Gabapentin (Neurontin) does all sorts of things, except for the one thing its inventors designed it to do, which is to act as a GABA-mimetic drug (hence the name). Although structurally similar to GABA, gabapentin shows no affinity for the main GABA receptor at normal concentrations. As I mentioned above, one of the things gabapentin does is bind to sites on the alpha subunit of the GABA receptor. Since these are the same sites that the benzodiazepines bind to, this makes gabapentin one of the best drugs for helping to taper off the benzodiazepines, as the sites formerly occupied by benzodiazepine molecules simply become occupied by gabapentin molecules instead. This also explains why gabapentin is addicting, since like the benzodiazepines, it is a positive allosteric modulator of the GABA receptor. However, gabapentin addiction is generally easier to deal with than benzodiazepine addiction. Unlike gabapentin, pregabalin (Lyrica) has no affinity for any sites on the GABA receptor.
Both gabapentin and pregabalin bind to the α2δ (alpha-2-delta) subunit of the voltage-dependent calcium channel in the central nervous system. Gabapentin blocks the action of substance P (SP) at the NK(1) receptor, thereby preventing SP from removing the magnesium block at the NMDA receptor. Pregabalin, however, directly decreases the release of SP, along with the neurotransmitters glutamate, norepinephrine, and calcitonin gene-related peptide. Both gabapentin and pregabalin are potassium channel openers.
So these two drugs have multiple, overlapping actions. The exact connection between these drugs' actions and their effects is not completely understood.