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EN
A lot of clinical processes following excessive stimulation of glutamate receptors seem to participate in pathophysiology of numerous acute and chronic neurologicla disorders.The whole of these reactions has been named as "glutamate cascade", because of the central role of glutamate in initiation and intensification of these processes.In this article, classification of different types of glutamate receptors and several hypotheses concerning mechanisms of glutamate neurotoxic activity are presented.A wide variety of neurological diseases, which etiologies are more or less connected with glutamate toxicity are discussed. At last, the future perspecives for treatment by drugs which action is though to be mediated through glutmate receptord are persented.
EN
The 2S, 3S, 4S-isomer (L-CCG-I) of 2-(carboxycyclopropyl)glycine (CCG) is a potent metabotropic glutamate receptor agonist. L-CCG-I depressed monosynaptic excitation in the newborn rat spinal motoneurone at low concentrations well below those causing postsynaptic depolarization. 2S,3R,4S-CCG (L-CCG-IV) is a potent N-methyl-D-aspartate (NMDA)-type agonist. In cultured rat hippocampal neurones, L-CCG-IV caused marked increase in intracellular Ca?+ concentrations. 6-Carboxylated L-CCG-IV (DCG-IV), which is a tricarboxylated CCG derivative containing both chemical moieties of L-CCG-I and L-CCG-IV, depressed preferentially monosynaptic excitation of spinal reflexes in lower concentrations than L-CCG-I. 4-(2-Methoxyphenyl)-2-carboxy-3-pyrrolidineacetic acid (MEPA), which is the most potent kainoid yet described, is superior to acromelic acid A in causing depolarization of the newborn rat spinal motoneurone. In addition to MFPA, some non-kainoids demonstrated considerably high depolarizing activities. These new compounds would provide useful probes for neuroscience research.
EN
A form of activity dependent, functional plasticity can be induced in the barrel cortex by sensory deprivation without damage to the sensory receptors. Changes of cortical representation of a spared C3 vibrissa, when all other whiskers were plucked out, were mapped with 2-deoxyglucose autoradiography in mice and rats after a short-lasting deprivation. An increase in the volume of cortical column activated by the spared vibrissa was found previously that if deprivation is commenced immediately after birth, yhe changes in cortical representation of the spared whisker appeared in the third week of life. In search of a possible reason for the delayed expression of functional plasticity in neonatal animals we examined the developmental curves of neurotransmitter receptor binding for several transmitters thought to be involved in plstic processes of the cerebral cortex. We found that the beta noradrenergic and miscarinic cholinergic receptor binding increased rapidly at the end of the second postnatal week and subsequently remained high. By contrast, the metabotropic glutamate receptor binding decreased during the first month of postnatal development. The AMPA receptors binding values rose during the first two weeks of life, and then decreased. Together with our previous data on the development of NMDA and GABA receptor and voltage dependent calcium channel binding, the results suggest that slow development of functional plasticity in neonatal animals may be due to low levels of receptors of several neurotransmitters implicated in brain plasticity.
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