Apamin and d-tubocurarine block the afterhyperpolarization of rat supraoptic neurosecretory neurons.
Magnocellular neurosecretory cells (MNCs) were impaled in perfused explants of rat hypothalamus. Evoked bursts of spikes were followed by an afterhyperpolarization (AHP) lasting 1-2 s. In each of 22 cells this AHP was selectively suppressed by low nanomolar concentrations of apamin (IC50 = 1.3 nM) or micromolar concentrations of d-tubocurarine (IC50 approximately 40 microM). Blockade of the AHP was accompanied by a decrease in spike accommodation and an unmasking of the late depolarizing afterpotential which induces burst firing in MNCs. Modulation of the Ca2+-dependent K+ (AHP) conductance by an endogenous apamin-like ligand could play an important role in the control of firing rate and pattern in MNCs.
M.R.C. Neuropharmacology Research Group, School of Pharmacy, University of London, U.K.
C W
CW
Bourque
D A
DA
Brown
D000200:Action Potentials / Q000187:drug effects; D000818:Animals; D001030:Apamin / Q000494:pharmacology*; D001514:Bee Venoms / Q000494:pharmacology*; D004594:Electrophysiology; D009474:Neurons / Q000187:drug effects / Q000502:physiology*; D009490:Neurosecretory Systems / Q000166:cytology / Q000187:drug effects / Q000502:physiology*; D009994:Osmolar Concentration; D011802:Quinidine / Q000494:pharmacology; D051381:Rats; D013495:Supraoptic Nucleus / Q000166:cytology / Q000187:drug effects / Q000502:physiology*; D014403:Tubocurarine / Q000494:pharmacology*
D001514:Bee Venoms; D001030:Apamin; D011802:Quinidine; D014403:Tubocurarine