Perturbations in complex media, due to their own dynamical evolution or to external effects, are often seen as detrimental. Therefore, a common strategy, especially for telecommunication and imaging applications, is to limit the sensitivity to those perturbations in order to avoid them. Here, instead, we consider enhancing the interaction between light and perturbations to produce the largest change in the output intensity distribution.
View Article and Find Full Text PDFActivity-dependent modulations of N-methyl-D-aspartate glutamate receptor (NMDAR) trapping at synapses regulate excitatory neurotransmission and shape cognitive functions. Although NMDAR synaptic destabilization has been associated with severe neurological and psychiatric conditions, tuning NMDAR synaptic trapping to assess its clinical relevance for the treatment of brain conditions remains a challenge. Here, we report that ketamine (KET) and other clinically relevant NMDAR open channel blockers (OCBs) promote interactions between NMDAR and PDZ-domain-containing scaffolding proteins and enhance NMDAR trapping at synapses.
View Article and Find Full Text PDFAutoantibodies directed against the N-methyl-D-aspartate receptor (NMDAR-Ab) are pathogenic immunoglobulins detected in patients suffering from NMDAR encephalitis. NMDAR-Ab alter the receptor membrane trafficking, synaptic transmission and neuronal network properties, leading to neurological and psychiatric symptoms in patients. Patients often have very little neuronal damage but rapid and massive (treatment-responsive) brain dysfunctions related to an unknown early mechanism of NMDAR-Ab.
View Article and Find Full Text PDFThis publisher's note contains a correction to Opt. Lett.48, 6027 (2023)10.
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