| Rapid onset | Receptor density on neuronal surfaces decreases by 40-60% within 2 hours of antibody exposure[@chen2020] |
| Subunit specificity | Only GluN1-containing receptors are affected; GluN1/GluN2B heteromers are preferentially lost over GluN1/GluN2A[@chen2020] |
| Recovery timecourse | Receptor density returns to baseline within 24-48 hours after antibody removal in vitro, consistent with the clinical observation that early treatment leads to faster recovery[@hughes2010] |
| Functional consequences | The loss of surface NMDARs reduces synaptic NMDAR-mediated currents, impairing calcium influx and downstream signaling cascades essential for synaptic plasticity[@badran2022] |
| CA1 pyramidal neuron hyperexcitability | Paradoxical increase in firing rates due to disinhibition when NMDAR-mediated excitation is reduced |
| Inhibitory interneuron vulnerability | Interneurons expressing parvalbumin may be particularly affected, contributing to circuit-level dysfunction |
| Astrocyte reactivity | Astrocyte-mediated glutamate reuptake is impaired, contributing to excitotoxic stress[@malter2023] |
| Microglial activation | Microglia activation in the hippocampus correlates with cognitive impairment severity[@malter2023] |
| Databases | OMIMOrphanetClinicalTrialsPubMed |
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