Effect of equal and random amounts of varied practice on transfer task performance.
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Adult↗
Biomedical subjects
M Lemke
Publications and source records attributed to M Lemke.
Decreases in tissue levels of ubiquinol-9 and -10, ascorbate and alpha-tocopherol following spinal cord impact trauma in rats.
Generation of free radicals and subsequent lipid peroxidation have been proposed to contribute to delayed tissue damage following traumatic spinal cord injury (SCI). Ubiquinols (reduced coenzyme Q), ascorbate (vitamin C), and alpha-tocopherol (vitamin E) are endogenous antioxidants; decreases in tissue levels of these compounds may, therefore, reflect ongoing oxidative reactions. In the present studies, alterations in tissue levels of ubiquinol-9 and -10, ascorbate, and alpha-tocopherol were examined after SCI of varying severity in the rat. Levels of alpha-tocopherol did not change significantly after injury. Ascorbate and ubiquinol levels were decreased after trauma. Changes in tissue levels of ubiquinol, but not ascorbate reflected the degree of trauma. Thus, ubiquinol levels may provide a useful marker of the oxidative component of the secondary injury response.
Animals↗
Lipid alterations correlate with tissue magnesium decrease following impact trauma in rabbit spinal cord.
Secondary neurochemical events contribute to progressive tissue damage and subsequent neurological deficit after traumatic spinal-cord injury (SCI). Among proposed injury factors are alterations of phospholipids and certain cations. To clarify the relationship of membrane lipid changes (phospholipids, cholesterol, and arachidonic acid) to changes in tissue content of water and selected ions (sodium, potassium, and magnesium) after SCI, these variables were examined in spinal-cord segments from anesthetized ventilated rabbits subjected to laminectomy or to moderate (40 g-cm) or severe (150 g-cm) impact trauma at the lumbar (L2) segment. Trauma caused significant increases in tissue sodium, water, and arachidonic acid content, and significant decreases in phospholipids, cholesterol, potassium, and magnesium content. Alterations in magnesium were significantly related to injury severity. In contrast, changes in spinal-cord water content occurred to a similar degree in the two injury groups, as did tissue sodium and potassium content. Decreases in phospholipids were strongly correlated with decreases in tissue magnesium content, whereas changes in sodium and potassium were less well-correlated. Because magnesium ions play a critical role with regard to cellular bioenergetic state, calcium flux, amino acid receptor function, and eicosanoid production, reductions in tissue magnesium after injury may be important in the progression of secondary tissue damage.
Animals↗
Edema development and ion changes in rat spinal cord after impact trauma: injury dose-response studies.
Changes in the total tissue content of water, sodium, potassium, and magnesium were measured in spinal cord from pentobarbital-anesthetized rats subjected to impact trauma (T9) of varying severity (low, 25 g-cm; moderate, 50 g-cm; severe, 100 g-cm). Laminectomized animals served as controls. Spinal cord samples were taken from rats in the high injury group at 15 min, 60 min, 4 hr, 24 hr, 3 days, or 7 days posttrauma. Samples from the low and moderate injury groups were taken at 24 hr postinjury. In all groups, spinal cord tissue was rapidly removed (less than 30 sec), frozen in liquid N2, and dissected into the injured segment and adjacent two caudal and rostral segments. Severe injury caused significant increases in tissue water content; changes were present at 15 min, peaked at 24 hr, and continued at 3-7 days. Sodium levels were increased at 4 hr and remained elevated for up to 7 days. Potassium levels were decreased at 60 min, remained at low levels for up to 3 days, and partially recovered at 7 days. Tissue magnesium levels were significantly decreased only at 4 hr and 24 hr. Changes in water content and total sodium at 24 hr were not correlated with injury severity. Although potassium decreases did correlate with injury severity, alterations in magnesium levels had a much higher degree of correlation. Thus, reductions in magnesium content may contribute to the development of irreversible tissue damage. In contrast, edema formation after spinal cord trauma may be an epiphenomenon, since it was found to an equal degree in low, moderate, and severe injuries.
Animals↗
Effects of TRH-analog treatment on tissue cations, phospholipids and energy metabolism after spinal cord injury.
