Semax, an ACTH(4-10) analogue with nootropic properties, activates dopaminergic and serotoninergic brain systems in rodents.

Corticotrophin (ACTH) and its analogues, particularly Semax (Met-Glu-His-Phe-Pro-Gly-Pro), demonstrate nootropic activity. Close functional and anatomical links have been established between melanocortinergic and monoaminergic brain systems. The aim of present work was to investigate the effects of Semax on neurochemical parameters of dopaminergic- and serotonergic systems in rodents.

Delta-sleep inducing peptide and neuronal activity after glutamate microiontophoresis: the role of NMDA-receptors.

The influence of microiontophoretic application of delta-sleep inducing peptide (DSIP) on a neuronal activity of sensorimotor brain cortex, dorsal hippocampus, ventral anterior thalamic nucleus and lateral hypothalamus was studied under the effects of glutamate and MK-801, a N-methyl-d-aspartate non-competitive antagonist, on male Wistar rats. DSIP microiontophoresis predominantly activated neurons of various brain regions, in particular, dorsal hippocampus and ventral anterior thalamic nucleus. A preliminary DSIP microiontophoresis prevented the augmentation of a neuronal activity in the studied structures under glutamate microiontophoresis.

Chronic neonatal N-methyl-D-aspartate receptor blockade induces learning deficits and transient hypoactivity in young rats.

A blockade of N-methyl-D-aspartate (NMDA)-type of glutamate receptor in rodents is believed to provide a pharmacological model of schizophrenia-related psychosis. Since neurodevelopmental abnormality, at least partly, could contribute to the pathogenesis of schizophrenia, the aim of this study was to recapitulate cognitive impairments accompanying this disorder in rats by a chronic neonatal treatment with a noncompetitive NMDA antagonist MK-801. Rat pups were treated with a low dose of MK-801 (0.

Effect of sulpiride on the amphetamine-induced changes in extracellular dopamine, DOPAC, and hydroxyl radical generation in the rat striatum.

The neurotoxic effects of psychostimulants are mediated by several mechanisms, which together lead to neuronal damage. These mechanisms include an increase in the extracellular content of dopamine, stimulation of dopamine oxidation, accumulation of extracellular glutamate, and an increase in body temperature. In the present study, the dopamine receptor antagonist sulpiride proved able to prevent the delayed loss of dopamine and 3,4-dihydroxyphenylacetic acid (DOPAC) and depressed the gradual generation of hydroxyl radicals induced in the rat striatum by D-amphetamine.