Time-Resolved IR Spectroscopy Reveals a Mechanism with TiO2 as a Reversible Electron Acceptor in a TiO2 - Re Catalyst CO2 Photoreduction System

Attaching the phosphonated molecular catalyst [Re$^{I}$Br(bpy)(CO)₃]⁰ to the wide-band gap semiconductor TiO₂ strongly enhances the rate of visible-light driven reduction of CO₂ to CO in dimethyl formamide (DMF) with triethanolamine (TEOA) as sacrificial electron donor. Herein, we show by transient mid-IR spectroscopy that the mechanism of catalyst photoreduction is initiated by ultrafast electron injection into TiO₂, followed by rapid (ps-ns) and sequential two-electron oxidation of TEOA that is coordinated to the Re center. The injected electrons can be stored in the conduction band (CB) of TiO₂ on a ms-s time scale, and we propose they lead to further reduction of the Re-catalyst and completion of the catalytic cycle. Thus, the excited Re catalyst gives away one electron and would eventually get three electrons back. The function of an electron reservoir would represent a role for TiO₂ in photo-catalytic CO₂ reduction that has previously not been considered. We propose that the increase in photocatalytic activity upon heterogenisation of the catalyst to TiO₂ is due to the slow charge recombination and the high oxidative power of the ReII species after electron injection, as compared to the excited MLCT state of the unbound Re catalyst or when immobilized on ZrO₂, which results in a more efficient reaction with TEOA.Knut and Alice Wallenberg Foundation, Swedish Energy Agency, Swedish Research Council, Austrian Christian Doppler Research Association, OMV Grou

Rapid-acting antidepressants and the regulation of TrkB neurotrophic signalling-Insights from ketamine, nitrous oxide, seizures and anaesthesia

Increased glutamatergic neurotransmission and synaptic plasticity in the prefrontal cortex have been associated with the rapid antidepressant effects of ketamine. Activation of BDNF (brain-derived neurotrophic factor) receptor TrkB is considered a key molecular event for antidepressant-induced functional and structural synaptic plasticity. Several mechanisms have been proposed to underlie ketamine's effects on TrkB, but much remains unclear. Notably, preliminary studies suggest that besides ketamine, nitrous oxide (N2O) can rapidly alleviate depressive symptoms. We have shown nitrous oxide to evoke TrkB signalling preferentially after the acute pharmacological effects have dissipated (ie after receptor disengagement), when slow delta frequency electroencephalogram (EEG) activity is up-regulated. Our findings also demonstrate that various anaesthetics and sedatives activate TrkB signalling, further highlighting the complex mechanisms underlying TrkB activation. We hypothesize that rapid-acting antidepressants share the ability to regulate TrkB signalling during homeostatically evoked slow-wave activity and that this mechanism is important for sustained antidepressant effects. Our observations urge the examination of rapid and sustained antidepressant effects beyond conventional receptor pharmacology by focusing on brain physiology and temporally distributed signalling patterns spanning both wake and sleep. Potential implications of this approach for the improvement of current therapies and discovery of novel antidepressants are discussed.Peer reviewe