Journal
NEUROREPORT
Volume 19, Issue 2, Pages 139-143Publisher
LIPPINCOTT WILLIAMS & WILKINS
DOI: 10.1097/WNR.0b013e3282f3da10
Keywords
ErbB4; long-term potentiation; neuregulin; paired-pulse facilitation; Schaffer collateral CAI synapses; synaptic plasticity; theta burst stimulation; transgenic mouse
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Funding
- Canadian Institutes of Health Research [12682-5] Funding Source: Medline
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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 CAI 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 LTR 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.
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