Synaptic stimulation and neuronal damage

Read Also

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.