Plexus Morphology Research Articles

The Cornea in Sjögren’s Syndrome: An In Vivo Confocal Study

To analyze the in vivo morphology of corneal cells and nerves in dry eye associated with primary (SSI) and secondary (SSII) Sjögren's syndrome and to study its relationship with the clinical evaluation. Thirty-five patients with SS and 20 age- and gender-matched control subjects were studied. Confocal microscopy was used to investigate corneal thickness, epithelial and stromal cellular density, and subbasal plexus morphology. Corneal central thickness was 514.74 +/- 19.85 microm in the SS group and 550 +/- 21.46 microm in the control group (P < 0.0001, t-test); stromal central thickness was 456.62 +/- 18.05 microm in the SS group and 487.35 +/- 20.40 microm in the control group (P < 0.0001). The density of the superficial epithelial cells in the SSI and SSII groups was 965.40 +/- 96.00 and 999.80 +/- 115.67 cells/mm(2), respectively, and 1488.55 +/- 133.74 cells/mm(2) in the control group (P < 0.001, ANOVA). The number of subbasal nerves was 3.34 +/- 0.76 in the SS group and 5.10 +/- 0.79 in the control group (P < 0.0001, t-test). The average grade of nerve tortuosity was 2.62 +/- 0.94 in the SS group and 1.20 +/- 0.70 in the control group (P < 0.0001). Statistically significant correlations were found between clinical data and confocal microscopy data. Corneal thickness, cells, and nerves show morphologic changes in patients with dry eye associated with SS. The in vivo confocal study of these alterations may be important in better understanding the complexity of the ocular surface morphofunctional unit and the potentials of therapeutic approaches for the control of the phlogistic process and neuroprotection.

Morphologic Alterations of Both the Stromal and Subbasal Nerves in the Corneas of Patients with Diabetes

To evaluate the subbasal and the stromal nerves of the corneas of patients with type 2 diabetes with in vivo confocal microscopy and to compare them with those of nondiabetic patients. Thirty-five corneas of patients with type 2 diabetes and 24 corneas of age-matched control subjects were included in the study. Patients with diabetes were further classified with respect to the stage of retinopathy. Subbasal and stromal nerve plexus morphology and thickness were evaluated with in vivo confocal microscopy. Subbasal long nerve fiber (LNF) and total nerve branch (NB) densities were calculated. The mean stromal nerve thickness was significantly higher in patients with diabetes (8.99 +/- 2.32 microm) than that of the control subjects (5.69 +/- 1.49 microm; Mann-Whitney U test; P < 0.001). The proportion of curved stromal nerves in patients with diabetes (45.7%) was also higher than that of normal subjects (20.8%; chi(2), P = 0.05). Subbasal LNF and NB densities were found to significantly lower in the corneas of patients with diabetes (28.3 +/- 10.4 and 39.7 +/- 13.2 nerve/mm(2), respectively) than those of the control subjects (34.1 +/- 5.7 and 58.5 +/- 12.4 nerve/mm(2), respectively; Mann-Whitney, P = 0.012 and P < 0.001). In addition, the subbasal nerve plexus of patients with diabetes appeared significantly thicker and more tortuous than those of the control subjects (Mann-Whitney, P = 0.002 and P = 0.001). Both stromal and subbasal nerves appear abnormal in the corneas of patients with diabetes. Patients with proliferative diabetic retinopathy show more pronounced nerve alterations than patients who do not have diabetic retinopathy.

The Effects of Venous Ischaemia on the Subependymal and Choroid Plexus Morphology in Rat

Morphological changes of ependyma, subependyma and choroids plexus regions were evaluated after experimental anastomotic venous occlusion in twenty male Sprague-Dawley rats. In this model, small burr holes were made over the anterior and posterior anastomotic veins and after precisely locating these vessels, bipolar coagulation and microscissors were used to perform permanent occlusion. Three days later, rats were sacrificed by perfusion and fixation and specimens were evaluated by histopathological techniques. Morphological changes of ependymal, subependymal and choroids plexus cells were evaluated in operated and intact hemispheres and revealed cell proliferation in the subventricular zone adjacent to the territory of venous occlusion in the operated hemisphere as well as midline shift, brain oedema, subcortical petechial haemorrhage, brain infarction and hemispheric swelling. In conclusion, following anterior (the vein of Throlard) and posterior (the vein of Labbé) anastomotic vein occlusion, cell proliferation can be seen in the choroids plexus, ependymal and subependymal regions in rats. We conclude that these morphological changes might be part of a self-repairing mechanism in the brain.

Morphological and functional alterations of the myenteric plexus in rats with TNBS-induced colitis.

The 2,4,6-trinitrobenzenesulfonic acid (TNBS)-induced model of experimental colitis was used to investigate the time-course of alterations in enteric neurotransmission and/or smooth muscle function that occur in chronic inflammation. Myenteric plexus morphology (immunocytochemical markers), functional integrity of cholinergic neurons (3H-choline uptake, acetylcholine release and contractile response to electrical field stimulation) and smooth muscle integrity (contractile response to exogenous acetylcholine) were determined 2, 7, 15, and 30 days after TNBS treatment. In TNBS-treated rats extensive ulcerations of the mucosa and/or the submucosa and increase in colonic weights were accompanied by significant reduction in 3H-choline uptake, acetylcholine release and contractile response to stimulation of enteric nerves. These changes were maximal 7 and 15 days after TNBS treatment. Immunocytochemical marker (PGP 9.5, SNAP 25, synaptophysin and S100 protein) expression was absent in necrotic areas of colons removed 7 days post-injury and partially reduced in colons removed 15 days after TNBS treatment. By contrast, the contractile response to exogenous acetylcholine was significantly increased after 7 days in both inflamed and uninflamed regions and returned to control values by day 30. Likewise, an almost complete recovery of neural cholinergic function and of myenteric plexus morphology was observed 30 days after TNBS treatment. These data suggest that TNBS-induced colitis is associated with progressive and selective alterations in myenteric plexus structure and function, with consequent reduction of cholinergic neurotransmission and abnormality in colonic contractility. The reversibility of myenteric plexus disruption is a clear indication of neuronal plasticity within enteric nervous system as an adaptative mechanism against inflammatory challenges.