title: [Memory and potassium channels].
abstract: The K(+)-channels of the surface membrane play a crucial role in the generation of electrical activity of a neuron. There is a large diversity of the K(+)-channels that depends on a great number (over 200) of genes encoding channels proteins. An evolutionary conservation of channel's proteins is determined. The K(+)-channels were found to have a great importance in the memory processes. It was shown on different model systems that K(+)-current of the surface membrane decreases during the learning. The antagonists of K(+)-channels were found to improve the learning and memory. It was revealed in electrophysiological experiments that K(+)-channels antagonists can either themselves induce a long-term synaptic potentiation or intensify the synaptic potentiation induced by a tetanization. The disfunction of K(+)-channels is believed to be an important link in the mechanisms of memory disturbances. In animal mutants with K(+)-channels disfunction, learning and memory are deficient. In behavioral experiments, the use of K(+)-channels openers make the learning worse. Amnesia caused by cerebral ischemia is explained by strong activity of K(+)-channels which not only inhibits neuronal excitement but also causes neurodegeneration. The question on the K(+)-channels involvement into pathophysiology of Alzheimer's disease is discussed. Neurotoxic peptide beta-amyloid, which is supposed to be involved into mechanisms of Alzheimer's disease, modulates K(+)-channels function. The effect of beta-amyloid depends on the subtype of K(+)-channels: A-channels are inhibited, and KDR-channels, on the contrary, become stronger. The effect of the cognitive enhancers (vinpocetine, piracetam, tacrine, linopirdine) on K(+)-current also depends on the subtype of K(+)-channels. Slow-inactivating K(+)-currents (IDR, IK(Ca), IM) are inhibited in the presence of these drugs, while fast-in-activating K(+)-current (A-current) remains unchanged or even increases.
authors.affiliation: Brain Research Institute, Russian Academy of Medical Sciences, Moscow.
authors.forename: E I
authors.initials: EI
authors.lastname: Solntseva
authors.forename: Iu V
authors.initials: IuV
authors.lastname: Bukanova
authors.forename: V G
authors.initials: VG
authors.lastname: Skrebitskiĭ
mesh_terms: D000544:Alzheimer Disease / Q000503:physiopathology; D000647:Amnesia / Q000503:physiopathology; D016229:Amyloid beta-Peptides / Q000502:physiology; D000818:Animals; D001921:Brain / Q000187:drug effects / Q000503:physiopathology; D001923:Brain Chemistry; D004594:Electrophysiology; D007858:Learning; D008568:Memory / Q000502:physiology*; D019636:Neurodegenerative Diseases / Q000503:physiopathology; D009474:Neurons / Q000187:drug effects / Q000502:physiology; D018696:Neuroprotective Agents / Q000494:pharmacology; D026902:Potassium Channel Blockers / Q000494:pharmacology; D015221:Potassium Channels / Q000187:drug effects / Q000235:genetics / Q000502:physiology*
chemical_list: D016229:Amyloid beta-Peptides; D018696:Neuroprotective Agents; D026902:Potassium Channel Blockers; D015221:Potassium Channels