The purpose of this work was to evaluate a potentially useful animal model, Meriones shawi (M.sh)-developing metabolic X syndrome, diabetes and possessing a visual streak similar to human macula-in the study of diabetic retinopathy and diabetic macular edema (DME). Type 2 diabetes (T2D) was induced by high fat diet administration in M.sh. Body weights, blood glucose levels were monitored throughout the study. Diabetic retinal histopathology was evaluated 3 and 7 months after diabetes induction. Retinal thickness was measured, retinal cell types were labeled by immunohistochemistry and the number of stained elements were quantified. Apoptosis was determined with TUNEL assay. T2D induced progressive changes in retinal histology. A significant decrease of retinal thickness and glial reactivity was observed without an increase in apoptosis rate. Photoreceptor outer segment degeneration was evident, with a significant decrease in the number of all cones and M-cone subtype, but-surprisingly-an increase in S-cones. Damage of the pigment epithelium was also confirmed. A decrease in the number and labeling intensity of parvalbumin- and calretinin-positive amacrine cells and a loss of ganglion cells was detected. Other cell types showed no evident alterations. No DME-like condition was noticed even after 7 months. M.sh could be a useful model to study the evolution of diabetic retinal pathology and to identify the role of hypertension and dyslipidemia in the development of the reported alterations. Longer follow up would be needed to evaluate the potential use of the visual streak in modeling human macular diseases.

The mouse somatosensory cortex is an excellent model to study the structural basis of cortical information processing, since it possesses anatomically recognizable domains that receive different thalamic inputs, which indicates spatial segregation of different processing tasks. In this work we examined three genetically labeled, non-overlapping subpopulations of GABAergic neurons: parvalbumin- (PV+), somatostatin- (SST+), and vasoactive intestinal polypeptide-expressing (VIP+) cells. Each of these subpopulations displayed a unique cellular distribution pattern across layers. In terms of columnar localization, the distribution of these three populations was not quantitatively different between barrel-related versus septal compartments in most layers. However, in layer IV (LIV), SST+, and VIP+, but not PV+ neurons preferred the septal compartment over barrels. The examined cell types showed a tendency toward differential distribution in supragranular and infragranular barrel-related versus septal compartments, too. Our data suggests that the location of GABAergic neuron cell bodies correlates with the spatial pattern of cortical domains receiving different kinds of thalamic input. Thus, at least in LIV, lemniscal inputs present a close spatial relation preferentially to PV+ cells whereas paralemniscal inputs target compartments in which more SST+ and VIP+ cells are localized. Our findings suggest pathway-specific roles for neocortical GABAergic neurons.

A thinning of the inner retina is one of the earliest potential markers of neuroretinal damage in diabetic subjects. The histological background is uncertain; retinal ganglion cell (RGC) loss and changes in the structure or thickness of the inner plexiform layer (IPL) have been suspected. Studies conducted on animal models on RGC pathology gave contradictory results. Hereby we present RGC numbers, distribution patterns and IPL thickness from Zucker Diabetic Fatty (ZDF) rats. After labelling RGCs on retinal whole mounts, isodensity maps were constructed, RGC numbers and distribution patterns analysed using a custom-built algorithm, enabling point-by-point comparison. There was no change in staining characteristics of the antibodies and no significant difference in average RGC densities was found compared to controls. The distribution patterns were also comparable and no significant difference was found in IPL thickness and stratification or in the number of apoptotic cells in the ganglion cell layer (GCL). Our results provide a detailed evaluation of the inner retina and exclude major RGC loss in ZDF rats and suggest that other factors could serve as a potential explanation for inner retinal thinning in clinical studies. Our custom-built method could be adopted for the assessment of other animal or human retinas.