Abstract
ErbB4 has emerged as a leading susceptibility gene for schizophrenia but the function of the ErbB4 receptor in the adult brain is unknown. Here, we show in the adult hippocampus that long-term potentiation (LTP) of transmission at Schaffer collateral CA1 synapses was markedly enhanced in mutant mice lacking ErbB4. Concordantly, LTP was enhanced by acutely blocking ErbB4 in wild-type animals, indicating that ErbB4 activity constitutively suppresses LTP. Moreover, increasing ErbB4 signaling further suppressed LTP. By contrast, altering ErbB4 activity did not affect basal synaptic transmission or short-term facilitation. Our findings suggest that cognitive deficits in schizophrenia may be a consequence of hyperfunction of ErbB4 signaling leading to suppressed glutamatergic synaptic plasticity, thus opening new approaches for the treatment of this disorder.
Original language | English (US) |
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Pages (from-to) | 139-143 |
Number of pages | 5 |
Journal | NeuroReport |
Volume | 19 |
Issue number | 2 |
DOIs | |
State | Published - Jan 2008 |
Externally published | Yes |
Keywords
- ErbB4
- Long-term potentiation
- Neuregulin
- Paired-pulse facilitation
- Schaffer collateral CA1 synapses
- Synaptic plasticity
- Theta burst stimulation
- Transgenic mouse
ASJC Scopus subject areas
- Neuroscience(all)