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  • 1
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Short (5 days)-to long-term (4 months) corticosterone (CORT) administration by injection, pellet implantation, or in the drinking water decreased glial fibrillary acidic protein (GFAP) by 20–40% in hippocampus and cortex of intact rats. In contrast to CORT, adrenalectomy (ADX) caused elevations (50–125%) in hippocampus and cortex GFAP within 12 days of surgery that persisted for at least 4 months. CORT replacement of ADX rats decreased GFAP amount in hippocampus and cortex. The effects of long-term CORT and ADX on GFAP in hippocampus and cortex were also seen in striatum, midbrain, and cerebellum, findings suggestive of brain-wide adrenal steroid regulation of this astrocyte protein. The changes in GFAP amount due to CORT and ADX were paralleled by changes in GFAP mRNA, indicating a possible transcriptional or at least genomic effect of adrenal steroids. Glucocorticoid regulation of GFAP was relatively specific; it could not be generalized to other astrocyte proteins or other major structural proteins of neurons. The negative regulation of GFAP and GFAP mRNA by adrenal steroids suggested that increases in GFAP that result from brain injury may be attenuated by glucocorticoids. However, chronic CORT treatment of intact rats did not reverse or reduce the large increases in GFAP caused by trauma-or toxicant-induced brain damage. Thus, glucocorticoids and injury appear to regulate the expression of GFAP through different mechanisms. In contrast to the lack of effects of CORT on brain damage-induced increases in GFAP, CORT treatment begun in 2-week ADX rats, after an increase in GFAP had time to occur, did reverse the ADX-induced increase in GFAP. These results suggest that the increase in GFAP resulting from ADX is not mediated through an injury-linked mechanism.
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  • 2
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Abstract: The effect of a single oral 750 mg/kg dose of tri-o-cresyl phosphate (TOCP) on the endogenous phosphorylation of brain and spinal cord proteins was assessed in hens during the development of and recovery from delayed neurotoxicity. Crude membrane and cytosolic fractions were prepared from the brains and spinal cords of control and TOCP-treated hens at 1, 7, 14, 21, 35, and 55 days after treatment. Brain and spinal cord protein phosphorylation with [γ-32P]ATP was analyzed by sodium dodecyl sulfate-polyacrylamide gel electrophoresis (SDS-PAGE), autoradiography, and microdensitometry. TOCP administration conferred calcium and calmodulin dependence on the phosphorylation of a few brain cytosolic proteins and caused an increase in the phosphorylation of a number of other cytosolic and membrane proteins. This effect of TOCP was large in magnitude, and its time course reflected the onset of and recovery from the signs of ataxia and paralysis associated with delayed neurotoxicity in the hen. The molecular weights (Mr) and maximal phosphorylation (percent of control) for the most prominently affected bands were as follows: brain cytosol—50K (183%), 55K (575%), 60K (529%), 65K (273%), and 70K (548%); brain membranes—50K (622%) and 60K (697%); and spinal cord cytosol—20K (182%). The role of endogenous phosphorylation reactions in and their potential usefulness as biochemical indicators of delayed neurotoxicity are being explored further.
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  • 3
    ISSN: 1440-1681
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: 1. Diets enriched with n-3 polyunsaturated fish oils, predominantly eicosapen-taenoic acid, are associated with a lower risk of atherosclerotic vascular disease. These oils purportedly reduce plasma triglycerides, total cholesterol and impair platelet aggregation. Recently, the present authors reported that rats fed a marine oil-enriched diet had significantly reduced levels of lyso-PAF, the immediate precursor of platelet-activating factor (PAF). As PAF has potent vasodilator and pro-aggregatory properties, the purpose of this study was to examine the hypothesis that fish oils affect the biosynthesis of PAF in man.2. Supplementation of a normal diet for 3 weeks with fish oil containing the equivalent of 2.7 g of eicosapentaenoic acid daily, increased the eicosapentaenoic acid content of platelet phospholipids as well as depleting the arachidonic acid. Platelet aggregation to PAF (measured in whole blood by impedance aggregometry) was significantly impaired and whole blood thromboxane suppressed.3. Two weeks after ceasing supplements, platelet aggregation remained impaired although thromboxane had reverted to baseline levels. There was a transient but significant fall in whole blood lyso-PAF apparent within 2 days of commencing supplements but returning to baseline levels by the end of the treatment period. Whole blood PAF followed a similar trend.4. The effects of dietary fish oil on whole blood aggregations to PAF, on thromboxane and plasma lyso-PAF levels may be relevant to the prevention of vascular disease and the treatment of disorders in which PAF could be an inflammatory mediator.
