Ketamine induces the expression of Ca²⁺-permeable AMPA receptors to enhance synaptic glutamatergic and Ca²⁺ activity in neurons to cause rapid antidepressant effects.

Neurons in the hypothalamus that promote satiety manifest plasticity of their response to the excitatory transmitter, glutamate, by re-organizing the composition of a specific glutamare receptor.

During parallel fibre activity in vivo, postsynaptic mGluR1 receptors in molecular layer interneurons of the cerebellar cortex are engaged in a frequency-dependent manner and in concert with inotropic glutamate receptors.

Excitotoxicity driven by NMDA receptor hyper-activation does not involve DAPK1-dependent events in vitro or in vivo, and previously described DAPK1-NMDAR disrupting peptides act by blocking the NMDA receptor.

Repression of the G protein-coupled chemokine receptor CCR5 enhances MAPK/CREB signaling, long-term potentiation, somatosensory cortical plasticity, and learning and memory, while CCR5 over-activation by viral proteins may contribute to HIV-associated cognitive deficits.