作者: Shuichiro Kinoshita , Hiroki Yasuda , Nobuaki Taniguchi , Ritsuko Katoh-Semba , Hiroshi Hatanaka
DOI: 10.1523/JNEUROSCI.19-06-02122.1999
关键词:
摘要: Brain-derived neurotrophic factor (BDNF) is reported to enhance synaptic transmission and play a role in long-term potentiation hippocampus neocortex. If so, shortage or blockade of BDNF might lead another form plasticity, depression (LTD). To test this possibility elucidate mechanisms if it the case, EPSCs evoked by stimulation layer IV were recorded from II/III neurons visual cortical slices young rats whole-cell voltage-clamp mode. LTD was induced low-frequency (LFS) at 1 Hz for 10–15 min each pulse LFS paired with depolarization −30 mV but not their membrane potentials kept −70 mV. Such an blocked exogenously applied BDNF, probably through presynaptic mechanisms. Suppression endogenous activity anti-BDNF antibody inhibitor receptors made otherwise ineffective stimuli (LFS without postsynaptic depolarization) effective induction, suggesting that may prevent inputs inducing developing cortex.