Blood Metabolomic Profiling of Systemic Responses to Dried Black Lychee in a Scopolamine-Induced Cognitive Impairment in Rats.

The sophisticated computations underlying brain function arise from highly interconnected and dynamically regulated microcircuits consisting of two fundamental neuronal classes: (1) glutamatergic projection neurons that establish the excitatory backbone of neural networks, and (2) GABAergic interneurons that precisely modulate signal transmission and shape network dynamics. Although GABAergic interneurons constitute only 10%–15% of hippocampal neurons, they exhibit remarkable diversity and exert disproportionately powerful control over circuit function. Historically, GABAergic interneurons have been classified by neurochemical markers, such as parvalbumin (PV), calretinin (CR), somatostatin (SST), vasoactive intestinal polypeptide (VIP), neuropeptide Y (NPY), cholecystokinin (CCK), tyrosine hydroxylase (TH), ionotropic serotonin receptor 5HT3a (5HT3aR), and others. However, the most comprehensive catalog of neuronal diversity based on transcriptomics has revealed the existence of over 100 molecularly distinct subtypes of inhibitory neurons across mice, marmosets, and humans. Based on their distinct gene expression profiles from single‐cell sequencing, they are further classified into five groups: PV, SST, VIP, Lamp5, and Sncg., , , Notably, PV interneurons constitute the largest subgroup, accounting for approximately 40% of all GABAergic neurons in many brain regions. Moreover, connections among cortical PV interneurons are more frequent than those among any other interneuron type, or between other interneurons and PV cells., , They play a fundamental role in maintaining the cortical excitation–inhibition balance, as pyramidal neurons dynamically fine‐tune their inhibitory inputs specifically from this population. PV interneurons serve as master regulators of neural circuit operations: they fire high‐frequency action potentials (up to 300 Hz), release GABA with millisecond precision, and thereby synchronize gamma and theta oscillations while maintaining optimal E/I balance across neural networks. Despite this remarkable functional homogeneity at the circuit level, PV interneurons are far from a uniform population. Within the hippocampal CA1 region, PV interneurons can be further subdivided into three major classes based on their morphological and synaptic targeting patterns: (1) PV basket cells (PVBCs) that form perisomatic synapses, (2) bistratified cells (BiCs) targeting dendritic compartments, and (3) axo‐axonic/chandelier cells (AACs) that specifically innervate axon initial segment (AIS). Additionally, a subset of oriens lacunosum‐moleculare interneurons (O‐LMs) also shows detectable PV expression though at substantially lower levels compared to the aforementioned PVBCs, BiCs, and AACs. Mounting evidence implicates PV interneuron dysfunction, whether through cellular loss, synaptic impairment, or metabolic compromise, as a key pathophysiological mechanism in several neuropsychiatric disorders, with particularly strong associations demonstrated in Alzheimer's disease (AD) pathogenesis.