Cholinergic interneurons (CINs) are essential elements of striatal circuits and functions. Although acetylcholine signaling via muscarinic receptors (mAChRs) has been well studied, more recent data indicate that postsynaptic nicotinic receptors (nAChRs) located on striatal GABAergic interneurons (GINs) are equally critical. One example is that CIN stimulation induces large disynaptic inhibition of striatal projection neurons (SPNs) mediated by nAChR activation of GINs. Although these circuits are ideally positioned to modulate striatal output, the neurons involved are not definitively identified because of an incomplete mapping of CINs-GINs interconnections. Here, we show that CINs modulate four GINs populations via an intricate mechanism involving co-activation of presynaptic and postsynaptic mAChRs and nAChRs. Using optogenetics, we demonstrate the participation of tyrosine hydroxylase-expressing GINs in the disynaptic inhibition of SPNs via heterotypic electrical coupling with neurogliaform interneurons. Altogether, our results highlight the importance of CINs in regulating GINs microcircuits via complex synaptic/heterosynaptic mechanisms.

Voltage imaging has emerged as a powerful tool for recording membrane potential changes in living cells, offering a direct measurement of rapid neuronal events with high temporal precision. Since the brain is a three-dimensional circuit, it is essential to record signals across a volume. However, achieving effective three-dimensional voltage imaging over large neuronal populations remains challenging due to the need for high imaging speed, high signal-to-noise ratio, and extensive volume coverage. In this study, we demonstrate in vivo three-dimensional voltage imaging in larval zebrafish using oblique plane microscopy and QFDBD-QUAS-driven expression of the genetically encoded voltage indicator Ace-mNeon2-Kv2.1, achieving volumetric imaging rates of up to 200 volumes per second (VPS). This approach enables dye-free voltage imaging, simplifying experimental workflows and improving the reproducibility of in vivo voltage imaging experiments for investigating neuronal circuit dynamics in the living zebrafish animal model.

The neurotransmitter acetylcholine (ACh) is essential in both the central and peripheral nervous systems. Recent studies highlight the significance of interactions between ACh and various neuromodulators in regulating complex behaviors. The ability to simultaneously image ACh and other neuromodulators can provide valuable information regarding the mechanisms underlying these behaviors. Here we developed a series of red fluorescent G-protein-coupled receptor activation-based ACh sensors, with a wide detection range and expanded spectral profile. The high-affinity sensor rACh1h reliably detects ACh release in various brain regions, including the nucleus accumbens, amygdala, hippocampus and cortex. Moreover, rACh1h can be coexpressed with green fluorescent sensors to record ACh release together with other neurochemicals in various behavioral contexts using fiber photometry, mesoscopic imaging and two-photon imaging with high spatiotemporal resolution.

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.

Cardiovascular disease remains the leading cause of morbidity and mortality among women globally, with growing evidence suggesting that cardiovascular risk can begin developing well before pregnancy, even during the preconception period. Among the most significant contributing factors is excess prepregnancy weight, which has been associated with a higher risk of adverse maternal and fetal outcomes, including hypertension-related disorders, gestational diabetes, preeclampsia, and long-term cardiovascular complications. As obesity rates continue to rise among women of reproductive age, preconception weight management has become an increasingly important area of focus in maternal and cardiovascular health. This review examines the relationship between prepregnancy weight and cardiovascular outcomes, explores the underlying mechanisms involved, and evaluates current evidence-based lifestyle interventions aimed at reducing cardiovascular risk before and during pregnancy.

Heart failure with preserved ejection fraction (HFpEF) is a highly heterogeneous syndrome characterized by impaired ventricular relaxation, systemic inflammation, and multisystem cardiovascular dysfunction. Despite growing recognition of HFpEF as a major global health burden, effective targeted therapies remain limited due to an incomplete understanding of its phenotypic diversity. Increasing evidence suggests that left atrial (LA) myopathy represents a central mechanistic and phenotypic axis in HFpEF rather than merely a secondary consequence of elevated left ventricular filling pressures. LA myopathy encompasses structural remodeling, fibrosis, impaired compliance, and electrical dysfunction that collectively disrupt reservoir, conduit, and booster pump function. These abnormalities contribute to elevated filling pressures, pulmonary venous congestion, pulmonary vascular remodeling, and impaired exercise hemodynamics. Emerging data demonstrate strong associations between impaired LA strain, reduced compliance, pulmonary hypertension, atrial fibrillation, and adverse clinical outcomes in HFpEF. Importantly, LA dysfunction may identify a distinct HFpEF phenotype characterized by disproportionate pulmonary vascular disease and severe exercise intolerance. Advances in multimodality imaging, including speckle-tracking echocardiography and cardiac magnetic resonance imaging, have improved the ability to characterize atrial structure and function and may enable earlier recognition of atrial disease. Therapeutic strategies targeting neurohormonal activation, fibrosis, pulmonary vascular coupling, rhythm control, and interatrial pressure modulation are increasingly being explored as potential approaches to modify this phenotype. This narrative review examines the mechanistic basis of LA myopathy in HFpEF, its relationship with pulmonary hypertension and exercise intolerance, contemporary diagnostic approaches, prognostic significance, and emerging therapeutic implications. Reframing LA myopathy as a central phenotypic axis may facilitate phenotype-directed management and improve therapeutic precision in HFpEF.

Type 2 myocardial infarction is defined by myocardial necrosis from supply-demand mismatch in the absence of acute atherothrombosis. It remains a heterogeneous entity without dedicated clinical guidelines or a validated management pathway. This challenge is particularly relevant in patients with cardiorenal vulnerability, including heart failure with reduced ejection fraction and chronic kidney disease, in whom limited physiological reserve may increase susceptibility to acute hemodynamic or metabolic stress. This narrative review explores how the cardiorenal substrate may contribute to type 2 myocardial infarction risk, with attention to possible roles of uremic myocardial toxicity, hypoalbuminemia, and catecholamine-mediated arrhythmic stress. We also review diagnostic challenges in this population, including troponin interpretation, electrocardiographic confounders, and the decision to pursue coronary angiography during active sepsis. A 5-step clinical pathway is proposed as a hypothesis-generating framework to support structured bedside reasoning in the absence of formal guidelines. Emerging biomarkers and recent guideline considerations are discussed as areas requiring further validation before clinical adoption.