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  • 1
    Electronic Resource
    Electronic Resource
    Springer
    Experimental brain research 31 (1978), S. 499-510 
    ISSN: 1432-1106
    Keywords: Monosynaptic reflex ; Post-tetanic potentiation ; Post-tetanic depression ; Primary afferent depolarization
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The effect of simultaneous tetanization of two antagonist nerves on the post-tetanic potentiation (PTP) of a test reflex was studied in decerebrate unanesthetized spinal cats. The PTP of an extensor or flexor monosynaptic reflex decreased significantly after simultaneous tetanization of Group I afferents from antagonist nerves. The non-potentiated control monosynaptic reflex was not affected by the tetanus of an antagonist nerve. The latter finding suggests that the tetanic stimulation of the antagonist nerve alone does not cause longlasting effects onto the agonist system-neither at primary afferent nor at motoneuronal level. It was established that the PTP of the agonist monosynaptic reflex was inversely related to the post-tetanic excitability of the Ia primary afferent terminals of the agonist nerve. A strong primary afferent depolarization of the Ia fibers from the agonist occurred during (but not after) tetanization of the Group I afferents of an antagonist nerve. The prolonged excitability decrease caused by the agonist tetanus (and which parallels the PTP) was less pronounced after a combined tetanus to agonists and antagonists. It was therefore concluded that the process of antagonist post-tetanic modulation of PTP occurs at the primary afferent level resulting from an interaction of the antagonist tetanus with the development of the agonist PTP.
    Type of Medium: Electronic Resource
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  • 2
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    London : Periodicals Archive Online (PAO)
    The RUSI journal. 73 (1928:Feb./Nov.) 659 
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  • 3
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    London : Periodicals Archive Online (PAO)
    The RUSI journal. 73 (1928:Feb./Nov.) 30 
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  • 4
    ISSN: 1432-5233
    Keywords: Key words Cadmium ; Diabetes ; VEP ; TBARS ; Rat
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Fifty-two healthy male Swiss albino rats, aged three months, were used in this study. They were divided into four groups: control (c), diabetic (D), cadmium (Cd), and diabetic + Cd (D+Cd). A diabetic condition was induced in D and D + Cd groups by administration of alloxane (5 mg/100 g). After this treatment, Cd and D + Cd groups were injected intraperitoneally with CdCl2 (2 mg/kg week). At the end of the 2-month experimental period, flash visual evoked potentials (FVEPs) of the four groups were recorded with disk electrodes attached with electrode paste 0.5 cm in front of and behind the bregma. The mean latencies off the P1, N1, P2, N2 and P3 components were significantly prolonged in the diabetic group compared with the control group. The mean latencies of P3 in the D + Cd group and of P1 and P3 in the Cd group were longer than those of the control group. P2N2 amplitude of Cd and D + Cd groups were significantly increased compared with the control group. On the other hand, thiobarbituric acid-reactive substances (TBARS) were determined as an indicator of lipid peroxidation. Our data showed that Cd treatment and diabetic condition caused a significant increase of lipid peroxidation in kidney, brain, retina and lens.
    Type of Medium: Electronic Resource
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  • 5
    ISSN: 1432-0703
    Source: Springer Online Journal Archives 1860-2000
    Topics: Energy, Environment Protection, Nuclear Power Engineering , Medicine
    Notes: Abstract The aim of the study was to investigate the effect of 10 ppm sulfur dioxide (SO2) exposure on visual evoked potentials (VEPs), thiobarbituric acid reactive substances (TBARS), and the activities of Cu,Zn superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), and catalase (CAT) in diabetes mellitus. Forty healthy male albino rats, aged 3 months, were divided into four equal groups: control (C), sulfur dioxide + control (CSO2), diabetic (D), and sulfur dioxide + diabetic (DSO2) groups. Experimental diabetes mellitus was induced by IV injection of alloxane monohydrate in a dose of 50 mg/kg body weight. Ten ppm sulfur dioxide was administered to the animals of sulfur dioxide–exposed groups in an exposure chamber for 1 h/day × 7 days/week × 6 weeks while control and diabetic groups were exposed to filtered air in the same condition. SO2 exposure, though markedly decreasing retina CAT and GSH-Px activities, significantly increased retina Cu,Zn-SOD activity in the diabetic and nondiabetic groups. In contrast to SO2-related increase in the activity of Cu,Zn-SOD, decrease in GSH-Px activity was observed in the brain of those groups. Brain CAT activity was unaltered. SO2 exposure caused the significant elevation in brain TBARS levels of CSO2 and DSO2 groups, whereas only in the retina TBARS level of the CSO2 group. SO2 exposure caused the significant prolongations of P1, N1, P2, and P3 components of VEPs in the nondiabetic and all components of VEPs in the diabetic groups. SO2 exposure also resulted in significant amplitude reductions in both experimental groups.
    Type of Medium: Electronic Resource
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  • 6
    ISSN: 1432-0703
    Source: Springer Online Journal Archives 1860-2000
    Topics: Energy, Environment Protection, Nuclear Power Engineering , Medicine
    Notes: Abstract. The effect of sulfur dioxide (SO2) on somatosensory-evoked potentials (SEPs), thiobarbituric acid reactive substances (TBARS), and the activities of Cu,Zn-superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), and catalase (CAT) were investigated in young (3 months), middle-age (12 months), and old (24 months) Swiss male albino rats. Ten ppm SO2 was administrated to the animals of SO2 groups in an exposure chamber for 1 h/day × 7 days/week × 6 while control groups were exposed to filtered air in the same condition. SO2 exposure caused increased levels of brain Cu,Zn-SOD activity and decreased levels of brain GSH-Px activity in all experimental groups with respect to their corresponding control groups. Brain CAT activities were unaltered. Brain TBARS levels of all SO2-exposed groups were significantly increased in comparison with their respective control groups. The mean latencies of P1, P2, and N2 components in the older group were either significantly different from the young or from the middle-age groups. The mean latency of the N1 component in the older group and that of P1 and N1 in the middle-age group were significantly increased compared with the young group. SO2 exposure caused the prolongation of all components in the young group, whereas it affected only the P2 component in the middle-age group, but it did not result in any latency change in the older group in comparison with their corresponding control groups.
    Type of Medium: Electronic Resource
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