Biomedical subjects

Anna Kalinchuk

Publications and source records attributed to Anna Kalinchuk.

3 recordsLinked to original sources

PubMed2004

The effect of age on prepro-orexin gene expression and contents of orexin A and B in the rat brain.

Orexin A and B (hypocretin 1 and 2) are hypothalamic peptides, which are synthesized in the lateral hypothalamus. Orexins participate in the regulation energy balance, food intake, vigilance and several endocrine and autonomic functions. The widespread projections of the orexin neurons suggest that they may have a role in coordination of different brain activities. The effects of ageing on the orexin system have not been studied previously. Prepro-orexin gene expression in the lateral hypothalamus, and the contents of orexin A and B peptides in the lateral hypothalamus and hypothalamus were measured in young, middle-aged and old (3, 12 and 24 months) rats. In the course of ageing, the expression of the prepro-orexin gene and the levels of orexin A and B decreased; the main decrease occurred by 12 months. Sleep deprivation for 6h increased slightly the expression of prepro-orexin gene in young rats. Deterioration of the orexin system may play a role in the phenomenon associated with aging, e.g. decreased consolidation of vigilance states, endocrine changes and dysfunctions of autonomic nervous system.

Aging↗

PubMed2003

Adenosine, energy metabolism, and sleep.

While the exact function of sleep remains unknown, it is evident that sleep was developed early in phylogenesis and represents an ancient and vital strategy for survival. Several pieces of evidence suggest that the function of sleep is associated with energy metabolism, saving of energy, and replenishment of energy stores. Prolonged wakefulness induces signs of energy depletion in the brain, while experimentally induced, local energy depletion induces increase in sleep, similarly as would a period of prolonged wakefulness. The key molecule in the induction of sleep appears to be adenosine, which induces sleep locally in the basal forebrain.

Adenosine↗

PubMed2002

Adenosine and sleep.

Adenosine is directly linked to the energy metabolism of cells. In the central nervous system an increase in neuronal activity enhances energy consumption as well as extracellular adenosine concentrations. In most brain areas high extracellular adenosine concentrations, through A(1) adenosine receptors, decrease neuronal activity and thus the need for energy. Adenosine seems to act as a direct negative feed-back inhibitor of neuronal activity. Hypoxia and ischemia induce very high extracellular adenosine levels, which may limit further brain damage. In brain areas that regulate cortical vigilance, particularly in the basal forebrain, high extracellular adenosine concentrations, induced by prolonged wakefulness, decrease the activity of presumably cholinergic cells and via this mechanism promote sleep. Our hypothesis is that in the cholinergic basal forebrain prolonged wakefulness induces local energy depletion that generates increases in extracellular adenosine concentrations in this area. In addition to the immediate effects, high extracellular adenosine concentrations also induce intracellular changes in signal transduction and transcription, e.g. increase in A(1) receptor expression and NF-kappaB binding activity. These changes may at least partially mediate the long term effects of prolonged wakefulness. Adenosine may also be a common mediator of the effects of several other sleep-inducing factors.

Adenosine↗