Biomedical subjects

D L Korol

Publications and source records attributed to D L Korol.

10 recordsLinked to original sources

PubMed1998

Glucose enhancement of 24-h memory retrieval in healthy elderly humans.

When administered soon before or after training, glucose facilitates memory in rodents and in several populations of humans, including healthy elderly people. Thus, glucose appears to enhance memory formation in a time- and dose-dependent manner. By assessing the effects of glucose at the time of memory tests, the present experiment examined the role of glucose on memory retrieval in healthy elderly people. On four sessions separated by a week, glucose or saccharin were administered immediately before hearing a narrative prose passage, as in previous experiments, or immediately before being tested for recall of the passage (24 h after training). Subjects recalled significantly more information after glucose ingestion than after saccharin ingestion whether the glucose was given before acquisition or memory tests. In addition, recall was significantly better in the preacquisition glucose condition relative to recall in the retrieval glucose condition. These findings provide evidence that glucose enhances both memory storage and retrieval.

Aged↗

PubMed1998

Glucose, memory, and aging.

Circulating glucose concentrations regulate many brain functions, including learning and memory. Much of the evidence for this view comes from experiments assessing stress-related release of epinephrine with subsequent increases in blood glucose concentrations. One application of this work has been to investigate whether age-related memory impairments result from dysfunctions in the neuroendocrine regulation of the brain processes responsible for memory. Like humans, aged rodents exhibit some memory impairments that can be reversed by administration of epinephrine or glucose. In elderly humans, ingestion of glucose enhances some cognitive functions, with effects best documented thus far on tests of verbal contextual and noncontextual information. Glucose also effectively enhances cognition in persons with Alzheimer disease or Down syndrome. Although earlier evidence suggested that glucose does not enhance cognitive function in healthy young adults, more recent findings suggest that glucose is effective in this population, provided the tests are sufficiently difficult. In college students, glucose consumption significantly enhanced memory of material in a paragraph. Glucose also appeared to enhance attentional processes in these students. Neither face and word recognition nor working memory was influenced by treatment with glucose. The neurobiological mechanisms by which glucose acts are under current investigation. Initial evidence suggests that glucose or a metabolite may activate release of the neurotransmitter acetylcholine in rats when they are engaged in learning. Consequently, the issue of nutrition and cognition becomes increasingly important in light of evidence that circulating glucose concentrations have substantial effects on brain and cognitive functions.

Adolescent↗

PubMed1997

Age-related differences in an ecologically based study of route learning.

Spatial learning abilities in younger adults and in healthy elderly adults were examined in 2 tasks. In the first task, participants were tested for their ability to recall relevant route information as well as to recognize and to order temporally landmark information observed along the route. Older participants had relatively greater difficulty retracing the route and temporospatially ordering landmarks but were equally good at recognition of landmarks occurring on the route. In the second task, participants memorized a 2-dimensional representation of a route and subsequently navigated the route from memory. Older participants had greater difficulty memorizing the route and navigating it. Errors of omission, commission, wrong, and forced choice were analyzed. Group differences in the pattern of errors differed by task.

Adolescent↗

PubMed1996

Increased susceptibility to induction of long-term depression and long-term potentiation reversal during aging.

Homosynaptic long-term depression (LTD) and reversal of long-term potentiation (LTP) were examined extracellularly at CA3-CA1 synapses in stratum radiatum of slices from adult (6-9 months) and aged (20-24 months) Fischer 344 rats. Prolonged low-frequency stimulation (LFS) (900 pulses/1 Hz) of the Schaffer collaterals depressed the initial slope of the excitatory postsynaptic potential (EPSP) in aged but not adult rats. LTD at aged synapses was pathway-specific, persistent, and sensitive to the NMDA receptor antagonist DL-2-amino-5-phosphonopentanoic acid (AP5). Adult slices exhibited AP5-sensitive LTD in high [Ca2+] medium, whereas LTD in aged slices was blocked by high [Mg2+], suggesting that differences in Ca2+ regulation may underlie susceptibility to LTD. Despite age-related differences in LTD induction, no age difference in LTP magnitude was revealed. Additionally, LFS delivered 60 min after LTP induction resulted in similar LTP reversal for both age groups. Susceptibility differences to LTP reversal were indicated after multiple short-duration LFS bursts (30 pulses/1 Hz), with each burst separated by 10 min. Aged synapses exhibited significant reversal after a single burst and complete reversal after three LFS episodes. In adult slices, LTP reversal appeared after the fourth burst, and at no time was LTP depressed to initial baseline levels. This study provides the first characterization of homosynaptic LTD/LTP reversal in the aged animal and demonstrates that one form of plasticity, depression attributable to LFS, is increased during aging.

