Neonatal Exposure to Bacterial Lipopolysaccharide Affects Behavior and Expression of Ionotropic Glutamate Receptors in the Hippocampus of Adult Rats after Psychogenic Trauma.

According to the two-hit hypothesis of psychoneuropathology formation, infectious diseases and other pathological conditions occurring during the critical periods of early ontogenesis disrupt normal brain development and increase its susceptibility to stress experienced in adolescence and adulthood. It is believed that these disorders are associated with changes in the functional activity of the glutamatergic system in the hippocampus. Here, we studied expression of NMDA (GluN1, GluN2a, GluN2b) and AMPA (GluA1, GluA2) glutamate receptor subunits, as well as glutamate transporter EAAT2, in the ventral and dorsal regions of the hippocampus of rats injected with LPS during the third postnatal week and then subjected to predator stress (contact with a python) in adulthood. The tests were performed 25 days after the stress. It was found that stress altered protein expression in the ventral, but not in the dorsal hippocampus. Non-stressed LPS-treated rats displayed lower levels of the GluN2b protein in the ventral hippocampus vs. control animals. Stress significantly increased the content of GluN2b in the LPS-treated rats, but not in the control animals. Stress also affected differently the exploratory behavior of LPS-injected and control rats. Compared to the non-stressed animals, stressed control rats demonstrated a higher locomotor activity during the 1st min of the open field test, while the stressed LPS-injected rats displayed lower locomotor activity than the non-stressed rats. In addition, LPS-treated stressed and non-stressed rats spent more time in the open arms of the elevated plus maze and demonstrated reduced blood levels of corticosterone. To summarize the results of our study, exposure to bacterial LPS in the early postnatal ontogenesis affects the pattern of stress-induced changes in the behavior and hippocampal expression of genes coding for ionotropic glutamate receptor subunits after psychogenic trauma suffered in adulthood.

Psychophysiological analysis of the influence of vasopressin on speech in patients with post-stroke aphasias.

Speech is an attribute of the human species. Central speech disorders following stroke are unique models for the investigation of the organization of speech. Achievements in neurobiology suggest that there are possible neuroendocrine mechanisms involved in the organization of speech. It is known that the neuropeptide vasotocin, analogous of vasopressin in mammals, modulates various components of vocalization in animals. Furthermore, the positive influence of vasopressin on memory, which plays an important role in the formation of speech, has been described. In this study, speech organization processes and their recovery with the administration of vasopressin (1-desamino-8-D-arginin-vasopressin) to 26 patients with chronic aphasias after stroke were investigated. Results showed that sub-endocrine doses of the neuropeptide with intranasal administration had positive influence primarily on simple forms of speech and secondarily on composite forms. There were no statistically significant differences between the sensory and integrative components of the organization of speech processes with vasopressin. In all cases, the positive effect of the neuropeptide was demonstrated. As a result of the effects, speech regulated by both brain hemispheres improved. It is suggested that the neuropeptide optimizes the activity both in the left and right hemispheres, with primary influence on the right hemisphere. The persistence of the acquired effects is explained by an induction of compensatory processes resulting in the reorganization of the intra-central connections by vasopressin.