Synaptic stimulation and neuronal damage
Excitatory synaptic stimulation can play an
important role in the development of neuron pathology. Strong and long-term
synaptic stimulation itself causes functional overstrain of the neuron, which
can be completed by degeneration of intracellular structures. These lesions are
amplified in violation of microcirculation and cerebral circulation, the action
of toxic factors.
Of paramount importance is the synaptic
stimulation of the development of anoxic (ischemic) injury. Culture neuronal
tissue becomes sensitive to anoxia only after the establishment of synaptic
contacts between neurons. Synaptic stimulation is realized through the action
of excitatory amino acids (glutamate, aspartate, L-homocystein), these lesions
are similar to those that occur during ischemia and are associated with
increased intracellular Ca2 + content. This effect is known as a neurotoxic (or
cytotoxic) action of excitatory amino acids. With synaptic hyperactivation, the
action of excitatory amino acids and hypoxia-associated damage and neuronal
death during status epilepticus in the postischemic period. In doing so, the
pathogenic action of these factors joined energy deficit.
In connection with the become clear beneficial
effects (ie, the weakening of the synaptic effects) reduce a functional load,
to prevent additional irritation, "protective" for IP Pavlov,
inhibition of reversibly damaged neurons.
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