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Biomedical subjects

K E Light

Publications and source records attributed to K E Light.

At least 19 recordsLinked to original sources
PubMed2006

Reliability of motor cortex transcranial magnetic stimulation in four muscle representations.

OBJECTIVE: Motor cortex plasticity may underlie motor recovery after stroke. Numerous studies have used transcranial magnetic stimulation (TMS) to investigate motor system plasticity. However, research on the reliability of TMS measures of motor cortex organization and excitability is limited. We sought to test the reliability of these TMS measurements. METHODS: Twenty healthy volunteers were tested twice over a two-week period using TMS to determine motor threshold, map topography, and stimulus-response curves for first dorsal interosseous (FDI), abductor pollicis brevis (APB), extensor digitorum communis (EDC), and flexor carpi radialis (FCR) muscles. RESULTS: We found moderate to good test-retest reliability TMS measurements of motor threshold (ICC=0.90-0.97), map area (ICC=0.63-0.86) and location (ICC=0.69-0.86), and stimulus-response curves (ICC=0.60-0.83). CONCLUSIONS: TMS assessments of motor representation size, location, and excitability are generally reliable measures, although their reliability may vary according to the muscle under investigation. SIGNIFICANCE: These results suggest that TMS measurements of motor cortex function are reliable enough to be potentially useful in investigation of motor system plasticity.

Adult↗
PubMed2002

Time course and manner of Purkinje neuron death following a single ethanol exposure on postnatal day 4 in the developing rat.

The present study was designed to evaluate the time course and manner of Purkinje cell death following a single ethanol dose delivered intragastrically on postnatal day (PN) 4 to rat pups. Analysis included immunolabeling of Purkinje cells with antibody specific for calbindin D28k and counting of Purkinje cells in each lobule of a mid-vermal slice. Terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling analysis and immunodetection for cleaved (activated) caspase-3 enzyme was used to identify apoptosis, with calbindin D28k co-immunolabeling to identify apoptotic Purkinje cells. Finally, immunodetection for cytochrome c, again with co-labeling using calbindin D28k antibody, identified intracellular release of cytochrome c from the mitochondria into the cytoplasm of Purkinje cells. The data demonstrate that a single dose of ethanol results in a significant and extensive, lobular dependent loss of Purkinje cells within 24 h after administration. Extensive loss in the early developing lobules (I-III, VIII-X) and less to no loss in the later developing lobules (IV-VII) is consistent with prior literature reports on the ethanol-induced effects on Purkinje cells at this age. Clear and consistent evidence of apoptotic Purkinje cells was identified and the pattern was transient in nature. Finally, cytochrome c is released from the mitochondria of Purkinje cells in a time course consistent with the activation of the mitochondrial pathway of apoptosis. These data support the hypothesis that ethanol-induced loss of Purkinje cells involves apoptotic mechanisms. Furthermore, the initiation of apoptosis by ethanol is consistent with ethanol-induced interruptions of Purkinje cell neurotrophic support leading to activation of the mitochondrial pathway of apoptosis.

Alcohol-Induced Disorders, Nervous System↗
PubMed2001

Early postnatal ethanol exposure selectively decreases BDNF and truncated TrkB-T2 receptor mRNA expression in the rat cerebellum.

Binge-like ethanol exposure on postnatal day (PN) 4 induces a concentration dependent loss of Purkinje cells in the rat cerebellum. The mechanism of this ethanol-induced Purkinje cell vulnerability is not presently understood. Nevertheless, the specific timing of this vulnerability leads us to consider the neurotrophin system crucial to the regulation of neuronal development. Differentiation, maturation, and survival of Purkinje cells are shown to involve an intimate interaction between brain-derived nerve growth factor (BDNF) and neurotrophin-3 (NT3) acting primarily through their specific tyrosine-kinase (Trk) receptors. We believe that the specific ethanol vulnerability, and the timing of this vulnerability result from alterations in the BDNF-NT3 interplay. We hypothesize that disruption of TrkB and/or TrkC mediated neurotrophin communication is, in part, responsible for the ethanol-induced loss of Purkinje cells during development. The current study was undertaken to define the impact of ethanol exposure at the onset of ethanol vulnerability on the relative concentrations of mRNA encoding the neurotrophic factor receptors TrkB and TrkC. The reverse transcriptase (RT) polymerase chain reaction (PCR) amplification technique was used to identify the relative expression levels of mRNA specific to these receptors as well as the truncated TrkB receptor isoforms. We identify a specific decrease in overall TrkB receptor mRNA expression that is primarily a function of the TrkB-T2 receptor isoform. Concurrent decreases in mRNA specific to BDNF were also identified. No significant alterations to the expression of TrkC mRNA were found indicating that ethanol-exposure appears to act selectively on the BDNF communication system.

