ABSTRACT The developmental origin and molecular specification of the lateral pallium remain incompletely understood, particularly with respect to the emergence of the claustrum and its relationship to neighboring pallial territories. Here, we provide a developmental and genoarchitectonic analysis of the feline lateral pallium and its derivatives, focusing on the expression of Nr4a2 and Fezf1 . Our results demonstrate that the lateral pallium acquires a distinct molecular identity before the onset of Nr4a2 expression. Beginning at E26/27, a Satb2 ‐positive and Fezf2 ‐low domain can be identified below the ventral rim of the cortical plate, preceding the appearance of a restricted Nr4a2 ‐positive claustral focus that subsequently expands to encompass both claustral and endopiriform populations, indicating that Nr4a2 is a marker of claustral differentiation rather than of lateropallial identity. The spatial organization of the developing claustral complex resembles that described in rodents and is consistent with the cortical ring theory. In contrast to the restricted developmental profile of Nr4a2 , Fezf1 exhibited a broad and dynamic expression pattern. Early Fezf1 expression was widely distributed among pallial progenitor populations, suggesting a role in neurogenesis rather than in regional specification, whereas later expression became restricted to selected populations of the piriform cortex and the amygdala. Comparisons with Otp and Sim1 expression further suggest contributions from both telencephalic and hypothalamic sources to Fezf1 ‐positive amygdalar populations. Our findings do not support a specific association between Fezf1 expression and the lateropallial mantle; instead, Fezf1 appears to participate in pallial neurogenesis and amygdalar differentiation. Collectively, our findings refine the current understanding of feline lateropallial development, clarify the significance of Nr4a2 and Fezf1 expression, and provide a comparative framework for interpreting claustral and amygdalar regionalization across mammals.
The Cairo spiny mouse (Acomys cahirinus), a promising animal model in neuroscience, lacks a detailed neuroanatomical map of its cerebral cortex. This study aims to delineate the location and internal subdivision of the sensorimotor cortex, specifically the region controlling the hindlimb. For this purpose, retrograde tracing from the lumbar spinal cord using Fast Blue was combined with immunohistochemical characterization using neuronal markers (NeuN, SMI-32, and calbindin 28 kDa) in adult animals. Fast Blue-labeled neurons were identified in layer V within the cortical region defined as the sensorimotor cortex responsible for hindlimb control. Within this region, the general cytoarchitecture was defined using NeuN, which allowed visualization of all cortical layers. The border between the lateral and medial sub-areas was clearly identified by SMI-32 immunostaining, which showed denser labeling in the lateral zone (presumably the primary somatosensory cortex) compared to the medial zone (presumably the secondary motor cortex). Within the defined layers and sub-areas, a comprehensive analysis of the calbindin-expressing interneuron population was performed, revealing significant interareal differences in soma size and cellular density of calbindin-positive neurons exclusively within layers III-IV. These findings provide the first detailed map of the hindlimb sensorimotor cortex in spiny mice, establishing a crucial neuroanatomical foundation for future studies using this novel model in sensorimotor research.
Understanding how the brain processes bodily signals requires mapping the circuits that transform interoceptive information into coordinated responses. Visceral signals converge in the nucleus of the solitary tract (NTS), which coordinates appetite, breathing, cardiovascular reflexes, and digestion. The NTS contains many intermingled subpopulations of neurons, and deciphering their functions requires understanding their connections. Here, we used cell-type-specific tracing to test whether molecularly distinct NTS neurons exhibit unique connectivity patterns. First, we found that Lmx1b-expressing excitatory neurons provide output to a broad array of NTS target regions in both the brainstem and forebrain, while inhibitory neurons in this region project predominantly within the brainstem. Next, we found that several genetically defined excitatory subpopulations-catecholaminergic (Th), neuropeptidergic (Cck, Npff, or Pdyn), and aldosterone-sensitive (Hsd11b2)-exhibit unique output patterns across multiple targets. As examples, the ventrolateral medulla receives moderate Th, Cck, and Pdyn, light Npff, and no Hsd11b2 input. The outer rim of the external lateral parabrachial subnucleus receives concentrated Th, Cck, and Npff input, contrasting a more uniform Pdyn input and a lack of Hsd11b2 input. The subcommissural bed nucleus of the stria terminalis receives broad Th, light Cck, sparse Pdyn, and virtually no Npff input, contrasting the focal Hsd11b2 input to its fusiform subnucleus. These divergent patterns demonstrate that molecular identity predicts connectivity and define the organizational logic by which interoceptive signals are transformed into coordinated autonomic and behavioral responses.
Sturgeons are an ancient and basal group of ray-finned fishes whose morphology is critical to our understanding of the evolution of teleosts, which form most of the ray-finned fish radiation. In sturgeons, the pallium, or area dorsalis, consists of lateral, medial, and posterior divisions. The connections of these pallial divisions were determined by injections of biotinylated dextran amine and DiI. All three divisions receive olfactory input, with the posterior division receiving the bulk of the secondary olfactory projections. All three pallial divisions also have extensive intratelencephalic connections, as well as input from the thalamus and the posterior tubercle. The posterior division also receives sparse input from the midbrain and secondary gustatory nucleus of the isthmus. All three pallial divisions project heavily to the hypothalamus of the ipsilateral inferior lobe, and more sparsely to the ipsilateral optic tectum, posterior tubercle, and midbrain tegmentum. Cytological and connectional data provide no evidence that either a dorsal or central pallial division exists in sturgeons, and these pallial divisions likely arose in ancestral teleosts.
Ceramide synthases (CerS) are key enzymes in sphingolipid metabolism that regulate fundamental cellular processes, including apoptosis, cell growth, and homeostasis. Among the six known mammalian isoforms (CerS1-CerS6), CerS5 has been particularly well studied for its involvement in the synthesis of the sphingolipid C16-ceramide. However, its expression, localization, and functional significance of CerS5 in the retina remain unclear. In the present study, we investigated the presence, distribution, and functional role of CerS5 in mouse retina using CerS5 knockout (KO) mice. We performed quantitative polymerase chain reaction, X-gal staining, and immunohistochemistry to analyze the expression and localization. Electroretinography (ERG) was employed to assess the impact of CerS5 deficiency on retinal function. Our results demonstrated that CerS5 is localized to the inner nuclear layer and ganglion cell layer, co-localizing with horizontal cells and specific subsets of amacrine and ganglion cells. The retina of CerS5 KO mice showed a reduction in overall thickness, with significant thinning observed in all retinal layers except the photoreceptor, whereas the outer plexiform layer showed increased thickness. Despite these structural alterations, ERG recordings revealed no significant changes in retinal function. These findings suggest that CerS5 contributes to the maintenance of retinal structural integrity, particularly through its presence in specific retinal cell types, whereas its loss does not markedly impair retinal function in adult mice. The observed structural alterations highlight its potential role in retinal physiology and possible implications for retinal pathophysiology, warranting further investigation into compensatory mechanisms by other ceramide synthase isoforms.
