APAMIN-SENSITIVE CA2-ACTIVATED K+ CHANNELS REGULATE PACEMAKER ACTIVITY IN NIGRAL DOPAMINE NEURONS()

MESENCEPHALIC dopamine-containing neurons exhibit a Ca2+-dependent osc illation in membrane potential believed to underlie the ability of the se cells to maintain spontaneous activity in the absence of afferent s ynaptic drive. In the present series of experiments, sharp electrode i ntracellular recording techniques were used in conjunction with an in vitro brain slice preparation to explore the ionic mechanisms underlyi ng rhythmogenesis in nigral dopamine neurons in the rat. Our results i ndicate that the K+ channel producing the prolonged post-spike afterhy perpolarization exhibited by these neurons is also principally respons ible for generating the falling phase of the autogenous pacemaker osci llation. Alterations in the expression of this conductance are associa ted with marked changes in neuronal firing pattern, indicating that mo dulation of ligand-gated Ca2+-activated K+ channels may constitute a f unctional means of altering temporal coding among the major mesotelenc ephalic dopamine systems.