Actins↗
PubMed2001

Concurrent and construct validity of scores on the Timed Movement Battery.

BACKGROUND AND PURPOSE: The Timed Movement Battery (TMB) is a new assessment tool designed to measure mobility in elderly individuals. "Mobility" was defined as a person's ability to maneuver his or her body independently in order to accomplish everyday tasks. The purpose of this study was to assess the concurrent and construct validity of scores obtained with the TMB as a measure of mobility in a group of elderly individuals who reported moderate or no difficulty in performing either basic or instrumental activities of daily living (BADL or IADL). SUBJECTS: Thirty community-dwelling elderly people, with a mean age of 77.5 years (SD=7.0, range=65-92), participated in this study. METHODS: Subjects responded to 2 questionnaires regarding their activities of daily living (ADL) (ie, Barthel Index and an 18-item ADL/IADL scale) and completed 3 assessments of mobility (ie, Berg Balance Scale, Timed "Up & Go" Test, and the TMB). Subjects were asked to perform the items on the TMB at a "self-selected" speed (their normal speed) and at a "maximum-movement" speed (as quickly as they could safely perform the items). Subjects' scores on the TMB were cross-correlated with data for 4 criterion tests (ie, Berg Balance Scale, Timed "Up & Go" Test, Barthel Index, and the 18-item ADL/IADL scale) using Spearman rank correlations and Pearson product moment correlations. RESULTS: Composite scores of the TMB performed at self-selected speeds correlated highly with data for the criterion tests and differentiated between those subjects reporting difficulty with ADL and those reporting no difficulty. CONCLUSION AND DISCUSSION: These results support the validity of scores obtained with the TMB as a measure of mobility in this sample of elderly individuals with moderate or no reported difficulty with ADL.

Activities of Daily Living↗
PubMed2000

Practice as an intervention to improve speeded motor performance and motor learning in Parkinson's disease.

Individuals with Parkinson's disease have difficulty initiating and performing complex, sequential movements. Practice generally leads to faster initiation and execution of movements in healthy adults, however, whether practice similarly improves motor performance in patients with Parkinson's disease remains controversial. To assess the effects of practice on motor performance, patients with Parkinson's disease and control subjects practiced two, rapid arm-reaching tasks with different levels of movement complexity for 120 trials each over 2 days. Response programming was studied by analyzing the overall reaction time latency of each movement and its fractionated sub-components, premotor and motor time. Practice effects were investigated by comparing pretest performance to immediate and delayed retention test performances (10-min and 48-h rest intervals, respectively). Both patients with Parkinson's disease and control subjects improved speeded performance of sequential targeting tasks by practice and retained the improvement across both retention test intervals. Finding a learning effect for persons with Parkinson's disease supports practice as an effective rehabilitation strategy to improve motor performance of specific tasks for patients with Parkinson's disease.

Acoustic Stimulation↗
PubMed2000

Effects of ethanol on working memory and attention in pigeons.

To determine whether the effects of ethanol on working memory are mediated by a secondary effect on attention, dose-response curves for ethanol were determined in eight pigeons trained under a titrating matching-to-sample (TMTS) procedure, in eight pigeons trained under a discrete-trial measure of attention, and in eight pigeons trained under a continuous-trial measure of attention. Ethanol decreased accuracy under the TMTS procedure following the three highest doses (1, 1.8, and 3 g/kg). Only the highest dose (3 mg/kg) decreased rates of responding. Attention, as measured under the discrete-trial procedure, was affected only by the two highest doses (1.8 and 3 g/kg). The 3-g/kg dose caused significant decreases in the probability of a hit and probability of a correct rejection, as well as significant increases in the probability of an error of omission and response latencies. Sensitivity to the signal decreased following 1.8 and 3 g/kg ethanol. Under the continuous-trial procedure, ethanol caused a peak in false alarms after the 1.8-g/kg dose, decreased the probability of a hit following the 1.8- and 3-g/kg doses, and increased probability of a miss at all doses. Sensitivity to the signal was not affected. A comparison of the dose-response curves for the TMTS procedure and the two measures of attention revealed that working memory (TMTS) was decreased by a lower dose than that affecting attention. This suggests that the effects of ethanol on working memory are not mediated by the subject's ability to pay attention to stimulus changes in the environment.

