SummaryThe subfornical organ (SFO) is a circumventricular organ with a chemosensitive function, and its vessels have no blood-brain barrier. Our study investigated the glial and vascular components in the SFO to determine whether their distributions indicate subdivisions, how to characterize the vessels and how to demarcate the SFO. To this end, we investigated glial markers (GFAP, glutamine synthetase, S100) and other markers, including vimentin and nestin (immature glia), laminin (basal lamina), β-dystroglycan (glio-vascular connections), and aquaporin 4 (glial water channels). We determined that the 'shell' of the SFO was marked by immunoreactivity for S100, GFAP and aquaporin 4. Nestin immunoreactivity was characteristic of the 'core'. Vimentin was almost evenly distributed. Glutamine synthetase immunoreactivity occurred in the shell but its expression was sparse. Vessels in the core were decorated with laminin but showed a discontinuous expression of aquaporin 4. Vimentin and GFAP staining was usually in separate glial elements, which may be related to their functional differences. Similar to other vessels in the brain, β-dystroglycan was detected along the shell vessels but laminin was not. The gradual disappearance of the laminin immunopositivity was attributed to the gradual disappearance of the perivascular space. Thus, our findings suggest that the shell and core glio-vascular structures are adapted to different sensory functions: osmoperception and the perception of circulating peptides, respectively.

This study demonstrates glial and gliovascular markers of organon vasculosum laminae terminalis (OVLT) in three planes. The distribution of glial markers displayed similarities to the subfornical organ. There was an inner part with vimentin‐ and nestin‐immunopositive glia whereas GFAP and the water‐channel aquaporin 4 were found at the periphery. This separation indicates different functions of the two regions. The presence of nestin may indicate stem cell‐capabilities whereas aquaporin 4 has been reported to promote the osmoreceptor function. Glutamine synthetase immunoreactivity was sparse like in the area postrema and subfornical organ. The laminin and β‐dystroglycan immunolabelings altered along the vessels such as in the subfornical organ indicating altering gliovascular relations. The different subdivisions of OVLT received glial processes of different origins. The posterior periventricular zone contained short vimentin‐immunopositive processes from the ependyma of the adjacent surface of the third ventricle. The lateral periventricular zone received forceps‐like process systems from the anterolateral part of the third ventricle. Most interestingly, the “dorsal cap” received a mixed group of long GFAP‐ and vimentin‐immunopositive processes from a distant part of the third ventricle. The processes may have two functions: a guidance for newly produced cells like radial glia in immature brain and/or a connection between distant parts of the third ventricle and OVLT.

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The so-called neurointermediate lobe is composed of the intermediate and neural lobes of the pituitary. The present immunohistochemical study investigated components of the basal lamina (laminin, agrin, and perlecan), the dystrophin-dystroglycan complex (dystrophin, beta-dystroglycan, alpha1-dystrobrevin, beta-dystrobrevin, utrophin, and alpha1-syntrophin), and the aquaporins (aquaporin-4 and -9). Glia markers (GFAP, S100, and glutamine synthetase) and components of connective tissue (collagen type I and fibronectin) were also labeled. In the neurohypophysis, immunostaining of basal lamina delineated meningeal invaginations. In these invaginations, vessels were seen to penetrate the organ without submerging into its parenchyma. On the parenchymal side of the invaginations, beta-dystroglycan was detected, whereas utrophin was detected in the walls of vessels. Immunostaining of alpha1-dystrobrevin and alpha1-syntrophin did not delineate the vessels. The cells of the intermediate lobe were fully immunoreactive to alpha1-dystrobrevin and alpha1-syntrophin, whereas components of the basal lamina delineated the contours of the cells. GFAP-immunoreactive processes surrounded them. Aquaporin-4 localized at the periphery of the neurohypophysis, mainly adjacent to the intermediate lobe but not along the vessels. It colocalized only partially with GFAP and not at all with alpha1-syntrophin. Aquaporin-9 was not detected. These results emphasize the possibility that the components of the dystrophin-dystroglycan complex localize differently and raise the question about the roles of dystrobrevins, alpha1-syntrophin, and aquaporin-4 in the functions of the intermediate and neural lobes, respectively.

The present paper provides novel findings on the temporo-spatial correlation of perivascular laminin immunoreactivity with the early postnatal astrocyte development. The cerebrovascular laminin immunoreactivity gradually disappears during development. The fusion of the glial and vascular basal laminae during development makes the laminin epitopes inaccessible for antibody molecules (Krum et al., 1991, Exp Neurol 111:151). The fusion is supposed to correlate with the maturation of the glio-vascular connections. Glial development was followed by immunostaining for GFAP (glial fibrillary acidic protein), S100 protein, glutamine synthetase as glial markers and for nestin to visualize the immature glial structures. Our investigation focused on the period from postnatal day (P)2 to P16, on the dorso-parietal pallium. In the wall of the telencephalon the laminin immunoreactivity disappeared between P5 and P10; in subcortical structures it persisted to P12 or even to P16. Its disappearance overlapped the period when GFAP-immunopositive astrocytes were taking the place of radial glia. Despite the parallel time courses, however, the spatial patterns of the two processes were just the opposite: disappearance of the laminin immunoreactivity progressed from the middle zone whereas the appearance of GFAP from the pial surface and the corpus callosum. Rather, the regression of the vascular laminin immunoreactivity followed the progression of the immunoreactivities of glutamine synthetase and S100 protein. Therefore, the regression really correlates with a 'maturation' of astrocytes which, however, affects other astrocyte functions rather than cytoskeleton.