Effects of thyrotropin-releasing hormone analog CG3703 on biochemical changes following impact spinal cord trauma were investigated by 31P magnetic resonance spectroscopy, atomic absorption spectrophotometry, high-pressure liquid chromatography and radioimmunoassay using parallel injury models in rabbits and rats. Treatment with CG3703 at 45 min after trauma in rabbits significantly attenuated decreases in intracellular pH and reversed increases in phosphodiester to phosphomonoester ratio, as shown by 31P magnetic resonance spectroscopy. The improved phosphodiester/phosphomonoester ratio was correlated with improved ATP status after treatment, although there was no improvement in aerobic bioenergetic capacity as reflected by phosphocreatine to inorganic phosphate ratios. In rats, treatment with CG3703 significantly reduced changes in tissue cations (Na+, K+, Mg2+) and water content following trauma, but did not significantly alter the accumulation of free fatty acids or thromboxane B2. Thus, the beneficial effects of treatment with thyrotropin-releasing hormone or thyrotropin-releasing hormone analogs on outcome following traumatic spinal cord injury may be due, in part, to actions relating to ion homeostasis.
Animals↗
Opiate-receptor antagonist improves metabolic recovery and limits neurochemical alterations associated with reperfusion after global brain ischemia in rats.
Opiate-receptor antagonists improve behavioral, electrophysiologic and/or histologic outcome in various experimental models of central nervous system ischemia. To address the potential mechanism(s) by which opiate-receptor antagonists may exert their protective actions in cerebral ischemia, metabolic and biochemical changes were measured in brain of rats pretreated with the opiate-receptor antagonist nalmefene or vehicle and subjected to 60 min of global ischemia followed by 2 hr of reperfusion. 31P and 1H magnetic resonance spectroscopy were used to follow the metabolic changes during ischemia and reperfusion, after which brain tissue was frozen in situ. Biochemical assays included free fatty acids, thromboxane B2, ascorbate, vitamin E and amino acids. Nalmefene-treated animals showed more rapid and complete recovery of cellular bioenergetic state (as indicated by the phosphocreatine to inorganic phosphate ratio), tissue acidosis and lactate levels during reperfusion than placebotreated controls. Ischemia/reperfusion caused significant increases of fatty free acids and thromboxane, associated with significant decreases of ascorbate and glutamate; nalmefene pretreatment limited each of these changes. The degree of metabolic improvement as reflected by recovery of high energy phosphates and reduction of lactic acidosis were highly correlated with changes in tissue levels of arachidonate and glutamate. Thus, the beneficial effects of opiate-receptor antagonists in cerebral ischemia may be due, in part, to an ability to enhance metabolic recovery with associated, reduction in phospholipid hydrolysis and excitotoxin release.
Adenosine Triphosphate↗
Spinal cord edema and changes in tissue content of Na+, K+, and Mg2+ after impact trauma in rats.
Changes in the tissue content of water, Na+, K+, and Mg2+ were measured in spinal cord samples from anesthetized rats subjected to impact trauma (T9 spinal segment) of varying severity: 25 g-cm (low injury), 100 g-cm (high injury). Laminectomized animals served as controls. Rats with high injury were killed at 15 min, 60 min, 4 hr, 24 hr, 3 days, or 7 days after trauma. Those with low injury were killed at 24-hr postinjury. In all groups, spinal cord tissue was rapidly removed (less than 30 sec), frozen in liquid nitrogen, and dissected into the injured segment and adjacent two caudal and rostral segments. Water content was determined as wet weight/dry weight ratios, and cations were measured by atomic absorption spectrophotometry. High injury resulted in statistically significant increases in water content as early as 15 min after trauma. There were concomitant increases in Na+ and decreases in K+ that were apparent at 15 min and were statistically significant by 60-min posttrauma. The increases in water content and Na+ were present to a similar degree in the 4-hr, 24-hr, 3-day, and 7-day groups. In contrast, tissue Mg2+ was reduced and significantly decreased at 4 hr and 24 hr; Mg2+ levels had recovered partially by 3 days and completely by 7 days. Whereas changes in the tissue content of water, Na+, and K+ occurred at 24 hr regardless of the injury severity, changes in total Mg2+ were correlated with the degree of injury. These data are consistent with the conclusion that edema formation (and associated Na+ and K+ changes) after spinal cord trauma may be an epiphenomenon and does not significantly contribute to injury progression. In contrast, reductions in Mg2+ content may represent an important factor in the development of irreversible tissue damage.
