Hyperactivity neuron

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Hyperactivity neuron caused significant emerging out of control imbalance between excitation and inhibition in favor of the neuron excitation. Functionally, it is the production of neuron amplified pulse stream, which can have a different character: the high-frequency action potentials; individual level; digits, grouped in packs, and so on. A special kind of hyperactivity is a paroxysmal depolarization shift (PDS) in the membrane, which occurs at the height of the high-frequency discharge. This type of hyperactivity is seen as a manifestation of epileptization neuron.

This shift in the balance between excitation and inhibition may be due to a primary enhanced neuronal excitation, overcoming the braking control, or primary failure of the brake control. The first mechanism is a significant membrane depolarization and increased input of Na + and Ca2 + into the neuron, the second - a disorder mechanisms for hyperpolarization of the membrane: breach of release of K + of the neuron and the neuron input C1.

An important endogenous regulator of the neuron activity is γ-aminobutyric acid (GABA). It causes inhibition of the neuron upon binding to its receptor. As a result in enhanced neuron C1 delivery.

When a neuron disinhibition due to the weakening of inhibition and membrane depolarization occurs gain admission Ca2 + into the neuron. Furthermore, Ca2 +, while in the cytosol delivery SH gives a neuron, thereby weakening, inside GABAergic inhibition. A related epileptization neuron that occurs under the influence of a convulsant that violate GABAergic inhibition. Many convulsant (eg, penicillin, korazol et al.) Have a complex effect on the neuron, stimulating at the same time activating and inactivating the brakes.

Chronic stimulation of the neuron (e.g., by direct electrical stimulation, synaptic effects influenced by excitatory amino acids, etc.), Even low intensity over time can lead to hyperactivation neuron.