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  • 4
    Electronic Resource
    Electronic Resource
    Oxford, UK : Blackwell Publishing Ltd
    Addiction 90 (1995), S. 0 
    ISSN: 1360-0443
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine , Psychology
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  • 5
    ISSN: 1360-0443
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine , Psychology
    Notes: Nitrous oxide is commonly used (abused) recreationally by inhaling it in a bolus form (i.e. single or several breaths). The time course of the psychoactive effects of nitrous oxide, via this mode of inhalation, has not been adequately characterized and thus formed the basis for this study. Twelve healthy volunteers participated in four sessions, using a randomized, cross-over, placebo-controlled design. In each session one of the following four measures were assessed: self-reported strength of drug effects, mood, memory and psyckomotor performance. Within sessions, subjects were exposed to four different concentrations of nitrous oxide in a randomized fashion: 0% (oxygen-placebo), 40%, 60% and 80%. At each concentration, or “trial”, subjects took four deep breaths of the gas. Peak drug effects, as reported by our subjects, occurred within 30 seconds after the last inhalation of nitrous oxide, persisted for about a minute, and then gradually subsided to near-baseline levels by 5 minutes post-inhalation. Certain aspects of mood were briefly affected by nitrous oxide, generally in a dose-related fashion with increases in visual analog scale ratings of “anxious”, “stimulated”, “coasting (spaced out)”, “lightheaded”, “confused”, and “high”. Free recall of words that had been presented between 30 and 60 seconds post-inhalation was significantly reduced after 80% nitrous oxide, relative to oxygen-placebo. There was a trend towards psychomotor impairment (Concentration x time: p – 0.08), as measured by the Digit Symbol Substitution Test, with peak decrements in performance (about a minute after inhalation) being greater after 80% nitrous oxide than after 0% nitrous oxide. Our results suggest that there arc acute, albeit brief, adverse effects of inhaling bolus concentrations of nitrous oxide.
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  • 6
    ISSN: 1369-1600
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Repeated exposure to psychostimulant drugs such as d-methamphetamine (d-METH) and cocaine can be associated with extremely long-lived changes in dopamine systems at the behavioral, cellular and molecular level. Sensitization or an enhanced response to drug exposure is one such change. Investigations of these phenomena at the cellular and molecular levels are being conducted in the hope that this will aid in understanding how such adaptations might contribute to drug addition. Repeated exposure to certain amphetamines can also result in damage to dopaminergic pathways. Although some of the same molecular adaptations and mechanisms are suspected to occur or play a role in the neurotoxic sequelae associated with psychostimulant exposure, there has been little attempt to examine the relationship among these phenomena. Here we utilized C57BL/6J female mice to examine whether exposure to a sensitizing regimen of d-METH would impact the degree of neural injury induced by a subsequent exposure to a neurotoxic regimen of the same psychostimulant. Every other day exposure to d-METH (1.0 or 2.0 mg/kg) for 11 days produced a behavioral sensitization, as evidenced by a significant increase in the degree of locomotor activity induced by each subsequent exposure to d-METH. Following a 5-day period of no drug exposure sensitized mice were given a neurotoxic regiment of d-METH (a total of four injections of 10.0 mg/kg, one every 2 hours) and striatal tissue examined 72 hours later. All groups, whether drug-naive or sensitized previously to d-METH, showed exactly the same degree of dopaminergic striatal damage induced by a neurotoxic regimen. This was evidenced by equivalent reductions in dopamine and elevations in GFAP protein, a marker of astrocytic response to injury, GFAP. The inability of a sensitizing regimen to either exacerbate or lessen the neurotoxic actions of the same compound suggests that the molecular and cellular control of these two aspects of psychostimulant exposure may differ.
