The effect of morphine on mammalian nerve fibres.
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Biomedical subjects
Publications and source records attributed to I Jurna.
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The effect of memantine (dimethylaminoadamantane), a new amantadinederivate with antiparknison-properties was investigated by the help of the sucrose gap method on sensory nerve fibres of the rat In normal Locke-solution memantine 10(-4) M reduced the amplitude of the compound action potential without change of the resting potential, increased the membrane resistance and depressed the repetitive activity elicited by depolarizing rectangular currents. The results of the experiments with changed concentrations of sodium, potassium and chloride ions in the suspensionmedium indicate that the membrane conductance of all three ions was reduced by memantine. Beside the antiparkinson properties these effects as well as those reported by others might be interpreted as a central muscle relaxing action of memantine. The possible implication of the demonstrated membrane effects of the drug is discussed in relation to its action on the dopaminergic transmission in the nigro-striatal system.
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The effect of morphine on the activity in ventrolateral tract axons was studied in intercollicularly decerebrate cats with and without spinal section. Activity was elicited by electrical stimulation of Adelta- and C-fibres in the sural nerves. In spinal animals, morphine injected intravenously in a dose as low as 0.5 mg/kg reduced the post-stimulus discharge of impulses recorded in ventrolateral tract axons below the site of transection. The depression was not only abolished but reversed by levallorphan and naloxone. Pretreatment with reserpine did not diminish the effect of morphine. The effect of morphine was considerably weaker in decerebrate cats. Reversible block of the spinal cord produced by cold revealed that morphine reduced inhibition from the brain stem controlling the impulse transmission to ventrolateral tract axons. It is concluded that a spinal effect contributes to the analgesic action of morphine.
The effect of dimethylaminoadamantane (DMAA), an amantadine derivative with an anti-Parkinson property, on rat sensory nerve fibres was studied with the sucrose gap method. DMAA 10(-4) M in normal Locke solution reduced the spike amplitude without changing the resting potential, increased the membrane resistance and depressed repetitive spike activity elicited by depolarizing currents. From experiments performed with changed concentrations of sodium, potassium, calcium and chloride ions in the suspension medium it appears that the permeability of sodium, potassium and chloride ions is reduced by DMAA. The possible implication of the membrane effects of the drug in its action on dopaminergic transmission in the brain is discussed.
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