2-Amino-5-phosphonovalerate↗

PubMed1994

LTP saturation and spatial learning disruption: effects of task variables and saturation levels.

The prediction that "saturation" of LTP/LTE at hippocampal synapses should impair spatial learning was reinvestigated in the light of a more specific consideration of the theory of Hebbian associative networks, which predicts a nonlinear relationship between LTP "saturation" and memory impairment. This nonlinearity may explain the variable results of studies that have addressed the effects of LTP "saturation" on behavior. The extent of LTP "saturation" in fascia dentata produced by the standard chronic LTP stimulation protocol was assessed both electrophysiologically and through the use of an anatomical marker (activation of the immediate-early gene zif268). Both methods point to the conclusion that the standard protocols used to induce LTP do not "saturate" the process at any dorsoventral level, and leave the ventral half of the hippocampus virtually unaffected. LTP-inducing, bilateral perforant path stimulation led to a significant deficit in the reversal of a well-learned spatial response on the Barnes circular platform task as reported previously, yet in the same animals produced no deficit in learning the Morris water task (for which previous results have been conflicting). The behavioral deficit was not a consequence of any after-discharge in the hippocampal EEG. In contrast, administration of maximal electroconvulsive shock led to robust zif268 activation throughout the hippocampus, enhancement of synaptic responses, occlusion of LTP produced by discrete high-frequency stimulation, and spatial learning deficits in the water task. These data provide further support for the involvement of LTP-like synaptic enhancement in spatial learning.

Animals↗

PubMed1993

Hippocampal synaptic enhancement and spatial learning in the Morris swim task.

The authors attempted to replicate the study of Castro, Silbert, McNaughton, and Barnes (1989) in which it was concluded that bilateral saturation of hippocampal synaptic enhancement produced a deficit in acquisition of a spatial navigation problem in the Morris swim task. The original protocol was followed as closely as possible, but no effect of long-term enhancement (LTE) saturation on spatial performance in this task was found. This negative result suggests either that the previous finding using the swim task reflected statistical error or that some as yet undetermined variable is of critical importance in this phenomenon. The present negative finding also raises a question concerning the reproducibility of the earlier results of McNaughton, Barnes, Rao, Baldwin, and Rasmussen (1986) in which LTE saturation apparently led to a prolonged deficit on a different spatial task. Although negative results in such experiments do not constitute grounds for rejecting the underlying hypothesis, the present lack of a positive effect renders uncertain, for the time being, one of the lines of experimental support for the theory that LTE at hippocampal synapses reflects a mechanism for the associative, distributed storage of new spatial information.

Animals↗

PubMed1992

Unilateral naris closure and vascular development in the rat olfactory bulb.

The blood supply to the brain has been linked closely to nervous system function and metabolism, thereby possibly playing a direct role in brain maturation. Previously, we demonstrated that closure of an external naris early in life results in large changes within the olfactory bulb, including reductions in laminar volume and cell number and a rapid decline in metabolism and protein synthesis. To understand the role of the blood supply in the dramatic changes following naris closure, the present study examines the development of olfactory bulb vasculature in unilaterally odor-deprived and control rats. On post-partum day 1 (P1; the day after birth), littermate rat pups underwent either unilateral naris occlusion or sham surgery. On P5, P10, P15, P20, P30 and P60, animals were perfused with an india ink-gelatin mixture to assess blood vessel amount and complexity. Densitometric analyses were performed to obtain values of blood vessel area ratios (vessel area/tissue area), branch point number and branch point density. Considerable vessel development in all bulbs occurred over the first two to three weeks post-partum. By P20, large reductions in vessel area ratios were observed in all constituent laminae of deprived bulbs. While similar reductions in number of vessel branch points/tissue area were seen, few changes were noted in the number of branch points/vessel area. The effects were primarily confined to early developmental periods: bulb vasculature in animals deprived at older ages (P40) appeared normal. The results indicate that the vasculature responds to alterations in sensory stimulation early in life, therefore potentially playing an important regulative role in neural development.