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  • 7
    ISSN: 1369-1600
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Specific protein phosphorylation pathways have been shown to play a role in cellular adaptation responses underlying addiction to psychostimulants such as methamphetamine and cocaine. Transcriptional regulation through fos-related antigens constitutes one element through which these dopaminergic agonists exert their persistent actions. In addition to their addictive properties, amphetamines are known to damage dopaminergic nerve terminals. Although not widely appreciated, protein phosphorylation cascades and fos-related antigens also may play a role in the neurotoxic actions of substituted amphetamines such as methamphetamine. Here we document the involvement of the dopaminoceptive phosphoprotein, DARPP-32, the fos-related antigen, FRA-2, and the growth associated protein kinase, MAP kinase, in the neurotoxic action of known dopaminergic neurotoxicants, including methamphetamine. The addictive and neurotoxic properties of psychostimulants may share some molecular signaling mechanisms.
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  • 8
    ISSN: 1440-1681
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: 1. Groups of mice interacting socially in complex population cages become hypertensive. Some also develop fatal chronic tubulointerstitial nephritis.2. Long-term administration of the cardioselective β-blocker metoprolol controls stress-induced elevation of plasma renin and adrenal tyrosine hydroxylase. It also normalizes blood pressure. Despite the effectiveness of this sympathetic blockade, the incidence of nephritis was not diminished.3. The fact that stress-induced increases of adrenal weight and plasma cortico-sterone persist during metoprolol treatment points to the independence of the pituitary-adrenal cortical system and its possible role in the aetiology of renal disease.
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  • 9
    Electronic Resource
    Electronic Resource
    Oxford, UK : Blackwell Publishing Ltd
    ISSN: 1440-1681
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: 1. Early research on blood volume as an independent parameter affecting kidney function took the approach that the sensors must be located in the most compliant, that is the reservoir portion, of the cardiovascular system. This encompasses the great veins and the cardiac atria.2. Small changes in volume were shown not to affect the compliance of this reservoir and messages from the atrial receptor network were shown to travel in the vagus nerve and to control urine volume by antidiuretic hormone.3. Although greatly affected by the water immersion stimulus, sodium excretion was not as dependent on vagus integrity. The ensuing search for the natriuretic arm of the blood volume mechanism persisted for the next 20 years.4. Finally, one aspect of the elusive natriuretic factor was found exactly where theory had suggested, namely the most distensible part of the system, in specialized granules in the cardiac atria.
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  • 10
    ISSN: 1440-1681
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: 1. This study investigates the effect of dietary eicosapentaenoic acid (EPA), in the form of ‘Max EPA’ fish oil, on leukotriene B4 (LTB4) production in ionophore-stimulated rat leukocytes. Male Wistar rats (200–250 g) were fed for 3 weeks on a synthetic chow supplemented with either 10% by weight Max EPA oil or a coconut oil/safflower oil mixture.2. The EPA-rich diet significantly increased the EPA content of leukocyte phospholipids and decreased the arachidonic acid level by 35% (P 〈 0.001) compared with the control diet.3. The concentration of leukotrienes in the ionophore (A23187) stimulated leukocytes was measured by reverse-phase HPLC using prostaglandin B2 as the internal standard. The EPA-supplemented diet caused a 50% decrease in LTB4 production (P 〈 0.001) and a concomitant increase in the formation of the biologically less active LTB5 compared with the control diet. The amount of LTB4 and LTB5 produced by stimulated leukocytes closely resembled the changes in arachidonic acid and EPA content of leukocyte phospholipids.4. Thromboxane B2 (TxB2) production in stimulated leukocytes from the EPA-fed animals was also decreased compared with the control group.5. Although the formation of platelet activating factor by stimulated leukocytes was not altered by dietary treatment, the ability of an EPA-rich diet to decrease LTB4 and TxB2 production suggests that these diets may attenuate leukocyte activity and have useful anti-inflammatory effects.
    Type of Medium: Electronic Resource
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