Algorithms↗
PubMed2000

Turning difficulty characteristics of adults aged 65 years or older.

BACKGROUND AND PURPOSE: Falls that occur while walking have been associated with an increased risk of hip fracture in elderly people. This study's purpose was to describe movement characteristics in older adults that serve as indicators of difficulty in turning while walking. SUBJECTS: Three groups were assessed: young adults who had no difficulty in turning (age range=20-30 years, n=20) (YNDT group), elderly adults who had no difficulty in turning (age range=65-87 years, n=15) (ENDT group), and elderly adults who had difficulty in turning (age range=69-92 years, n=15) (EDT group). METHODS: All subjects were videotaped performing a self-paced 180-degree turn during the Timed "Up & Go" Test. Movement characteristics of each group were identified. Four characteristics were used to identify difficulty in turning: (1) the type of turn, (2) the number of steps taken during the turn, (3) the time taken to accomplish the turn, (4) and staggering during the turn. RESULTS: In general, the EDT group took more steps during the turn and more time to accomplish the turn than the YNDT and ENDT groups. Although the only turning strategy used by the YNDT group was a pivot type of turn, there was an almost total absence of a pivot type of turn in the EDT group. No differences were found among the groups on the staggering item, yet the EDT group was the only group in which staggering was present. We believe these changes observed in the 4 characteristics only in the EDT group are indicators of difficulty in turning while walking. CONCLUSION AND DISCUSSION: These indicators of difficulty may be useful for the early identification of individuals aged 65 years or older who are having difficulty in turning and may well serve as the basis for the development of a scale for difficulty in turning in older adults. Preliminary findings indicate the need for further study into the reliability, validity, and sensitivity of measurements obtained with such a scale.

Accidental Falls↗
PubMed1999

Purkinje cell vulnerability to developmental ethanol exposure in the rat cerebellum.

BACKGROUND: Ethanol exposure is a consistent and reliable producer of neuronal toxicity, especially during periods of enhanced neuronal vulnerability. For rat cerebellar Purkinje cells, the postnatal period during the time of the brain growth spurt exhibits the greatest vulnerability to ethanol. Analyses of studies completed over more than 20 years provides sufficient detail to allow for the determination of the specific vulnerable window for ethanol-induced loss of Purkinje cells. METHODS: Data reporting Purkinje cell counts after ethanol exposure were compiled from 18 studies published since 1975. We conducted linear regression analysis between peak blood ethanol concentration (BEC) and percent reduction in Purkinje cells for the following individual postnatal (PN) days: PN4, PN5. PN6, PN7, and PN8 or beyond (+). The slope of the regression and the coefficients of determination (r2) were the primary factors of interest. Analysis of variance of the regressions was conducted to identify whether the slopes were significantly different from zero, or from each other. RESULTS: Exposures involving the PN4-6 period demonstrated the greatest significance in the relationship between BEC and reduction of Purkinje cell number. No significant differences were identified between different ethanol exposure techniques or for different Purkinje cell counting techniques. In addition, the initial day of exposure and the duration of exposure were not identified as critical variables. CONCLUSIONS: The literature database, developed over the past 20 years is clear in its direction that studies designed to identify the ethanol-specific mechanisms of Purkinje cell death are best designed to involve ethanol exposure during the vulnerable window of postnatal days 4-6.

Animals↗
PubMed1998

Intragastric intubation: important aspects of the model for administration of ethanol to rat pups during the postnatal period.

One technique for the controlled delivery of ethanol to neonatal rat pups is intragastric intubation. Often, the vehicle used for delivery of ethanol is composed of a nutrient mixture to compensate for decreased suckling or other possible nutritional compromise. This study analyzed the selection of nutrient vehicle, the combination of experimental treatment groups within a litter, and the overall litter size on the growth rate of ethanol-intubated and intubated-control pups, compared with mother-raised control pups. Sprague-Dawley rat pups were raised in litters of 8 or 10, and administered ethanol by intragastric intubation with 20% (v/v) Sustacal or 80% (v/v) Intralipid-II nutrient vehicle. Pups were treated between postnatal days 2 and 10, and body weight was analyzed on day 10. Pups were assigned to a treatment group as either intubated ethanol, intubated control, or nonintubated mother-raised controls. Experimental comparison by statistical analyses was performed to identify the optimal treatment design (mixed treatment groups in a single litter or a single treatment group per litter), the optimal vehicle (Sustacal or Intralipid-II), and the optimal number of pups per litter (8 vs. 10). The analyses demonstrate that the mixing of intubated control, intubated ethanol, and nonintubated mother-raised control treatment groups within a single litter introduced an uncontrolled variable that confounded measurement of ethanol-specific alterations. The sensitivity of treatment groups to inclusion in mixed litters was dependent on the nutrient vehicle and thus nutritional adequacy. Our results suggest that an optimal design was achieved with eight pups per litter. Furthermore, ethanol intubated and intubated control pups grow at a rate identical to parallel litters of eight mother-raised control pups when Intralipid-II is used as nutrient vehicle, and a single treatment group is present in a litter. Optimization of these experimental parameters has provided an excellent neonatal rat model for analysis of specific ethanol effects on brain development during the third trimester.

