Further observations on cerebellar climbing fibers. A study by means of light microscopy, confocal laser scanning microscopy and scanning and transmission electron microscopy

The intracortical pathways of climbing fibers were traced in several vertebrate cerebella using light microscopy, confocal laser scanning microscopy, scanning and transmission electron microscopy. They were identified as fine fibers up to 1(micron thick, with a characteristic crossing-over bifurcation pattern. Climbing fiber collaterals were tridimensionally visualized forming thin climbing fiber glomeruli in the granular layer. Confocal laser scanning microscopy revealed three types of collateral processes at the interface between granular and Purkinje cell layers. Scanning electron microscopy showed climbing fiber retrograde collaterals in the molecular layer. Asymmetric synaptic contacts of climbing fibers with Purkinje dendritic spines and stellate neuron dendrites were characterized by transmission electron microscopy. Correlative microscopy allowed us to obtain the basic three-dimensional morphological features of climbing fibers in several vertebrates and to show with more accuracy a higher degree of lateral collateralization of these fibers within the cerebellar cortex. The correlative microscopy approach provides new views in the cerebellar cortex information processing.(AU)

Neutrophil signaling alteration: an adverse inflammatory response after burn shock

The inflammatory response syndrome in shock-like states might frequently be accompained by an oxidative cell/tissue demage in one or more organ-systems in the body. The inflammatory response related hyperactivation of neutrophils can contribute to oxidative cell/tissue damage. Studies discussed in this review examined the role of cell sgnaling pathways in the hyperactivation of neutrophils in an early stage of burn injury shock. The studies were carried out in peripheral blood neutrophils isolated from rats with a 25 per cent body surface area scald burn. Neutrophil cell signaling responses were evaluated by measuring cytosolic [Ca2+] and protein kinase C activity, and were correlated with neutrophil superoxide production. The cytosolic [Ca2+] and protein kinase C responses were highly upregulated along with enhanced superoxide production in the early phase of burn injury. The treatment of burn-injured rats with the calcium antagonist diltiazem abrogated enhanced Ca2+ and protein kinase C signaling and superoxide generation. The signaling upregulation in neutrophils could result from potentiation of actions of burn-injury induced chemotactic mediators on the leukocytes. The neutrophil signaling upregulation leading to increased superoxide generation could thus be responsible for the oxidative cell/tissue damage. The organ-system dysfunction/failure accompanying burn shock may be initiated with the oxidative cell/tissue damage. (AU)

Calcium- and zinc-binding proteins in intracellular transport

The complex mechanism of intracellular transport is regulated by free calcium in different manners. Calcium binding proteins regulate several aspects of the vesicle fusion mechanism mediated by NSF (N-ethylmaleimide sensitive fusion factor). At least in some regulated exocytosis, calcium-binding proteins are the trigger for fusion downstream of NSF, Still, calcium-binding proteins, such as annexins, may be part of a different fusion mechanism mediating some specific transport steps or working in parallel to the NSF-dependent fusion process. Calcium is not the only ion necessary for the function of factors involved in vesicular transport. A zinc requirement has been also proposed. One of the zinc-dependent factors is probably a protein with a cysteine-rich region that coordinates zinc and binds phorbol esters. Although protein kinase C is the more prominent family of proteins carrying this domain, the factor necessary for transport does not appear to function as a kinase.(AU)