ABSTRACT
Antiamnesic activity of Noopept was studied on the original three-way model of conditioned passive avoidance response, which allows studying spatial component of memory. Cholinoceptor antagonists of both types (scopolamine and mecamylamine) decreased entry latency and reduced the probability for selection of the safe compartment. Noopept abolished the antiamnesic effect of cholinoceptor antagonists and improved spatial preference.
Subject(s)
Dipeptides/pharmacology , Memory Disorders/prevention & control , Memory/drug effects , Nootropic Agents/pharmacology , Animals , Cholinergic Agonists/metabolism , Cholinergic Agonists/pharmacology , Cholinergic Antagonists/metabolism , Cholinergic Antagonists/pharmacology , Male , Mecamylamine/metabolism , Mecamylamine/pharmacology , Nicotinic Antagonists/metabolism , Nicotinic Antagonists/pharmacology , Rats , Scopolamine/metabolism , Scopolamine/pharmacologyABSTRACT
Experiments on adult Wistar rats showed that injection of beta-amyloid25-35 (2 microg) into Meynert basal nuclei caused long-term memory deficiency which was detected 24 days after this injection by the memory trace retrieval in conditioned passive avoidance reflex (CPAR). The effects of noopept, an original nootropic and neuroprotective dipeptide, on the severity of this cognitive deficiency were studied. Preventive (for 7 days before the injury) intraperitoneal injections of noopept in a dose of 0.5 mg/kg completely prevented mnestic disorders under conditions of this model. Noopept exhibited a significant normalizing effect, if the treatment was started 15 days after the injury, when neurodegenerative changes in the basal nuclei, cortex, and hippocampus were still acutely pronounced. The mechanisms of this effect of the drug are studied, including, in addition to the choline-positive effect, its multicomponent neuroprotective effect and stimulation of production of antibodies to beta-amyloid25-35. Noopept efficiency in many models of Alzheimer disease, its high bioavailability and low toxicity suggest this dipeptide for further studies as a potential agent for the treatment of this condition (initial and moderate phases).
Subject(s)
Alzheimer Disease/drug therapy , Amyloid beta-Peptides/pharmacology , Basal Nucleus of Meynert/drug effects , Dipeptides/therapeutic use , Nootropic Agents/therapeutic use , Peptide Fragments/pharmacology , Alzheimer Disease/physiopathology , Amyloid beta-Peptides/administration & dosage , Animals , Basal Nucleus of Meynert/physiology , Disease Models, Animal , Humans , Male , Memory Disorders/prevention & control , Peptide Fragments/administration & dosage , Random Allocation , Rats , Rats, WistarABSTRACT
The effect of original nootropic preparation Noopept on learning and long-term memory was studied with BALB/c mice. Scopolamine (1 mg/kg) impaired long-term memory trace, while Noopept (0.5 mg/kg) had no significant effect. Noopept completely prevented the development of cognitive disorders induced by scopolamine (blockade of muscarinic cholinergic receptors). Our results confirmed the presence of choline-positive effect in dipeptide piracetam analogue Noopept on retrieval of learned skill of finding a submerged platform (spatial memory). We conclude that the effectiveness of this drug should be evaluated in patients with Alzheimer's disease.