Animals↗
PubMed1997

Nutritional factors modify the inhibition of CNS development by combined exposure to methadone and ethanol in neonatal rats.

The consequences resulting from the combined exposure to methadone and ethanol during a time period equivalent to the third trimester brain growth spurt was the purpose of this study. Rat pups were treated on postnatal days 6-10 and sacrificed on postnatal day 11. Body weight along with the heart, liver, kidneys, whole brain, cerebrum, cerebellum, and brain stem weights were measured. The impact of nutritional factors were identified by delivery of the drug solutions in one of two intubation vehicles differing in both caloric density and composition. Ethanol and methadone in combination result in significantly increased detrimental effects compared to methadone alone only when possible nutritional compromise was present. The combined effect of both drugs significantly inhibited body growth and the development of all brain regions studied. Neither drug alone, nor in combination, produced significant inhibition of growth in the liver, heart, or kidney. The nutritional status of the pup, as represented by vehicle composition, was able to modify the specific drug effects and suggests that nutritional status can mask or enhance the determination of specific drug effects.

Animal Nutritional Physiological Phenomena↗
PubMed1997

Microencephaly and selective decreases in cerebellar Purkinje cell numbers following combined exposure to ethanol and methadone during rat brain development.

This study evaluated the neuroanatomical effects of combined ethanol and methadone exposure on cerebellar development. Ethanol, methadone or a combination of both drugs was delivered twice daily to rat pups using intra-gastric intubation from postnatal day 6 (PN6) to PN10 inclusive. The intubated control group (IK) received equal volumes of isocaloric vehicle. Purkinje cell numbers in cerebellar lobules I-X were quantified from midsagittal sections of the cerebellar vermis at PN11. Deficits of 15-23% in body, total brain, cerebrum, cerebellum and brainstem weights were exhibited for the ethanol/methadone-treated (IEM) group compared to IK. Purkinje cell deficits resulting from IEM treatment were found in lobules VI through X compared to IK with significant decreases of 31 and 23%, respectively, for lobules VIII and X. In contrast, neither ethanol nor methadone exposures under these treatment conditions caused cerebellar deficits.

Animals↗
PubMed1993

Intragastric intubation of alcohol during postnatal development of rats results in selective cell loss in the cerebellum.

Postnatal alcohol exposure produces reductions in the number of Purkinje cells in the rat cerebellum. The goal of this study was to determine if the method of postnatal alcohol exposure would influence the degree of vulnerability of the Purkinje cells. Previously reported studies from other laboratories have demonstrated cerebellar Purkinje cell count reductions following postnatal alcohol exposure via artificial rearing and vapor inhalation techniques. This study used gastric intubation to administer alcohol (3.6 g ethanol/kg body weight, bid) to male rat pups from postnatal days 4-10. Peak blood alcohol levels were 203 +/- 12.7 mg/dl on postnatal day 6. On postnatal day 10, the animals were perfused, and brain weights were obtained. Body weight was not significantly altered by the postnatal alcohol exposure, yet the wet weights of the cerebral cortex and whole brain were significantly reduced. Although the cerebellar weight was not significantly reduced, the overall number of Purkinje cells measured in the cerebellar vermis was significantly reduced by 24% compared with the isocaloric and normal control groups. The pattern of vulnerability for the individual cerebellar lobules was similar to the previously reported studies, indicating that alcohol's teratogenicity transcends experimental paradigm and is remarkably consistent, when relatively similar blood alcohol profiles are established.

Animals↗
PubMed1990

Effects of adult aging on the movement complexity factor of response programming.

The interaction effects between adult aging and incremental levels of movement complexity were studied in young, middle-aged, and older healthy females. Utilizing a two-choice reaction time (RT) paradigm, movement complexity as a factor of response programming was varied in a microswitch pressing task by altering the number of sides of the body and the number of fingers controlled. The speed of response programming was found to be age dependent and to interact with movement complexity across age groups. The results confirmed that as movement complexity increases, the effects of adult aging on RT increase. This study further emphasizes the robustness of the movement complexity x age effect, in that older individuals were found to be much more sensitive to small changes in movement complexity than younger subjects. The comparison results of three adult age groups suggested this sensitivity to movement complexity is progressive over the adult life span.