Animals↗
Traumatic spinal cord injury in rabbits decreases intracellular free magnesium concentration as measured by 31P MRS.
The mechanisms by which traumatic injury to the central nervous system cause irreversible tissue damage remain speculative. Recent reports suggest that a decrease in tissue total and free Mg2+ concentration may be an important factor in the development of such injury after experimental brain trauma. Although total Mg changes have been reported following spinal cord trauma, no studies have examined spinal cord-free Mg2+. In the present study, we have used phosphorus magnetic resonance spectroscopy to determine intracellular free Mg2+ concentration and atomic absorption spectrophotometry to measure total tissue Mg concentration in rabbit spinal cord prior to and following impact trauma. We report that intracellular free Mg2+ concentration decreases from a pre-injury value of 0.80 +/- 0.12 mM (mean +/- S.E.M.) to 0.31 +/- 0.05 mM at 2 h post-trauma. Following injury there was an associated decrease in total tissue Mg and K concentration, but no alterations in tissue Na or water content.
Animals↗
[Animal experiment studies on the neurohumoral control of female puberty. 2. Studies on the influence of amygdala and of the hippocampus on sex maturation].
Immature female rats were bilaterally lesioned in the rostral or caudal part of the mediocortical amygdala (MCA) or in the ventral hippocampus (VHPC) at 21 days of age. In a second experiment, simultaneous lesioning of the MCA or VHPC and the medial preoptic area or hypothalamic ventromedial-arcuate region was performed in 21-day-old rats. Finally, discrete lesions were placed into the anterior or posterior parts of the medial (MAN) or cortical amygdaloid nuclei ath 21, 26 or 32 days of age. The effects of the different treatments on the onset of puberty were evaluated by recording the age at vaginal opening and first ovulation, the body weight on the day of vaginal opening, and the subsequent ovarian or vaginal cyclicity. The following conclusions may be drawn from the findings obtained: 1. At three weeks of age, the MCA exerts a gonadotropininhibiting function that is localized in the anterior part of the MAN. This activity is not demonstrable in older females. 2. The MAN, particularly its posterior part, may play an important role in the prepuberal maturation of the maturation of the neurohormonal ovulatory mechanisms that takes place in female rats during the fourth week of life. 3. The VHPC may be involved in the control of female sexual development mainly by its growth-stimulating activity. The results suggest an essential role of the subcortical limbic system in female sexual maturation and offer an explanation of contradictory findings on the gonadotrophin-controlling function of the MCA before puberty.
Amygdala↗
Studies on the puberty-controlling function of the mediocortical amygdala in the immature female rat.
The puberty-controlling function of the mediocortical amygdala in immature female rats was investigated by lesioning this region at different ages and by studying the effects on the onset of spontaneous and experimentally-induced precocious puberty. At 21 days of age, bilateral lesions in the anterior mediocortical amygdala (AMCA) caused precocious puberty and enhanced the puberty-accelerating effect of bilateral lesions produced simultaneously in the medial preoptic area (MPA). Similar lesions, ineffective on day 26, delayed the onset of puberty when produced on day 32 in otherwise untreated rats. Lesions in the posterior mediocortical amygdala (PMCA) at 26 or 32 days of age postponed puberty in untreated rats and inhibited the advancement of their 1st pubertal ovulation that resulted from damage to the ventromedial-arcuate region (VAH) or daily administration of 0.05 mug estradiol benzoate (EB) per 100 g b.w. The results confirm earlier findings of different gonadotropin-controlling activities of the AMCA and PMCA in immature female rats and suggest maturational changes in the function of both areas. The gonadotropin-inhibiting action exerted by the AMCA at 3 weeks of age is lost when puberty approaches; a gonadotropin-stimulating activity seems to develop in both the AMCA and PMCA.
Age Factors↗