ProBDNF Dependence of LTD and Fear Extinction Learning in the Amygdala of Adult Mice.

Neurotrophins are secreted proteins that control survival, differentiation, and synaptic plasticity. While mature neurotrophins regulate these functions via tyrosine kinase signaling (Trk), uncleaved pro-neurotrophins bind preferentially to the p75 neurotrophin receptor (p75NTR) and often exert opposite effects to those of mature neurotrophins. In the amygdala, brain-derived neurotrophic factor (BDNF) enables long-term potentiation as well as fear and fear extinction learning.

Neurotrophin signalling in amygdala-dependent cued fear learning.

The amygdala is a central hub for fear learning assessed by Pavlovian fear conditioning. Indeed, the prevailing hypothesis that learning and memory are mediated by changes in synaptic strength was shown most convincingly at thalamic and cortical afferents to the lateral amygdala. The neurotrophin brain-derived neurotrophic factor (BDNF) is known to regulate synaptic plasticity and memory formation in many areas of the mammalian brain including the amygdala, where BDNF signalling via tropomyosin-related kinase B (TrkB) receptors is prominently involved in fear learning.

Pristine and hydrated fluoroapatite (0001).

The surface structure of fluoroapatite (0001) (FAp) under quasi-dry and humid conditions has been probed with surface X-ray diffraction (SXRD). Lateral and perpendicular atomic relaxations corresponding to the FAp termination before and after HO exposure and the location of the adsorbed water molecules have been determined from experimental analysis of the crystal truncation rod (CTR) intensities. The surface under dry conditions exhibits a bulk termination with relaxations in the outermost atomic layers.

Impact of Chronic BDNF Depletion on GABAergic Synaptic Transmission in the Lateral Amygdala.

Brain-derived neurotrophic factor (BDNF) has previously been shown to play an important role in glutamatergic synaptic plasticity in the amygdala, correlating with cued fear learning. While glutamatergic neurotransmission is facilitated by BDNF signaling in the amygdala, its mechanism of action at inhibitory synapses in this nucleus is far less understood. We therefore analyzed the impact of chronic BDNF depletion on GABA-mediated synaptic transmission in BDNF heterozygous knockout mice (BDNF).