The cortico-basal ganglia pathways that mediate vocal learning in zebra finches ( Taeniopygia guttata ) are localized in parallel circuits formed by CORE and SHELL subregions. These circuits traverse a specialized region of the basal ganglia essential for vocal learning (Area X), which includes intermixed striatal and pallidal neurons. The pallidal neurons within Area X exhibit analogs of mammalian direct and indirect pathways that may have opposing effects and thereby increase or inhibit thalamic activity respectively. Direct pallidal neurons of Area X send projections to the medial portion of the dorsolateral anterior thalamic nucleus (DLM), whereas indirect pallidal neurons form intrinsic connections onto DLM-projecting neurons. Expression of the transcription factor FoxP2 in the basal ganglia is necessary for normal vocal learning and production in both humans and songbirds. We used tract-tracing techniques to label direct pallidal Area X→DLM projection neurons and immunohistochemical techniques to label neurons expressing the transcription factor FoxP2 in adult and juvenile male zebra finches. Our results showed that DLM-projecting neurons did not express FoxP2 in either adults or juveniles. Measurements of nuclear sizes revealed a population of large neurons that expressed FoxP2 but were not retrogradely-labeled from DLM. A putative marker of striatal neurons (DARPP-32) did not co-localize with FoxP2 in many of these large neurons, suggesting that they form a class of indirect pallidal neurons. These findings offer FoxP2 as a possible marker for indirect pallidal neurons and support the existence of different subpopulations of neurons that correspond to direct and indirect pathways within Area X.

Introduction: Venous thromboembolism (VTE), encompassing deep vein thrombosis (DVT) and pulmonary embolism (PE), is a major cardiovascular disorder and a leading cause of vascular mortality. MicroRNAs (miRNAs) are small endogenous noncoding RNAs that regulate gene expression post-transcriptionally by binding to the target messenger RNAs (mRNAs), inducing mRNA degradation or translational repression. miRNA dysregulation likely contributes to VTE pathogenesis. This review comprehensively summarizes current evidence on miRNAs in VTE, offering a structured overview of the existing literature. Materials and Methods: Eligibility criteria were defined using the Population, Intervention/Exposure, Comparator, Outcomes, and Study design (PICOS) framework. A comprehensive literature search in PubMed and EMBASE was conducted in accordance with Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) guidelines. Given methodological heterogeneity, a narrative synthesis was undertaken. Results: Among the 156 studies included in this review, 99 investigated miRNAs in DVT, 25 examined the role of miRNAs in PE, and 32 evaluated miRNA involvement in VTE. These miRNAs were categorized as prothrombotic, antithrombotic, or unclassified based on their reported functional roles. Conclusions: This systematic review highlights the impact of miRNAs in the pathophysiology of VTE and provides a resource for future mechanistic and translational research. The findings emphasize the need for standardized, large-scale studies focusing on human-specific models to validate miRNAs as diagnostic, prognostic biomarkers, and as therapeutic targets in VTE.