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Background: The gut microbiota regulates brain function through metabolite, immune, and neural signaling, and emerging evidence identifies the blood–brain barrier (BBB), gatekeeper of the neurovascular unit, as a principal target of this influence. BBB disruption is increasingly recognized in major psychiatric disorders, suggesting microbiota-driven neurovascular change contributes to neuroinflammation in depression and schizophrenia. Objective: To synthesize evidence that gut microorganisms and metabolites regulate BBB structure and function, link these mechanisms to psychiatric pathophysiology, and evaluate microbiota-targeted interventions acting through the neurovascular axis. Methods: Narrative review of preclinical, mechanistic, and clinical literature, including germ-free and antibiotic-depletion models, in vitro BBB models, case-control microbiome studies, barrier-dysfunction biomarkers, and randomized trials of probiotics and fecal microbiota transplantation (FMT). Results: Germ-free mice show increased BBB permeability with reduced occludin and claudin-5, reversible by bacterial colonization and short-chain fatty acids such as butyrate and propionate, acting via G-protein-coupled receptors, histone deacetylase inhibition, and NF-κB/Nrf2 signaling; trimethylamine-N-oxide and endotoxins instead promote barrier loss. The microbiota drives sex- and time-dependent microglial maturation, and stress-induced gut hyperpermeability with endotoxin translocation links to systemic inflammation and BBB compromise. Human studies show reduced claudin-5 in the nucleus accumbens and hippocampus in depression and schizophrenia, elevated S100B, and dysbiotic signatures with depleted butyrate-producing taxa. Probiotic trials show modest improvement; FMT remains experimental with unresolved durability. Conclusions: Microbial control of neurovascular function is a plausible, mechanistically rich pathway linking gut to psychiatric disease. Translation requires standardized methodology, prospective causal designs, sex-aware analysis, and biomarker-guided trials targeting the BBB as an endpoint.