The effect of dimethylaminoadamantane on neuronal membranes.
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.
D000547:Amantadine / Q000031:analogs & derivatives*; D000818:Animals; D002118:Calcium / Q000494:pharmacology; D002462:Cell Membrane / Q000187:drug effects / Q000502:physiology; D002463:Cell Membrane Permeability / Q000187:drug effects; D002712:Chlorides / Q000494:pharmacology; D004558:Electric Stimulation; D005071:Evoked Potentials / Q000187:drug effects; D066298:In Vitro Techniques; D008559:Memantine / Q000494:pharmacology*; D009474:Neurons / Q000187:drug effects* / Q000502:physiology / Q000648:ultrastructure; D009994:Osmolar Concentration; D011188:Potassium / Q000494:pharmacology; D051381:Rats; D011984:Sensory Receptor Cells / Q000187:drug effects; D012964:Sodium / Q000494:pharmacology / Q000502:physiology; D013126:Spinal Nerve Roots / Q000502:physiology
D002712:Chlorides; D012964:Sodium; D000547:Amantadine; D011188:Potassium; D002118:Calcium; D008559:Memantine