CSB332H1 Lecture Notes - Lecture 15: Default Mode Network, Eef2, Prefrontal Cortex
Document Summary
Recap: ketamine has been found to induce very fast anti-dep effects: associated with rapid synaptic genesis, particularly in prefrontal cortex, mediated by mtor -> increase in translation. Argument by one paper: found diff effects of ketamine: weren"t able to replicate the activation of mtor by ketamine, this protein is called eef2 -> a kinase is important in translational machinery. Found phosphorylation of another protein in the hippocampus -> responsible for memory and motor processing. The action of ketamine is independent of mtor. Ketamine eventually leads downstream to the phosphorylation of this kinase -> inhibit this activity -> inhibiting protein synthesis. We know ketamine is an nmdar receptor antagonist so what ketamine does is it blocks nmdar activity -> reducing ca influx -> series of biochemical pathways leading to phosphorylation of the protein kinase. This transmission is via electrophysio process that is independent of ap firing in the pre synaptic neuron.