Electrophysiological characterization of voltage-gated K(+) currents in cerebellar basket and purkinje cells: Kv1 and Kv3 channel subfamilies are present in basket cell nerve terminals.
To understand the processes underlying fast synaptic transmission in the mammalian CNS, we must have detailed knowledge of the identity, location, and physiology of the ion channels in the neuronal membrane. From labeling studies we can get clues regarding the distribution of ion channels, but electrophysiological methods are required to determine the importance of each ion channel in CNS transmission. Dendrotoxin-sensitive potassium channel subunits are highly concentrated in cerebellar basket cell nerve terminals, and we have previously shown that they are responsible for a significant fraction of the voltage-gated potassium current in this region. Here, we further investigate the characteristics and pharmacology of the voltage-dependent potassium currents in these inhibitory nerve terminals and compare these observations with those obtained from somatic recordings in basket and Purkinje cell soma regions. We find that alpha-DTX blocks basket cell nerve terminal currents and not somatic currents, and the IC(50) for alpha-DTX in basket cell terminals is 3.2 nM. There are at least two distinct types of potassium currents in the nerve terminal, a DTX-sensitive low-threshold component, and a second component that activates at much more positive voltages. Pharmacological experiments also reveal that nerve terminal potassium currents are also markedly reduced by 4-AP and TEA, with both high-sensitivity (micromolar) and low-sensitivity (millimolar) components present. We suggest that basket cell nerve terminals have potassium channels from both the Kv1 and Kv3 subfamilies, whereas somatic currents in basket cell and Purkinje cell bodies are more homogeneous.
Southan
A P
AP
Electrophysiology Group, Department of Biochemistry, Imperial College of Science, Technology and Medicine, London SW7 2AY, United Kingdom.
Robertson
B
B
D015761:4-Aminopyridine / Q000494:pharmacology; D000818:Animals; D001030:Apamin / Q000494:pharmacology; D001923:Brain Chemistry / Q000502:physiology; D018999:Charybdotoxin / Q000494:pharmacology; D004305:Dose-Response Relationship, Drug; D004546:Elapid Venoms / Q000494:pharmacology; D015640:Ion Channel Gating / Q000187:drug effects / Q000502:physiology*; D051662:Kv1.1 Potassium Channel; D051663:Kv1.2 Potassium Channel; D008297:Male; D008564:Membrane Potentials / Q000187:drug effects / Q000502:physiology; D051379:Mice; D008815:Mice, Inbred Strains; D009498:Neurotoxins / Q000494:pharmacology; D018408:Patch-Clamp Techniques; D015221:Potassium Channels / Q000502:physiology*; D024642:Potassium Channels, Voltage-Gated; D017729:Presynaptic Terminals / Q000737:chemistry / Q000502:physiology; D011689:Purkinje Cells / Q000737:chemistry* / Q000502:physiology*; D012604:Scorpion Venoms; D051670:Shaw Potassium Channels; D019789:Tetraethylammonium / Q000494:pharmacology
D004546:Elapid Venoms; C496947:Kcna1 protein, mouse; C496970:Kcna2 protein, mouse; D051663:Kv1.2 Potassium Channel; D009498:Neurotoxins; D015221:Potassium Channels; D024642:Potassium Channels, Voltage-Gated; D012604:Scorpion Venoms; D051670:Shaw Potassium Channels; D018999:Charybdotoxin; D051662:Kv1.1 Potassium Channel; D001030:Apamin; C077910:margatoxin; D019789:Tetraethylammonium; C020273:dendrotoxin; D015761:4-Aminopyridine