Adult↗
PubMed1990

Information processing for motor performance in aging adults.

Movement control systems are altered by the aging process. A growing body of research exists that explains the known changes that occur with aging, and many of those changes are related to central nervous system (CNS) effects. This article reviews motor control and learning issues related to CNS information-processing effects of aging and the effects of practice and physical conditioning on reactive capacity. The extensive variability in motor-performance abilities of older people is addressed, and the significance of individual differences is emphasized.

Adult↗
PubMed1989

Exposure of rats to ethanol from postnatal days 4 to 8: alterations of cholinergic neurochemistry in the cerebral cortex and corpus striatum at day 20.

Male and female rat pups were administered ethanol (3 g/kg/dose) twice daily by intragastric intubation between postnatal Day (PN) 4 and 8. Pups were maternally reared throughout the exposure period and until sacrifice on PN20. The consequences of this growth spurt exposure to ethanol were measured by an impact upon body growth, as well as upon specific growth parameters and cholinergic neurochemical factors within the cerebral cortex and corpus striatum. Specific endpoints included muscarinic receptor binding dynamics, acetylcholinesterase (AChE) and choline acetyltransferase (CAT) activities, regional wet weights, and subcellular protein content. In male pups, ethanol resulted in a significant enhancement of body weight gain and an increase in striatal but not cortical mass. Additionally, ethanol exposure resulted in a significant increase in striatal muscarinic receptor affinity, regardless of gender. This was accompanied by evidence of a significantly greater density of striatal muscarinic receptors in males versus females, regardless of treatment. Overall, the ethanol-associated effects are suggestive of a drug-induced developmental delay. Gender-specific, treatment-independent differences were also detected in the developing brain regions. Thus, regardless of treatment, cerebral cortical S1-level protein content was found to be significantly greater in males than in females. Furthermore, there were gender-based, significant differences in AChE activity within the striatum of control pups (males greater than females). Ethanol exposure resulted in a loss of this gender-based difference. We conclude that the cholinergic neurochemical development occurring in the striatum of the female rat brain between PN4 and 8 is exquisitely sensitive to ethanol-induced developmental delays which are not remediable by 12 subsequent days of maternal rearing in the absence of ethanol exposure.

Acetylcholinesterase↗
PubMed1989

Exposure of rats to ethanol from postnatal days 4 to 8: alterations of cholinergic neurochemistry in the hippocampus and cerebellum at day 20.

Brief neonatal ethanol exposure (3.0 g/kg/dose, twice daily; postnatal day (PN) 4 to PN8) resulted in cholinergic neurochemical alterations in the cerebellum, but not the hippocampus of rats assayed on PN20. Analysis revealed that the binding affinity of cerebellar muscarinic receptors for [3H]quinuclidinyl benzilate was decreased by ethanol, but only in female pups. Other gender-specific but treatment-independent cerebellar differences were identified as well, including lower levels of choline acetyltransferase activity and S1-level (1,000 x g) crude protein in males and females, respectively. No evidence of ethanol-induced cholinergic change was noted in the hippocampus of the same pups on PN20. However, collapsed across treatment, male hippocampi were found to contain less S1-level protein than their female counterparts. Neither muscarinic receptor density nor acetyl cholinesterase activity were found to differ between treatments or genders, in either brain region. Consistent with the developmental timetables for regional cholinergic synaptogenesis in the rat, observations on PN20 confirm a hypothesis of cerebellar cholinergic vulnerability and hippocampal cholinergic resilience to neonatal ethanol insult.

Acetylcholinesterase↗
PubMed1986

Antagonistic activity of tiotidine and ranitidine on guinea-pig and rabbit atria.

Isolated, spontaneously beating atrial pairs from rabbits and guinea-pigs were used to determine and to compare the activity of ranitidine and tiotidine as antagonists of histamine stimulated chronotropic activity. Ranitidine produced a classical competitive, reversible antagonism of histamine effects with a pA2 in rabbit atria of 8.2. In contrast, tiotidine produced both a dextral shift of the log dose-response curve, as well as a previously unreported suppression in the maximal response produced by histamine. In accordance with receptor theory, this type of activity represents a dualistic antagonism of histamine chronotropic responses.

Animals↗