[Interlevel relations in neural memory: extrasynaptic reception of mediators, potentiation, and spontaneous activity].
The firing of "spontaneous" spikes is regarded as a result of mediator propagation to extrasynaptic receptors. Receptor-receptor interaction unites them in dimer and dimer clusters, which accept three conformational states under agonist action. There are two cooperative and potential dependent transitions between the states, where cluster accumulates or releases energy. The released energy can trigger a mechanism of endogenous (spontaneous) neuron firing in potentiation condition. These accumulating and triggering properties are absent in third (passive) conformational state, where gating charges immobilization reduces conformational mobility. The features of ionotropic, metabotropic and combined mediator action are discussed for different level of slow potential. Conformational effect depends on conformity of pattern space-temporal structure to geometric and functional features of metabotropic mediator sources in cluster environment. Each cluster appears to be adjusted for recognizing a certain vast set of afferent patterns. Number, structure and dimensionality of the recognized patterns are given by: 1) threshold of conformational transition, 2) allocation of synaptic and extrasynaptic mediator ejecting points in gap-hole environment of the receptive cluster 3) combinatorial connections of presynaptic cells with inhibit and excite synapses and 4) signal delays in presynaptic ways and neuropil. Numerous receptive clusters of soma-dendrite membrane are capable to write down information, to keep and accumulate it and to recover. Engram stored as passive/active conformational receptive cluster states is recovered in inversion by "spontaneous" neuronal activity. The original information may be recovered by reading via inhibit synapses.
Radchenko
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AN
Russian Academy of Science, St. Petersburg Institute for Informatics and Automation.
D000200:Action Potentials; D000818:Animals; D017774:Long-Term Potentiation / Q000502:physiology*; D009474:Neurons / Q000502:physiology*; D018377:Neurotransmitter Agents / Q000502:physiology*; D013569:Synapses / Q000502:physiology*
D018377:Neurotransmitter Agents