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  • 5-Hydroxytryptophan  (1)
  • Carbamyl derivatives  (1)
  • 1
    Electronic Resource
    Electronic Resource
    Springer
    European journal of pediatrics 148 (1989), S. 540-542 
    ISSN: 1432-1076
    Keywords: Sodium benzoate ; Hyperammonaemia ; Carbamyl derivatives
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Sodium benzoate has been recommended for the treatment of hyperammonaemia in humans. However, benzoate potentiates ammonia toxicity and reduces urea synthesis in vitro and in vivo by decreasing the intramitochondrial levels of N-acetyl glutamate. Pretreatment of mice with carbamyl glutamate, a structural analogue of N-acetyl glutamate, decreases mortality induced by ammonium acetate and sodium benzoate administration. The protective effect of carbamyl glutamate is accompanied by an increase in urea production and of carbamyl phosphate synthetase activity.
    Type of Medium: Electronic Resource
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  • 2
    ISSN: 1432-2072
    Keywords: 5-Hydroxytryptophan ; Imipramine ; Brainstem auditory evoked response ; Middle latency auditory evoked response ; Rat
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The neurophysiological effects of acute and chronic treatment with the tricyclic antidepressant drug imipramine were investigated. Brainstem (BAER) and middle latency (MLR) auditory evoked responses were monitored in the alert and immobile rat. Daily injection of imipramine (10 mg/kg, IP) for 2 weeks produced a 13% increase in the latency and a 35% reduction in the amplitude of the N17 component of the MLR. Acute imipramine treatment had no effect. There was no observable change in the BAER after either acute or chronic drug administration. Serotonergic function was assessed by studying the inhibitory effects of 5-hydroxytryptophan on the BAER and MLR. Chronic application of imipramine caused an apparent reduction of the effects of 5-hydroxytryptophan (75 mg/kg, IP) on the N17 component of the MLR. This may, however, be due to the shift in baseline latency and amplitude. Inhibition of the BAER by 5-hydroxytryptophan was unaltered by long term exposure to imipramine. Acute treatment with imipramine was without effect on the modulation of the BAER and the MLR by 5-hydroxytryptophan. These results provide evidence that chronic, as opposed to acute, administration of imipramine had an inhibitory effect on auditory processing at the level of the MLR and that this may be associated with a change in the net output of the serotonergic system.
    Type of Medium: Electronic Resource
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