The pharmacology of the nootropics; new insights and new questions

Mondadori, Cesare

doi:10.1016/0166-4328(93)90145-g

Cited by 27 publications

(12 citation statements)

References 83 publications

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“…This attests to the involvement of hormonal mechanisms into the development of mnestic defects, which agrees with the hypothesis that individual variations in the nootropic effect of piracetam can be related to individual hormonal differences [10]. This work was supported by the Russian Humanitarian Scientific Foundation (grant No.…”

Section: Groupsupporting

confidence: 87%

Early Postnatal Effects of Noopept and Piracetam on Declarative and Procedural Memory of Adult Male and Female Rats

2005

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We studied the effect of a new nootropic dipeptide Noopept and reference nootropic preparation piracetam injected subcutaneously on days 8-20 of life on learning of alternative feeding response in a 6-arm-maze in male and female rats. Early postnatal administration of Noopept disturbed the dynamics of learning by parameters of declarative and procedural memory. Piracetam impaired learning by parameters of procedural, but not declarative memory (only in males). Both preparations decreased the ratio of successfully learned males (but not females). The observed effects were not associated with changes in locomotor activity.

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Section: Groupsupporting

confidence: 87%

Early Postnatal Effects of Noopept and Piracetam on Declarative and Procedural Memory of Adult Male and Female Rats

2005

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“…Even more surprising is the fact that the primary pharmacological sites of action of these substances are very heterogeneous. Among others, the list includes cholinergic agonists at the muscarinic and nicotinic receptors (1, 2); cholinesterase inhibitors such as physostigmine (3); calcium-channel blockers such as nimodipine (4); angiotensin-converting enzyme (ACE) inhibitors such as captopril (5); transmitters such as, e.g., norepinephrine (6); t-aminobutyric acid type B (GABAB) receptor blockers such as CGP 36742 (7); peptides such as vasopressin and corticotropin (8); glucose (9); and, not least, the large group of so-called nootropics including oxiracetam and piracetam (10,11). Despite their different primary sites of action, all of the above-mentioned substances have a similar effect in a simple one-trial passive avoidance task; if administered, e.g., 1 h before the learning trial, they improve the retention performance at retest 24 h later (12, 13).…”

mentioning

confidence: 99%

Delayed emergence of effects of memory-enhancing drugs: implications for the dynamics of long-term memory.

Mondadori

Hengerer

Ducret

et al. 1994

Proc. Natl. Acad. Sci. U.S.A.

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Many theories of memory polate that processing of information outlasts the earning situation and involves several different physiological substrates. If such physiologically distinct mecanism or stages of memory do in fact exist, they should be differentially affected by particular experimental manipulations. Accordingly, a selective improvement of the processes underlying short-term memory should be detectable only while the information is encoded in the shortterm mode, and a selective influence on long-term memory should be detectable only from the moment when memory is based on the long-term trace. Our comparative study of the time course of the effects of the cholinergic agonist arecoline, the -aminobutyric acid type B receptor antagonist CGP 36742, the angiotensin-converting enzyme inhibitor captopril, and the nootropic oxiracetam, four substances with completely different primary sites of action, show that the memoryenhancing effects consistently come into evidence no sooner than 16-24 h after the learning trial. On the one hand, this finding suggests that all these substances act by way of the same type of mechanism; on the other hand, it demonstrates that the substrate modulated by the compounds forms the basis of memory only after 16-24 h. From the observation that animals also show clear signs of retention during the first 16 h-i.e., before the effects of the substances are measurable-it can be inferred that retention during this time is mediated by other mechanisms that are not influenced by any of the substances.The group of preparations already found to display memoryenhancing effects in experimental learning situations is surprisingly large. Even more surprising is the fact that the primary pharmacological sites of action of these substances are very heterogeneous. Among others, the list includes cholinergic agonists at the muscarinic and nicotinic receptors (1, 2); cholinesterase inhibitors such as physostigmine (3); calcium-channel blockers such as nimodipine (4); angiotensin-converting enzyme (ACE) inhibitors such as captopril (5); transmitters such as, e.g., norepinephrine (6); t-aminobutyric acid type B (GABAB) receptor blockers such as CGP 36742 (7); peptides such as vasopressin and corticotropin (8); glucose (9); and, not least, the large group of so-called nootropics including oxiracetam and piracetam (10,11). Despite their different primary sites of action, all of the above-mentioned substances have a similar effect in a simple one-trial passive avoidance task; if administered, e.g., 1 h before the learning trial, they improve the retention performance at retest 24 h later (12, 13). At the time of retention testing, the changes induced by the substances have already been expressed at a stage generally reckoned to be in long-term memory, but it is not known when these changes occurred. Indeed, it is often implicitly assumed that the facilitatory effects occurred concomitantly with the initial learning itself, demonstrable at short retention intervals. By making a comparative study o...

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“…Numerous biochemical and electrophysiological effects of nootropics of the piracetam family suggest numerous targets of their action [10,12]. Voltage-dependent ion channels of the neuronal membrane responsible for the generation of nerve impulses can presumably be counted among these targets.…”

Section: Abstract: High-threshold Ca 2 § Channels; High-threshold K mentioning

confidence: 99%

Effects of the nootropics piracetam and GVS-111 on voltage-dependent ion channels of neuronal membranes

et al. 1996

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The effect of two nootropics, piracetam and N-phenylacetyI-L-prolylglycine ethyl ester , is studied by measuring high-threshold K+ and Ca 2 § currents in isolated snail neurons using a two-microelectrode patch-clamp technique. Piracetam and GVS-111 are shown to reduce the amplitude of both the K § and the Ca 2 § (to a lesser extent) current. The threshold concentrations for GVS-111 and piracetam are 10-9-10 .8 M and 1-5• -4 M, respectively. It is assumed that the antiamnestic effect of the nootropics is partially mediated by a blockade of ion channels of the neuronal membrane. Key Words: high-threshold Ca 2 § channels; high-threshold K § channels; nootropic drugs; snail neuronsNumerous biochemical and electrophysiological effects of nootropics of the piracetam family suggest numerous targets of their action [10,12]. Voltage-dependent ion channels of the neuronal membrane responsible for the generation of nerve impulses can presumably be counted among these targets. This assumption is based on the positive therapeutic effect of ion channel antagonists in cognitive disorders [12]. In light of this it is obviously very important to study the effect of nootropics on ion channel conductance. However, little is known about the effect of the drugs on ion currents in the neuronal membrane, there just being a few contradictory reports on the effect of piracetam nootropics on Ca 2 § channels. Both inhibitory [8,9,16]

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The pharmacology of the nootropics; new insights and new questions

Cited by 27 publications

References 83 publications

Early Postnatal Effects of Noopept and Piracetam on Declarative and Procedural Memory of Adult Male and Female Rats

Early Postnatal Effects of Noopept and Piracetam on Declarative and Procedural Memory of Adult Male and Female Rats

Delayed emergence of effects of memory-enhancing drugs: implications for the dynamics of long-term memory.

Effects of the nootropics piracetam and GVS-111 on voltage-dependent ion channels of neuronal membranes

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