Naunyn-Schmiedeberg's Archives of Pharmacology

, Volume 332, Issue 3, pp 230–235 | Cite as

Endplate channel actions of a hemicholinium-3 analog, DMAE

  • Karim A. Alkadhi
Original Articles


The effect of the hemicholium-3 analog, DMAE, on endplate currents (EPC) was investigated in the transected cutaneous pectoris muscle of the frog using a conventional two-microelectrode voltage clamp. At a low concentration (5 μM), DMAE produced a long-lasting decrease in the rate constant of decay (α) and an increase in the peak current amplitude (Ip). At higher concentrations (10–100 μM), DMAE produced biphasic changes characterized by a transient, marked decrease of α and increase of Ip followed by a long-lasting marked increase of α and decrease of Ip. When DMAE was removed from the bath recovery from block was asymmetrical in that α recovered more quickly than did Ip. Pretreatment with neostigmine or collagenase partially antagonized the initial effects without affecting the steady state effects of DMAE, indicating that the initial effects of DMAE may be, at least in part, due to inhibition of the enzyme acetylcholinesterase. The drug reverses the normal voltage dependence of α without altering the single exponential nature of decay of the EPC. The inward EPC was more markedly blocked than outward EPC, resulting in a highly non-linear current-voltage relation with Ip decreasing with increasing hyperpolarization. This effect may indicate that DMAE causes a voltage-dependent block of closed acetylcholine-activated ion channels.

Key words

Neuromuscular junction Voltage clamp Neostigmine Prejunctional effect Anticholinesterase effect Endplate current 


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Copyright information

© Springer-Verlag 1986

Authors and Affiliations

  • Karim A. Alkadhi
    • 1
  1. 1.Department of PharmacologyUniversity of HoustonHoustonUSA

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