Clonidine activates membrane potassium conductance in myenteric neurones

1 Intracellular recordings were made from neurones in the myenteric plexus of the ileum removed from guinea-pigs. The effects of clonidine and adrenaline on membrane potential and resistance were observed.2 Clonidine (100 pM-30 nM) caused a concentration-dependent membrane hyperpolarization associated with a fall in neurone input resistance.3 The amplitude of the clonidine hyperpolarization, but not the conductance increase, was greater in cells with lower resting potentials and smaller in more polarized neurones. In a given cell, membrane hyperpolarization decreased and membrane depolarization increased the clonidine effect.4 Low potassium solutions enhanced and high potassium solutions reduced the hyperpolarizing action of clonidine but did not significantly change the conductance increase caused by clonidine.5 The concentration-effect curve for clonidine was displaced to the left when the extracellular calcium concentration was reduced. Conversely, clonidine was almost ineffective in elevated calcium concentrations. This was true for both the hyperpolarization and the conductance increase.6 It is suggested that clonidine activates a potassium conductance by causing an elevation in the free intracellular calcium concentration.7 Clonidine reversibly depressed the amplitude of the nicotinic fast excitatory postsynaptic potential and the noncholinergic slow excitatory postsynaptic potential.8 All the effects of clonidine were shared by adrenaline and the actions of both were reversed or prevented by phentolamine (100 nM-1 muM).