Aging↗

PubMed1991

Unilateral olfactory deprivation: effects on succinate dehydrogenase histochemistry and [3H]leucine incorporation in the olfactory mucosa.

Surgically closing one external naris reduces airflow through one half of the nasal cavity, decreasing the access of odors to the receptor sheet. In rats, unilateral naris occlusion performed near birth results in large reductions in the size of the olfactory bulb, the primary central relay, when examined 30 days later. Previous research has demonstrated that there is a rapid reduction in [3H]2-deoxyglucose (2-DG) and [3H]leucine uptake in the bulb within hours after naris closure. The present study examined whether similar rapid changes could be observed in the sensory periphery. Pups occluded on P1 and examined on P3 with succinate dehydrogenase histochemistry exhibited reduced staining on the closed side of the nasal cavity, suggesting occlusion results in reductions in mucosal metabolism. Larger differences in staining were observed in pups examined at P6. [3H]Leucine incorporation was quite similar on both sides of the nasal septum as late as 30 days post occlusion, suggesting less dramatic changes in protein synthesis. The results suggest that naris closure does indeed have rapid effects on mucosal function, but indicate that the changes are different than those observed in the bulb.

Animals↗

PubMed1990

Rapid changes in 2-deoxyglucose uptake and amino acid incorporation following unilateral odor deprivation: a laminar analysis.

Unilateral naris occlusion in neonatal rats results in large alterations in the olfactory bulb, including substantial changes in laminar volume and enhanced cell death. These gross changes are undoubtedly the result of a cascade of more basic cellular regulatory events. The present study assesses the possibility of rapid post-deprivation changes in two such processes: glucose metabolism and protein synthesis. On the day after the day of birth rat pups underwent unilateral naris occlusion or sham surgery. In one study, either 1, 12, 24 or 48 h following surgery [3H]2-deoxyglucose [( 3H]2-DG) was administered to gauge patterns of glucose uptake. In a second study, [3H]leucine was injected to assess patterns of protein synthesis. Autoradiographs were then subjected to quantitative analyses. As early as 1 h following occlusion reduced 2-DG uptake was observed in many bulb regions. By 24 h, leucine incorporation was also uniformly diminished. While 2-DG uptake remained suppressed 48 h after deprivation, levels of amino acid incorporation returned to normal patterns in most laminae, with the exception of the mitral cell layer, where increased uptake was encountered. To evaluate whether the effects were developmental by nature a group of P40-P45 animals treated similarly were also examined. While 24 h of deprivation impaired 2-DG uptake in older animals, no alterations in amino acid incorporation were observed. The results indicate that early odor deprivation has rapid and specific effects on cellular functioning within the developing olfactory bulb.

Animals↗

PubMed1989

Prenatal neurogenesis in the telencephalon of the precocial mouse Acomys cahirinus.

[3H]thymidine autoradiography was employed to examine the times of formation of the major neuronal classes in the forebrain of the precocial mouse Acomys cahirinus. Dams received 3 thymidine injections over a 24 h period on either embryonic Day 14, 18, 20, 22, 29 or 36. Age-related changes in the distribution and number of heavily labeled cells were noted. Acomys exhibited later onset and more protracted periods of cell generation than the phylogenetically related, altricial laboratory rat or mouse, indicating considerable differences in patterns of early growth between the species. Understanding the factors responsible for these differences could lend important insights into evolutionary mechanisms involved in the process of speciation.

Animals↗