Premium
Dendritic D‐type potassium currents inhibit the spike afterdepolarization in rat hippocampal CA1 pyramidal neurons
Author(s) -
Metz Alexia E.,
Spruston Nelson,
Martina Marco
Publication year - 2007
Publication title -
the journal of physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.802
H-Index - 240
eISSN - 1469-7793
pISSN - 0022-3751
DOI - 10.1113/jphysiol.2006.127068
Subject(s) - bursting , neuroscience , hippocampal formation , depolarization , afterdepolarization , soma , biophysics , pyramidal cell , apical dendrite , potassium channel , chemistry , patch clamp , dendritic spike , electrophysiology , biology , inhibitory postsynaptic potential , excitatory postsynaptic potential , repolarization
In CA1 pyramidal neurons, burst firing is correlated with hippocampally dependent behaviours and modulation of synaptic strength. One of the mechanisms underlying burst firing in these cells is the afterdepolarization (ADP) that follows each action potential. Previous work has shown that the ADP results from the interaction of several depolarizing and hyperpolarizing conductances located in the soma and the dendrites. By using patch‐clamp recordings from acute rat hippocampal slices we show that D‐type potassium current modulates the size of the ADP and the bursting of CA1 pyramidal neurons. Sensitivity to α‐dendrotoxin suggests that Kv1‐containing potassium channels mediate this current. Dual somato‐dendritic recording, outside‐out dendritic recordings, and focal application of dendrotoxin together indicate that the channels mediating this current are located in the apical dendrites. Thus, our data present evidence for a dendritic segregation of Kv1‐like channels in CA1 pyramidal neurons and identify a novel action for these channels, showing that they inhibit action potential bursting by restricting the size of the ADP.