Details

Autor(en) / Beteiligte

• Berger, Thomas
• Senn, Walter
• Luscher, Hans-R

Titel

Hyperpolarization-Activated Current Ih Disconnects Somatic and Dendritic Spike Initiation Zones in Layer V Pyramidal Neurons

Ist Teil von

• Journal of neurophysiology, 2003-10, Vol.90 (4), p.2428-2437

Ort / Verlag

United States: Am Phys Soc

Erscheinungsjahr

2003

Quelle

MEDLINE

Beschreibungen/Notizen

• Institute of Physiology, University of Bern, CH-3012 Bern, Switzerland Submitted 16 April 2003; accepted in final form 4 June 2003 Layer V pyramidal cells of the somatosensory cortex operate with two spike initiation zones. Subthreshold depolarizations are strongly attenuated along the apical dendrite linking the somatic and distal dendritic spike initiation zones. Sodium action potentials, on the other hand, are actively back-propagating from the axon hillock into the apical tuft. There they can interact with local excitatory input leading to the generation of calcium action potentials. We investigated if and how back-propagating sodium action potentials alone, without concomitant excitatory dendritic input, can initiate calcium action potentials in the distal dendrite. In acute slices of the rat somatosensory cortex, layer V pyramidal cells were studied under current-clamp with simultaneous recordings from the soma and the apical dendrite. A train of four somatic action potentials had to reach high frequencies to induce calcium action potentials in the dendrite ("critical frequency," CF 100 Hz). Depolarization in the dendrite reduced the CF, while hyperpolarization increased it. The CF depended on the presence of the hyperpolarization-activated current I h : blockade with 20 µM 4-( N -ethyl- N -phenylamino)-1,2-dimethyl-6-(methylamino) pyridinium chloride (ZD7288) reduced the CF to 68% of control. If the neurons were stimulated with noisy current injections, leading to in-vivo-like irregular spiking, no calcium action potentials were induced in the dendrite. However, after I h channel blockade, calcium action potentials were frequently seen. These data suggest that I h prevents initiation of the dendritic calcium action potential by proximal input alone. Dendritic calcium action potentials may therefore represent a unique signature for coincident somatic and dendritic activation. Address for reprint requests and other correspondence: T. Berger, Institute of Physiology, University of Bern, Bühlplatz 5, CH-3012 Bern, Switzerland (E-mail: berger{at}pyl.unibe.ch ).