The Effect of Blood Glucose Concentration on the Error Monitoring and Processing System in Alcohol Users During Intensive Mental Activities

Background:The error monitoring and processing system (EMPS) located in the substantia nigra of the midbrain; basal ganglia and cortex of the forebrain; plays a leading role in error detection and correction. Although recent data show that alcohol disrupts the EMPS; the mechanism of alcohol's effect on this system remains unknown.Aims: To suggest a hypothesis that explains the processes and mechanism of alcohol-related disruption of EMPS. Methods:We critically examined our recent research data; as well as peer-reviewed literature on the effect of alcohol on blood glucose levels; and cognitive functions. The role of blood glucose concentration in the EMPS; including associated theories and hypothesis were also reviewed. Databases utilised were African Journals On Line; Elsevier; Science Direct; Medline from January 1940 to February 2010 . Results: Blood glucose concentration plays a vital role in the EMPS. The effect of blood glucose concentration on the EMPS is realised through the modulation of the activity of the dopaminergic system by proportional changes in the brain glucose level. Based on current literatures and the results of our recent study; here we suggest a hypothesis of alcohol-related glucose-dependent system of error monitoring and processing.The main postulate of this hypothesis holds that the disruption of EMPS by ethanol is related to disorders in glucose metabolism; which in turn may determine the dopamine level the major component of EMPS.Conclusion: Alcohol may disrupt the EMPS indirectly by affecting dopamine level through disorders in glucose homeostasis regulation

Histamine-correcting drug pherofunginum and bone tissue regeneration.

It has been shown that a histamine-correcting preparation (Pherofunginum) speeds up bone tissue regeneration. Other histamine correcting preparations behave in a similar way. We conclude that the application of these preparations in traumatology may have beneficial results.

[Analysis of changes in serotonin, histamine, and prostaglandin E2 levels in cerebrospinal fluid and body tissues during hyperthermia of various origins]. / Analiz izmenenii soderzhaniia serotonina, gistamina i prostaglandina E2 v spinomozgovoi zhidkosti i tkaniakh organizma pri gipertermiiakh razlichnogo proiskhozhdeniia.

Physical hyperthermia caused distinct increase in content of serotonin in liquor and its decrease in hypothalamus of rabbits and rats, while histamine and PGE2 were unaltered in liquor of these animals. Considerable increase of PGE2 in liquor simultaneously with unaltered content of serotonin and histamine were detected in rabbits with pyrogenal-caused fever. A decrease in PGE2 content and elevation of serotonin were found in animals liquor after normalization of body temperature within 7 hrs of the pyrogenal treatment. The biogenic amines studied appear to serve as constituents of the natural antipyretic body system in animals, whereas PGE2 belongs to factors responsible for elevation of body temperature.

[The effect of serotonin and histamine administered in low doses on body temperature]. / Vliianie serotonina i gistamina, vvodimykh v malykh dozakh, na temperaturu tela.

Experiments on white rats and mice have shown that intraventricular administration of serotonin (10 mg) or intraabdominal administration of histamine (0.5 mg/kg) do not affect body temperature, whereas simultaneous administration of these drugs leads to a reliable drop of body temperature due to intensification of the heat output and the inhibition of heat production. These biogenic amines seem to act as the substances with additive hypothermal properties and, probably, are the components of natural antipyretic system of the warm-blooded organism.

[Neuromediator mechanisms of the effect of the antihistamine agent dimebone on the brain]. / Neiromediatornye mekhanizmy deistviia antigistaminnogo preparata dimebona na mozg.

Dimebone was shown to inhibit monoamine oxidase (MAO) deaminating dopamine and serotonin, decrease dopamine metabolism in the basal ganglia of the rat brain, increase noradrenaline level and depress dopamine deamination in the hypothalamus. Dimebone first increased and then diminished the release of dopamine in the cortex, with the concomitant MAO activation and the increase in dopamine and noradrenaline levels. The in vitro experiments have demonstrated that dimebone (10(-4)) preferentially inhibited MAO activity, type B and dopamine deamination in homogenates of different rat brain structures. The role of MAO inhibition in the mechanism of dimebone action on the catecholamine metabolism in the brain structures and its stimulating effect on CNS are discussed.