cAMP/PKA pathway and mitochondrial protection in oxidative stress-induced optic nerve head astrocytes

Oxidative stress and cyclic adenosine 3′,5′-monophosphate(cAMP)/protein kinase A(PKA)pathway in the optic nerve head astrocytes:Glaucoma is a leading cause of blindness worldwide in individuals 60 years of age and older.Despite the widely appreciated disease relevance of structural and functional abnormalities of astrocyte in the optic nerve head(ONH)that is associated with retinal ganglion cell(RGC)axon degeneration,the molecular mechanisms underlying astrocyte dysfunction in glaucomatous ONH degeneration are poorly understood.Oxidative stress is strongly linked to glaucoma pathogenesis,and astrocytes are the responsible cell type that is mostly related to oxidative stress and glaucomatous ONH degeneration.

Phylogeny of nucleus medianus of the posterior tubercle in ray-finned fishes

The brains of ray-finned fishes form a morphocline of increasing complexity,from cladistians through teleosts.This is particularly apparent in the posterior tubercle of the diencephalon.In cladistians,the posterior tubercle consists of a periventricular nucleus and a migrated nucleus medianus that is fused across the midline.In more advanced ray-finned fishes,such as gars and bowfins,the posterior tubercle comprises numerous additional mi-grated nuclei,termed the preglomerular complex,in addition to a more well developed nucleus medianus.In teleosts,the most derived ray-finned fishes,there is an even more elaborate preglomerular complex,but there is no recognizable nucleus medianus.In an attempt to explain the variation in the posterior tubercle of the diencephalon in ray-finned fishes,the immunohistochemistry and connections of nucleus medianus were examined in cladistians,gars and bowfins.In each of these taxa,nucleus medianus exhibits large numbers of calretinin-positive neurons and has ascending projections that terminate in several divisions of the pallium.Although teleosts,such as goldfish,also exhibit numerous cell groups in the posterior tubercle that are rich in calretinin,none of these cell groups has connections that are comparable to those of nucleus medianus in non-teleost ray-finned fishes.It is possible,therefore,that nucleus medianus was lost with the origin of teleosts.

Store-operated calcium entry in neuroglia

Neuroglial cells are homeostatic neural cells. Generally, they are electrically non-excitable and their activation is associated with the generation of complex intracellular Ca^2＋ signals that define the ＂Ca^2＋ excitability＂ of glia. In mammalian glial cells the major source of Ca^2＋ for this excitability is the lumen of the endoplasmic reticulum （ER）, which is ultimately （re）filled from the extracellular space. This occurs via store-operated Ca^2＋ entry （SOCE） which is supported by a specific signaling system connecting the ER with plasmalemmal Ca^2＋ entry. Here, emptying of the ER Ca^2＋ store is necessary and sufficient for the activation of SOCE, and without Ca^2＋ influx via SOCE the ER store cannot be refilled. The molecular arrangements underlying SOCE are relatively complex and include plasmalemmal channels, ER Ca^2＋ sensors, such as stromal interaction molecule, and possibly ER Ca^2＋ pumps （of the SERCA type）. There are at least two sets of plasmalemmal channels mediating SOCE, the Ca2＊-release activated channels, Orai, and transient receptor potential （TRP） channels. The molecular identity of neuroglial SOCE has not been yet identified unequivocally. However, it seems that Orai is predominantly expressed in microglia, whereas astrocytes and oligodendrocytes rely more on TRP channels to produce SOCE. In physiological conditions the SOCE pathway is instrumental for the sustained phase of the Ca^2＋ signal observed following stimulation of metabotropic receptors on glial cells.