Hi Dan
A typical example would be:
Elinor Ben-Menachem - Pregabalin Pharmacology and Its Relevance to Clinical Practice - Epilepsia -Volume 45, Issue Supplement s6, pages 13–18, August 2004 - Article first published online: 17 AUG 2004
“Pregabalin has no effect on GABAergic mechanisms
Evidence suggests that pregabalin, although structurally related to GABA, is not functionally related, and as such does not act via the GABAergic system. Pregabalin itself is inactive at GABAA, GABAB, and benzodiazepine receptors, and is not converted metabolically into GABA or a GABA agonist (5–7). In addition, clinically effective concentrations of pregabalin have no effect on GABA uptake or degradation. Furthermore, experiments conducted in the rat forebrain and in the rat optic nerve demonstrate that pregabalin does not elevate GABA levels acutely in these tissues (15).
A non-GABAergic mechanism of action for pregabalin could have important clinical implications. First, it is possible that a drug that influences brain excitability by a different mechanism may be effective in patients who are resistant to existing AEDs with a more traditional mechanism involving GABAergic transmission. Second, lack of interaction with GABAergic systems, particularly its failure to elevate GABA levels in the optic nerve, may explain why pregabalin exhibits no retinal or optic nerve toxicity (16)”.
I have seen the following information on secondary sites such as Drugs Forum, but I can't find any journal articles that back it up, so I have to regard it as suspect:
“Pregabalin increases the activity of the glutamic acid decarboxylase enzyme; which converts glutamate into GABA, so GABA concentrations increase. Continued application of pregabalin use increases the concentration of GABA transporter proteins, which increases the rate of GABA transport.”