The effects of various cognition-enhancing drugs on in vitro rat hippocampal synaptosomal sodium dependent high affinity choline uptake

MDL 26,479: a potential cognition enhancer with benzodiazepine inverse agonist‐like properties

“…It has been suggested that inverse agonists at the benzodiazepine receptor may enhance cognition because of their ability to selectively disinhibit cholinergic neurones in the basal forebrain (Sarter et al, 1988b;. Several studies (Shih & Pugsley, 1985;Spignoli et al, 1986;Nakahiro et al, 1988;Lorez et al, 1988) report that 'nootropic' drugs (e.g. pramiracetam, oxiracetam and pantoyl-GABA) stimulate cortical or hippocampal HACU after in vivo administration.…”

“…pramiracetam, oxiracetam and pantoyl-GABA) stimulate cortical or hippocampal HACU after in vivo administration. Benzodiazepine inverse agonists also have been reported to enhance cognition (Venault et al, 1986;Lorez et al, 1988;Sarter et al, 1988a;Sarter & Stecker, 1989) and these compounds stimulate HACU after in vivo drug treatment (Miller & Chmielewski, 1990 reported for several potential nootropic agents (Shih & Pugsley, 1985;Spignoli et al, 1986;Nakahiro et al, 1988) suggesting that this may be a common mechanism for cognition enhancement among a diverse number of compounds. (Bowen et al, 1976;Arendt et al, 1983 Several studies have demonstrated that drugs with cognition enhancing potential can enhance LTP in the hippocampus (Olpe & Lynch, 1982;Ito et al, 1988;Tanaka et al, 1989;Pugliese et al, 1990).…”

“…Several studies (Shih & Pugsley, 1985;Spignoli et al, 1986;Nakahiro et al, 1988;Lorez et al, 1988) report that 'nootropic' drugs (e.g. pramiracetam, oxiracetam and pantoyl-GABA) stimulate cortical or hippocampal HACU after in vivo administration.…”

Pyritinol facilitates the recovery of cortical cholinergic deficits caused by nucleus basalis lesions

“…These various drugs have demonstrated differing effects on brain acetylcholine levels, acetylcholine release (basal, induced), high affinity choline uptake activity, cGMP levels, muscarinic receptor functionality, etc. However, their cellular and the subcellular targets in the cholinergic system and in the cognitive process have not been well defined up to now (Greiner et al, 1988;Martin and Vyas, 1987;Martin and Widdowson, 1990;Pepeu and Spignoli, 1989;Pilch and M/,iller, 1988;Seyfried, 1989;Shih and Pugsley, 1985). Although pharmacological effects on other non cholinergic systems (monoaminergic, aminoacidergic, peptidergic) have been rejected (Greiner et al, 1988) or considered to be minimal (Pepeu and Spignoli, 1989), other trophic or regulatory effects have been postulated in relation to corticosteroids and other factors (Mondadori and Petshke, 1987) and to phospholipid/cholinergic system interactions (Martin and Widdowson, 1988;Gelbmann and Miiller, 1991).…”

In vitro Effect of <i>Ginkgo biloba</i> Extract (EGb 761) on the Activity of Presynaptic Cholinergic Nerve Terminals in Rat Hippocampus

“…a marker of the activity of presynaptic septohippocampal cholinergic nerve termi nals. A significant increase (e.g., 3,4-diaminopyridine, pramiracetam, oxiracetam, pyritinol, ginsenoside Rb| [12][13][14]), no change (e.g., piracetam, aniracctam, 4-aminopyridine [12,13]) and even a decrease of HACU levels after in vivo administration (centrophenoxine, tacrine [12,15]) have been reported. Cognition-enhancing prop erties of nootropic drugs with a direct effect on presynap tic cholinergic terminals (i.e.…”