Onset Of Hyperactivity Research Articles

Neonatal rotenone lesions cause onset of hyperactivity during juvenile and adulthood in the rat

Attention deficit hyperactivity disorder (ADHD) is characterized by behavioral and cognitive symptoms. Longitudinal studies demonstrated that the symptoms remains clinically significant for the majority of ADHD children into adulthood. Furthermore, a population-based birth cohort provided the initial evidence of adult ADHD that lacks a history of childhood ADHD. We previously demonstrated that neonatal exposure to bisphenol A, an environmental chemical caused hyperactivity in the juvenile. Here, we extend to examine other chemical such as rotenone, a dopaminergic toxins. Oral administration of rotenone (3mg/kg) into 5-day-old male Wistar rats significantly caused hyperactivity at adulthood (8∼11 weeks old; p<0.05). It was about 1.3∼1.4-fold more active in the nocturnal phase after administration of rotenone than control rats. Higher dose (16mg/kg) or repeated lower dose of rotenone (1mg/kg/day for 4days) caused hyperactivity in the juvenile. Furthermore, DNA array analyses showed that neonatal exposure to rotenone altered the levels of gene expression of several molecules related to apoptosis/cell cycle, ATPase, skeletal molecule, and glioma. Bivariate normal distribution analysis indicates no correlation in gene expression between a hyperactivity disorder model and a Parkinson’s disease model by rotenone.Thus, we demonstrate a rotenone models of ADHD whose onset varies during juvenile and adulthood.

Rapid down regulation of hippocampal adenosine receptors following brief anoxia

Adenosine A 1 receptors, as demonstrated by [ 3H]cyclohexyladenosine (CHA) binding to cryostat sections of the brain, were studied utilizing quantitative autoradiographic techniques. A brief period of global CNS anoxia resulted in the rapid and persistent down regulation of [ 3H]CHA binding sites in the hippocampus but not in the neocortex or striatum. The density of adenosine A 1 receptors in a given brain region has previously been shown to be a critical factor in determining the strength of the inhibitory action of adenosine. Since the down regulation of these sites is correlated temporally with the onset of hyperactivity following transient anoxia, it is suggested that a reduction in the strength of the neuromodulatory action of adenosine contributes to the postanoxic hyperactivity of CA1 pyramidal cells and perhaps to their selective vulnerability.

Comparative toxicity of cis-cypermethrin in rainbow trout, frog, mouse, and quail

The synthetic α-cyano-phenoxybenzyl-containing pyrethroid insecticides act on the CNS of vertebrates and show a species-selective toxicity in the order fish > amphibians ⪢ mammals > birds. Concentrations of [ 14C] cis-cypermethrin in the brains of representative members of each of these classes of chordates were measured at toxic signs (an onset of hyperactivity followed by seizures and loss of balance/equilibrium) as an indicator of target organ sensitivity. The concentration of cis-cypermethrin in brain, associated with toxic signs, in micrograms per gram (mean ± SE) as determined by high-performance liquid chromatography was 0.08 ± 0.03 (frog), 0.23 ± 0.05 (trout), 1.71 ± 0.33 (mouse), and 3.94 ± 0.88 (quail). Trout brain was equally sensitive to the cis and trans isomers of cypermethrin. In both mouse and quail, some 90% of the radioactivity in the brain was parent pyrethroid. Trout and frog, however, afforded only 56 and 32%, respectively, of the brain 14C as cypermethrin, with the remaining radioactivity in both extractable and no-nextractable metabolites, including 4′-hydroxy- cis-cypermethrin, which is potentially neuroactive. Following oral administration, cis-cypermethrin was readily absorbed and metabolized by quail. Intestinal uptake was far less rapid in trout and mouse, with unchanged cypermethrin dispersed in secreted bile, being readily eliminated from the intestines of fish. The uptake and metabolism of cis-cypermethrin and the brain sensitivities of these animals to the pyrethroid account for the observed differences in acute toxicity.

Development of locomotor activity of rat pups exposed to heavy metals

Cadmium (Cd), triethyltin (TET), and trimethyltin (TMT) are heavy metals which are neurotoxic to developing animals. In the present experiment, preweaning assessment of locomotor activity was used to detect and differentiate between the developmental toxicity of these metals. On postnatal day (PND) 5, rat pups received a single injection of either Cd, TET, or TMT. A within-litter design was used for dosing; 1 male and 1 female pup from each litter (N = 10 litters/compound) received either the vehicle, low, medium, or high dosage of the compound. Preweaning motor activity was assessed in 30-min sessions in figure-eight mazes from PND 13 to 21. Motor activity of control animals progressively increased in the initial days of testing, and then both within-session and between-session habituation developed. A single exposure to Cd, TET, and TMT produced hyperactivity by the end of the preweaning period but these metals differed in the day of peak activity, the onset of hyperactivity, and the development of habituation.

Glutathione and non-protein sulfhydryl in cerebral cortex and lung in mice exposed to high oxygen pressure

Mice were exposed to 6 atm of 100% O 2, and killed at the onset of hyperactivity, convulsions, and 10(s) post convulsions. Examination of brain cortex from mice killed at these stages of O 2 toxicity revealed no change in oxidized glutathione (GSSG), non-protein sulfhydryls (NPSH), total glutathione (GSH + GSSG), the GSH/GSSG ratio, glutathione reductase and glutathione peroxidase. Mice exposed to 4 atm for 1 h or 6 atm for 16 min exhibited a 36% and 33% decrease in lung NPSH respectively, but no change in cortical NPSH was observed. Although intraventricular diethylmaleate (DEM) decreased cerebral NPSH 72%, no change in the susceptibility of mice to O 2 convulsions was found. Disulfiram, an effective O 2 convulsive protectant had no effect on either cortical NPSH or total glutathione.

Effects of DDT on oxygen consumption of Rhodnius prolixus Stål.

When fasting fifth-instar larvae of Rhodnius prolixus Stål were poisoned with a lethal dose of DDT, the rate of oxygen consumption increased from the onset of hyperactivity, reached a marked peak shortly after knockdown, and then declined. For some days after the peak the oxygen consumption was markedly in excess of that prior to poisoning with DDT. Eventually, the oxygen consumption fell below the pre-teatment value and continued at this low level for some days, although the insect was then undoubtedly dead and in one case had been bisected. There was no marked discontinuity in the declining phase of oxygen consumption and therefore there is no indication of when death occurred. It is concluded that the time of death in DDT-poisoned larvae of Rhodnius cannot be determined by measurements of oxygen consumption.The total oxygen consumed from poisoning until death was always less than that consumed in the normal use of all metabolic reserves by the fasting insect, and these experiments do not support the hypothesis that death in DDT poisoning is due to total exhaustion of metabolic reserves. However, it is pointed out that, in Rhodnius, some of the metabolic reserves are contained in the undigested residue of the blood-meal and in the massive endocuticle and that there is no reason to think that either digestion of the remaining blood-meal or resorption of the endocuticle could be speeded up during DDT poisoning. Hence there is a strong possibility that, in DDT-killed Rhodnius, death is brought about by exhaustion of the available reserves.The peak rate of oxygen consumption during poisoning was greatest in very recently fed larvae and decreased as the interval between moulting and DDT-treatment was increased. This suggests that knockdown occurs when the fuel demands of the DDT-induced activity exceed the rate at which the fuel can be mobilised from the metabolic reserves.