Apamin blocks the slow AHP in lamprey and delays termination of locomotor bursts.
The effects of apamin on the slow afterhyperpolarization (sAHP) in spinal neurones and on the frequency of rhythmic bursting during fictive locomotion were investigated in the lamprey spinal cord in vitro. Apamin, which is a selective blocker of a small conductance KCa channel responsible for the sAHP in many types of neurones, was also found to reduce the sAHP in lamprey neurones. The summation of the sAHP is considered to be an important burst terminating factor in the spinal locomotor network and thereby to regulate the frequency of fictive locomotion. In support of this view, apamin was found to reduce the frequency of rhythmic bursting during fictive locomotion induced by kainate and NMDA. Serotonin, which has previously been shown to reduce the sAHP and slow the rate of rhythmic bursting, may therefore act, at least in part, on apamin-sensitive KCa channels.
Hill
R
R
Nobel Institute for Neurophysiology, Karolinska Institutet, Stockholm, Sweden.
Matsushima
T
T
Schotland
J
J
Grillner
S
S
D000200:Action Potentials / Q000187:drug effects; D000818:Animals; D001030:Apamin / Q000494:pharmacology*; D066298:In Vitro Techniques; D007608:Kainic Acid / Q000494:pharmacology; D007798:Lampreys / Q000502:physiology*; D008124:Locomotion / Q000502:physiology*; D016202:N-Methylaspartate / Q000494:pharmacology; D009467:Neuromuscular Depolarizing Agents / Q000494:pharmacology*; D009474:Neurons / Q000187:drug effects*; D015221:Potassium Channels / Q000187:drug effects; D013116:Spinal Cord / Q000166:cytology / Q000187:drug effects / Q000502:physiology
D009467:Neuromuscular Depolarizing Agents; D015221:Potassium Channels; D001030:Apamin; D016202:N-Methylaspartate; D007608:Kainic Acid