BDNF restores impaired long-term potentiation of GABAergic synapses induced by chronic ethanol exposure in the VTA and attenuates reward-seeking behavior - PubMed
3 hours ago
- #BDNF
- #alcohol use disorder
- #GABAergic plasticity
- Chronic ethanol exposure impairs long-term potentiation (LTP) of GABAergic synapses in the VTA by reducing presynaptic GABA release.
- BDNF expression in the VTA is reduced by chronic ethanol exposure but recovers after 7 days of withdrawal.
- BDNF signaling through TrkB is necessary and sufficient for LTPGABA induction.
- BDNF application rescues impaired LTPGABA in VTA slices from chronic ethanol-exposed mice.
- In vivo, BDNF microinjection into the VTA restores hyperactive DA neuron activity and attenuates ethanol-seeking behavior.
- The effects of BDNF are dependent on TrkB activation and can be blocked by TrkB or GABAA receptor antagonists.
- BDNF-TrkB signaling is identified as a novel therapeutic target for alcohol use disorder (AUD).