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Erdem Tuzun, Neurologist Istanbul, Turkey
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The finding that exposure to environmental lead during the first seven years of life is associated with cognitive deficits that persist into later childhood is quite interesting from many point of views. There are disapproving studies on this issue and it is well known that even lesioning of both amygdaloid complex and accumbens nucleus at very early stages of life may not produce significant changes in memory functions, at least in rodents. Sparing and quick recovery of memory functions may be explained by functional reorganization and maturation of memory-related anatomical structures in the later stages of life. There is a large body of evidence about the roles of different types of potassium channels of memory-related anatomical structures in the development of cognitive functions. Presence of both small conductance potassium channels and apamin-binding sites in amygdala and accumbens nucleus have been previously demonstrated. Both of these structures play vital roles in memory and learning and potassium channels are also known to be involved in these processes. Apamin treatment has been demonstrated to improve learning and memory facilities in various animal experiments. On the other hand, apamin-binding sites are affected by learning disorders including Alzheimer's disease and changes in the sensitivity to apamin may result in memory disorders. On this basis, lack of apamin-binding sites in amygdala and accumbens nucleus of fetal tissue may be presumed to have a somewhat considerable importance in ontogenesis and development of cognitive functions. There are no reports testifying the role of potassium channels in the maturation and ontogenesis of memory functions. However, certain chemical and functional differences are known to exist between memory and learning-related structures of new-born and adult. Bilateral injections of nicotinic agents into the amygdaloid nucleus of new-born rats, for instance, does not reveal any changes in learning functions, but show some significant facilitatory effects at later stages of life. Autoradiography studies performed on both fetal and adult brain by using radioactive iodine (I125) labelled potassium channel blockers (apamin, charybdotoxin, dendrotoxin) may yield an answer to this question. The highest levels of binding on fetal rodent brain with all these ligands are observed in neocortex, hippocampus, dentate gyrus and neuroepithelium of caudate-putamen. Although high levels of binding can be observed in amygdala and lateral amygdaloid nucleus by charybdotoxin autoradiography, only moderate levels of binding can be seen in amygdala by using other two ligands and there seems to be no binding in lateral amygdaloid nucleus by these ligands at all. On the other hand high levels of binding can be observed on fetal accumbens nucleus by using charybdotoxin and dendrodotoxin autoradiography but no binding can be demonstrated by apamin autoradiography. However, significant binding activity can be observed in adult rodent amygdala and accumbens nucleus by any of these ligands in autoradiography studies. Maturation of cognition takes longer time than that of the other central nervous system facilities and many molecules that are vital for memory and learning may be produced in later stages of life. The differential expression of various molecules may explain the quick recovery of cognitive functions and such molecular differences as the lack of certain types of potassium channels may even be explanatory for a very distinguished phenomenon known as infantile amnesia - the inability to recall the events experienced in the first few years of life. The questions about the ontogenic development of learning and memory may be answered in the future by more studies on comparisons of molecular differences of memory-related structures of adult and new-born. |
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