory mediators, including adiponectin and IL-1 receptor antagonists, demonstrate protective effects by restoring autonomic balance and reducing arrhythmic risk. Collectively, the neuroimmune-cardiac axis provides a unified mechanistic framework for understanding arrhythmogenesis and highlights novel therapeutic opportunities targeting both inflammatory and autonomic pathways beyond conventional antiarrhythmic strategies.

Kawasaki disease (KD) and multisystem inflammatory syndrome in children (MIS-C) are pediatric inflammatory conditions with significant cardiovascular involvement, particularly affecting the coronary arteries. KD remains the leading cause of acquired heart disease in children worldwide, while MIS-C has emerged as a postinfectious complication of severe acute respiratory syndrome coronavirus 2 with overlapping but distinct cardiovascular manifestations. Coronary artery abnormalities, including dilation and aneurysm formation, represent the most important cardiovascular sequelae in KD, whereas coronary involvement in MIS-C appears less frequent and often transient, although its long-term implications remain incompletely understood. Early detection and longitudinal assessment of coronary involvement are essential for optimizing outcomes. Echocardiography is the first-line imaging modality for both KD and MIS-C due to its accessibility and high sensitivity in detecting proximal coronary abnormalities. However, advanced imaging techniques such as coronary computed tomography angiography and cardiac magnetic resonance imaging provide superior visualization of distal coronary segments, vessel wall characteristics, myocardial perfusion, and fibrosis. These modalities are increasingly integrated into follow-up strategies, especially in patients with complex or persistent lesions. Risk stratification is guided by coronary artery Z scores, inflammatory biomarkers, and clinical severity, enabling tailored therapeutic approaches, including antiplatelet and anticoagulation therapy. Despite advances in treatment, a subset of patients with KD develops persistent coronary artery abnormalities with potential progression to ischemic heart disease later in life. In contrast, current evidence suggests that most cardiovascular abnormalities in MIS-C improve over time, although long-term longitudinal data remain limited. This review synthesizes current evidence on the pathophysiology, imaging strategies, risk assessment, and long-term cardiovascular outcomes in KD and MIS-C. A multimodal imaging approach combined with individualized risk stratification is essential for improving prognosis and guiding lifelong surveillance in affected patients.