The pre- and postsynaptic mechanisms of the involvement of the serotonin of the amygdaloid body in the reproduction of the conditioned passive avoidance reaction in rats

A previous study reported that intercellular adhesion molecule-1 (ICAM-1) expression by human vascular endothelial cells (HUVEC) is augmented by intracellular signal transmission mainly through the protein kinase C (PKC) system stimulated by TXA2 receptors. In the present study, we show that a TXA2 receptor agonist, U46619, augments the expression of not only ICAM-1, but also vascular cell adhesion molecule-1 (VCAM-1) or endothelial leucocyte adhesion molecule-1 (ELAM-1) in HUVEC both at protein and mRNA levels. Pretreatment with SQ29,548 (a TXA2 receptor antagonist) or PKC inhibitors greatly diminished the extent of U46619-induced mRNA accumulation and surface expression of the adhesion molecules. An inhibitor of nuclear factor kappaB (NF-kappaB) activation, PDTC, diminishes U46619-induced VCAM-1 mRNA accumulation. NAC, which inhibits NF-kappaB and activation protein 1 (AP-1) binding activity, inhibits the expression of ICAM-1 or ELAM-1 at protein and mRNA levels. These findings suggest that ICAM-1 or ELAM-1 expression of HUVEC stimulated via TXA2 receptors is augmented by induction of NF-kappaB and AP-1 binding activity through the PKC system, and that VCAM-1 expression is augmented by induction of NF-kappaB binding activity.     

The mechanisms of the emotiogenic regulation of memory

The determining mechanism of memory regulation is a system involving the right temporal region and two anterior frontal regions. This is a cortical part of the integral system of the emotional regulation of memory. The dopaminergic mechanism forms the basis for fortifying the emotiogenic memory system, promoting the facilitation of retrieval. The selective emotional set of aggressive and submissive mice determines both the processes of extinction, development of amnesia, and subsequent reactivation of a memory trace induced by neuropharmacological agents. The GABA system is shown to enter the mechanism that controls the activity of dopamine system--dopamine release from the terminals of the nigrostriatal and mesolimbic dopaminergic systems is stimulated. The neurochemical background in the development of amnesia or forgetting determines the subsequent retrieval of a memory trace. The dopamine and GABA systems are common links in the retrieval of amnestic and forgetting memory traces, respectively. A substantial rise of met-enkephaline levels along with the maximum increase of D2-receptor density in the frontal cortex, amygdala, striatum, and hippocampus were observed in rats after learning. In vitro experiments indicated that met-enkephaline and beta-endorphine stabilized the kinetics of dopamine-receptor interactions.     

Oxidative metabolic changes, antioxidantion, and platelet activation rat phagocytes during development of experimental specific tuberculous changes

Efficacy and possibility of direct operations on the macular area of the retina in humid (exudative) maculopathies (senile maculodystrophy) is validated theoretically, morphologically, and clinically. A hypothesis on the mechanism of exudative process development in the macular area in degenerative diseases is formulated on the basis of pathohistological analysis of removed subpigmental material. Indications for such operations are defined.