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Depolarization potentials in mouse lateral septal nucleus neurons mediated by TRPC4‐like channels
Author(s) -
Tian JinBin,
Zhu Yingmin,
Lu Yungang,
Zhu Michael Xi
Publication year - 2012
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.26.1_supplement.1048.17
Subject(s) - depolarization , excitatory postsynaptic potential , neuroscience , plateau (mathematics) , electrophysiology , chemistry , patch clamp , biophysics , transient receptor potential channel , anatomy , biology , inhibitory postsynaptic potential , receptor , biochemistry , mathematical analysis , mathematics
The lateral septal nucleus (LSN) neurons express high levels of Canonical Transient Receptor Potential type 4 (TRPC4). In this study, we examined electrophysiological properties evoked by manipulations known to activate TRPC4 channels in LSN neurons from mouse brain slices using whole cell current clamp recordings. We show that: 1) pressure injection of (S)‐3,5‐DHPG to LSN neurons induced an instant burst firing on top of a prolonged depolarization plateau, 2) superfusion of the slice with DHPG caused membrane potential oscillations and repetitive burst firing of LSN neurons, 3) depolarization current injection increased the occurrence of depolarization plateau induced by DHPG and prolonged the plateau duration, 4) pretreatment of brain slices with pertussis toxin suppressed DHPG‐induced depolarization plateau in majority of the LSN neurons, 5) the DHPG‐induced depolarization plateau was blocked by a novel TRPC4 channel blocker, shown to be selective for TRPC4 and TRPC5 in heterologous expression systems, suggesting that the major component of the depolarization plateau is mediated by TRPC4 channels. These results demonstrate the involvement of TRPC4 channels in the integration of excitatory inputs of LSN neurons through metabotropic receptor and G protein signaling. Supported by NIH grant DK081654