title: [Role of functional state of neuronal mitochondria of cerebral cortex in mechanisms of nootropic activity of neuroprotectors in rats with alloxan hyperglycemia].
abstract: The influence of citicoline, phenylpiracetam, pentoxifylline and N-phenylacetyl-L-prolylglycine on cognitive processes and functional state of mitochondria in the neocortex of alloxan-diabetic rats has been studied. The drug effects on cognitive processes were assessed using passive avoidance tests in the dark-light camera. Latent period and the number of animals with amnesia skill on 6th and 20th days of drug administration were recorded. Functional status of mitochondria was assessed by mitochondrial pore opening and mitochondrial transmembrane potential (Y) on 20th day. It has been established that course administration of phenylpiracetam, citicoline and to a lesser extent N-phenylacetyl-L-prolylglycine, but not pentoxifylline, improves the processes of learning and storing conditional skill. At the same time, the nootropic activity of studied drugs was comparable to their effect on the functional state of mitochondria in neocortical neurons in rats with chronic hyperglycemia. According to mitoprotective activity (prevention of opening of mitochondrial cyclosporin-A-sensitive pores and restoration of mitochondrial transmembrane potential), the maximum potential was observed for citicoline and phenylpiracetam, and the minimum--for pentoxifylline. The results point out the importance of mitoprotective properties in nootropic effects of studied drugs.
authors.forename: V I
authors.initials: VI
authors.lastname: Zhiliuk
authors.forename: V I
authors.initials: VI
authors.lastname: Mamchur
authors.forename: S V
authors.initials: SV
authors.lastname: Pavlov
mesh_terms: D000496:Alloxan; D000647:Amnesia / Q000150:complications / Q000188:drug therapy / Q000503:physiopathology; D000818:Animals; D001362:Avoidance Learning / Q000187:drug effects; D002540:Cerebral Cortex / Q000187:drug effects* / Q000378:metabolism / Q000473:pathology; D003071:Cognition / Q000187:drug effects; D003566:Cytidine Diphosphate Choline / Q000494:pharmacology*; D003921:Diabetes Mellitus, Experimental / Q000150:complications / Q000188:drug therapy / Q000503:physiopathology; D004151:Dipeptides / Q000494:pharmacology*; D006943:Hyperglycemia / Q000150:complications / Q000188:drug therapy / Q000503:physiopathology; D008297:Male; D053078:Membrane Potential, Mitochondrial / Q000187:drug effects; D008928:Mitochondria / Q000187:drug effects* / Q000378:metabolism / Q000473:pathology; D033681:Mitochondrial Membrane Transport Proteins / Q000819:agonists / Q000378:metabolism; D000083162:Mitochondrial Permeability Transition Pore; D009474:Neurons / Q000187:drug effects / Q000378:metabolism / Q000473:pathology; D018697:Nootropic Agents / Q000494:pharmacology*; D010431:Pentoxifylline / Q000494:pharmacology*; D010889:Piracetam / Q000031:analogs & derivatives* / Q000494:pharmacology; D051381:Rats; D017208:Rats, Wistar
chemical_list: D004151:Dipeptides; D033681:Mitochondrial Membrane Transport Proteins; D000083162:Mitochondrial Permeability Transition Pore; D018697:Nootropic Agents; C103871:ethyl phenylacetyl-Pro-Gly; D003566:Cytidine Diphosphate Choline; D000496:Alloxan; C037917:4-phenylpiracetam; D010431:Pentoxifylline; D010889:Piracetam