[quote]Rusty Barbell wrote:
I was just throwing the possibility out there. I’ve noticed piracetam to change the THC high a little bit (stronger). It seems to make alcohol more potent with stronger hangovers.
Also caffeine is supposedly enhanced (I noticed this when I first started the two but it has worn off). Just these three represent a fairly wide variety of drugs, so without real testing who is to say the effects of a benzo wouldn’t be changed also? Personally I stay away from benzos so I can’t say for sure.[/quote]
Not so farfetched, perhaps. A quick search brought up three abstracts of some interest, actually. Bushy can deconstruct these 
Psychopharmacology (Berl). 1983;81(4):332-34.
Facilitation of diazepam action by anticonvulsant agents against picrotoxin induced convulsions.
Kulkarni SK, Jog MV.
A subeffective dose (2 mg/kg) of diazepam produced only 50% protection against picrotoxin-induced (PTX) convulsions in rats. Simultaneous administration of GABA and other GABA-ergic substances such as piracetam and sodium valproate, which did not have any effect by themselves, [b]potentiated diazepam action[/b]. The onset of convulsions and mortality due to PTX were significantly delayed.
The other conventional anticonvulsants phenobarbitone, phenytoin and ethosuximide also enhanced the protective effect of diazepam. Inosine, a putative benzodiazepine ligand, also enhanced diazepam action.
These observations are explained on the basis of data from in vitro studies indicating that GABA-ergic agents and barbiturates enhance both the number of benzodiazepine binding sites and benzodiazepine binding.
The protective effect of clonidine, however, may be mediated by a different mechanism unrelated to the GABA-ergic system.
more recently -
Epilepsy Res. 2004 Feb;58(2-3):167-74.
Anticonvulsant effects of levetiracetam and levetiracetam-diazepam combinations in experimental status epilepticus.
Mazarati AM, Baldwin R, Klitgaard H, Matagne A, Wasterlain CG.
Department of Neurology, Geffen School of Medicine at UCLA.
Status epilepticus (SE) is a neurological emergency, with high mortality and high morbidity among survivors, and novel therapeutic agents are needed to improve this picture.
We examined the effects of the antiepileptic drug levetiracetam (LEV) in an experimental model of self-sustaining status epilepticus (SSSE), induced in rats by electrical stimulation of the perforant path.
LEV’s unique spectrum of anticonvulsant activity, very high therapeutic index, and neuroprotective properties, make it a potentially interesting agent in the treatment of SE. Pretreatment with LEV intravenously reduced (30 mg/kg) or prevented (50-1000 mg/kg) the development of self-sustaining seizures.
Treatment during the maintenance phase of SSSE diminished (at 200 mg/kg) or aborted seizures (in doses of 500 or 1000 mg/kg). Addition of LEV significantly enhanced the anticonvulsant effects of diazepam (DZP), even when both drugs where given in doses far below their therapeutic level. We conclude that LEV deserves further evaluation in the treatment of status epilepticus.
and finally, wrt the mechanics of a hypothetical racetam-diazepam, interaction -
Br J Pharmacol. 2004 Jun;142(3):594-608. Epub 2004 May 17.
Piracetam and TRH analogues antagonise inhibition by barbiturates, diazepam, melatonin and galanin of human erythrocyte D-glucose transport.
Naftalin RJ, Cunningham P, Afzal-Ahmed I.
Physiology Division, Centre for Vascular Biology and Medicine, King’s College London, Guy’s Campus, New Hunt’s House, London.
1 Nootropic drugs increase glucose uptake into anaesthetised brain and into Alzheimer’s diseased brain. Thyrotropin-releasing hormone, TRH, which has a chemical structure similar to nootropics increases cerebellar uptake of glucose in murine rolling ataxia.
This paper shows that nootropic drugs like piracetam (2-oxo 1 pyrrolidine acetamide) and levetiracetam and neuropeptides like TRH antagonise the inhibition of glucose transport by barbiturates, diazepam, melatonin and endogenous neuropeptide galanin in human erythrocytes in vitro.
2 The potencies of nootropic drugs in opposing scopolamine-induced memory loss correlate with their potencies in antagonising pentobarbital inhibition of erythrocyte glucose transport in vitro (P<0.01).
Less potent nootropics, D-levetiracetam and D-pyroglutamate, have higher antagonist Ki’s against pentobarbital inhibition of glucose transport than more potent L-stereoisomers (P<0.001).
3 Piracetam and TRH have no direct effects on net glucose transport, but competitively antagonise hypnotic drug inhibition of glucose transport. Other nootropics, like aniracetam and levetiracetam, while antagonising pentobarbital action, also inhibit glucose transport.
Analeptics like bemigride and methamphetamine are more potent inhibitors of glucose transport than antagonists of hypnotic action on glucose transport.
4 There are similarities between amino-acid sequences in human glucose transport protein isoform 1 (GLUT1) and the benzodiazepine-binding domains of GABAA (gamma amino butyric acid) receptor subunits. Mapped on a 3D template of GLUT1, these homologies suggest that the site of diazepam and piracetam interaction is a pocket outside the central hydrophilic pore region.
5 Nootropic pyrrolidone antagonism of hypnotic drug inhibition of glucose transport in vitro may be an analogue of TRH antagonism of galanin-induced narcosis.
