ketamine


Remember that ketamine blocks the NMDA receptor of some brain cells, which stops the cell from functioning as it normally would. In the case of a blocked NMDA receptor, there is a decrease in production of the neurotransmitter called gamma-aminobutyric acid (GABA). Ketamine also seems to influence the transmission of dopamine-another neurotransmitter. The neurotransmitter GABA tends to regulate brain cells by keeping the calm and functioning smoothly while dopamine is an excitatory neurotransmitter-it encourages brain cells to action.

So there are two things going on when you are on ketamine: a decrease in the calming influence of GABA and an increase of the excitatory effects of dopamine. Without GABA and with dopamine present, brain cells (neurons) become more active than normal.

Overactive cells heat up and produce waste in the form of free radicals. These effects occur within 15 minutes of being exposed to the drug. One of the ways that a cell deals with being overexcited is through the release of something called a heat shock protein-proteins that help turn an over-excited cell off so that it can recoup from the damage. If the source of the excitation is still present (i.e., the drug), there is a risk of cell death. At the same time, as ketamine is metabolized, any number of metabolites are produced-all of which can contribute to cell death.

The body hates dead cells and will mount an immune response as a result, sending in a variety of helper cells to consume the dead cell (creating the lesions). In animal studies, these effects were noted four hours after exposure to ketamine. Brain cells cannot regenerate-once they are gone, they are gone. There are two consequences worth thinking about here. The first is that this cell death is brain damage. Second, as the cells die that are affected by ketamine, you will need more of the drug to feel any effect. In the end, this means more product for less effect--and more brain damage.

back to the main ketamine articletop