Piracetam induces plasma membrane depolarization in rat brain synaptosomes.

Piracetam makes neurons more excitable by inducing neuronal membrane depolarization. It also states that it induces chloride efflux from the neuron. This is what leads to the depolarization, the clearing of the magnesium blockage, and the ability for the NMDA receptor channels to open and allow calcium into the neuron, causing cascading signals to be propagated.

The AMPA receptors are glutamate receptors that control the sodium/potassium channels, whereas the NMDA receptors control the channels that also allow calcium into the neuron. When a neuron is in a resting state, the charge of the membrane pulls positively charged magnesium molecules into the NMDA channels, which blocks them from allowing calcium into the cell. When the AMPA receptors are activated, they open to allow sodium and potassium into the cell. This changes the charge, and brings the neuron to excitability, allowing the magnesium blockage to clear. In a similar fashion, protein pumps can pump ions like calcium and chloride out of the cell. This also changes the charge of the cell, bringing it to excitability. Once the magnesium blockage has cleared, then glutamate can bind to the NMDA receptors and open the calcium channels and allow for CA^2+ to enter, instigating the cascading signal release I spoke to earlier. Then once the charge reaches the appropriate level again, the magnesium molecule blocks the channels again, and the process starts over.

This paper was stating that piracetam increased the membrane potential of the neuron by increasing the efflux of chloride from the cell. This allowed the neuron to depolarize quicker, and allow for faster firing.