The distribution of monoamines and their metabolites in the brain structures of rats at later periods after exposure to 12C ions

2015 ◽  
Vol 9 (3) ◽  
pp. 214-220 ◽  
Author(s):  
K. V. Belokopytova ◽  
O. V. Belov ◽  
V. S. Kudrin ◽  
V. B. Narkevich ◽  
P. M. Klodt ◽  
...  
2018 ◽  
Vol 64 (6) ◽  
pp. 511-516 ◽  
Author(s):  
I.V. Karpova ◽  
V.V. Mikheev ◽  
V.V. Marysheva ◽  
N.A. Kuritcyna ◽  
E.R. Bychkov ◽  
...  

The experiments were performed in male albino outbred mice kept in a group and under the conditions of long-term social isolation. The changes in the monoaminergic systems of the left and right hemispheres of the brain after acute hypoxia with hypercapnia have been studied. The levels of dopamine (DA), serotonin (5-HT) and their metabolites – dioxyphenylacetic (DOPAC), homovanillic (HVA), and 5-hydroxyindoleacetic (5-HIAA) acids – were determined by HPLC in the cerebral cortex, hippocampus and striatum of the right and left sides of the brain. In the control mice kept both in the group and under the conditions of social isolation, a higher content of DA in the cortex of the left hemisphere has been found. In the other brain structures the monoamine content was symmetric. In the cerebral cortex of the mice in the group, acute hypoxia with hypercapnia led to a right-sided increase in the DA and 5HT levels. At the same time, the DOPAC content decreased in the left cortex. In mice in the group, under the hypoxia with hypercapnia conditions, the DA level in the left hippocampus increased. In the striatum, the content of monoamines and their metabolites did not change significantly. In animals kept for a long time under the conditions of social isolation, hypoxia with hypercapnia no statistically significant changes in the monoamines and their metabolites levels were found. It has been concluded that the preliminary maintenance under the conditions of prolonged social isolation changes the reaction of central monoaminergic systems to acute hypoxia with hypercapnia.


2020 ◽  
Vol 168 (5) ◽  
pp. 605-609 ◽  
Author(s):  
N. A. Krupina ◽  
N. N. Khlebnikova ◽  
V. B. Narkevich ◽  
P. L. Naplekova ◽  
V. S. Kudrin

2014 ◽  
Vol 5 (2) ◽  
pp. 56-64
Author(s):  
Inessa Vladimirovna Karpova ◽  
Sergey Nikolayevich Proshin ◽  
Ruslan Ivanovich Glushakov ◽  
Vladimir Vladimirovich Mikheyev ◽  
Evgeny Rudolfovich Bychkov

The Sex differenses in the content and metabolism of dopamine and serotonin were studied in symmetrical brain structures of C3H-A mice. With HPLC the contents of norepinephrine (NE), dopamine (DA), serotonin (5-HT) and their metabolites, such as dihydroxyphenylacetic acid (DOPAC), homovanillinic acid (HVA) and 5-hydroxyindolacetic acid (5-HIAA), were measured in the cortex, tuberculum olfactorium, hippocampus and striatum of both the right and the left hemispheres of the brain in male and female mice. The following sex differences in monoamines and their metabolites in brain areas were found: the NE content was higher in the male striatum and in the female tuberculum olfactorium; in males the DA content in cortex and hippocampus was higher, but in tuberculum olfactorium and striatum was lower than that in females; in females the 5-HT and 5-HIAA levels in hippocampus and tuberculum olfactorium were hither than that in males. In the female left striatum the 5-HIAA content was higher than in males. In males three cases of neurochemical cerebral hemisphere asymmetries were found: 1) the NE content is higher in the right tuberculum olfactorium, 2) the DA level is higher in the right hippocampus, 3) the 5-HIAA content is higher in the left hippocampus. In females the only one case of cerebral asymmetry was found, i. g. the 5-HT level was higher in the right tuberculum olfactorium.


2021 ◽  
Vol 22 (11) ◽  
pp. 6071
Author(s):  
Suzanne Gascon ◽  
Jessica Jann ◽  
Chloé Langlois-Blais ◽  
Mélanie Plourde ◽  
Christine Lavoie ◽  
...  

Alzheimer’s disease (AD) is a devastating neurodegenerative disease characterized by progressive neuron losses in memory-related brain structures. The classical features of AD are a dysregulation of the cholinergic system, the accumulation of amyloid plaques, and neurofibrillary tangles. Unfortunately, current treatments are unable to cure or even delay the progression of the disease. Therefore, new therapeutic strategies have emerged, such as the exogenous administration of neurotrophic factors (e.g., NGF and BDNF) that are deficient or dysregulated in AD. However, their low capacity to cross the blood–brain barrier and their exorbitant cost currently limit their use. To overcome these limitations, short peptides mimicking the binding receptor sites of these growth factors have been developed. Such peptides can target selective signaling pathways involved in neuron survival, differentiation, and/or maintenance. This review focuses on growth factors and their derived peptides as potential treatment for AD. It describes (1) the physiological functions of growth factors in the brain, their neuronal signaling pathways, and alteration in AD; (2) the strategies to develop peptides derived from growth factor and their capacity to mimic the role of native proteins; and (3) new advancements and potential in using these molecules as therapeutic treatments for AD, as well as their limitations.


2019 ◽  
Vol 9 (1) ◽  
pp. 11 ◽  
Author(s):  
Ángel Romero-Martínez ◽  
Macarena González ◽  
Marisol Lila ◽  
Enrique Gracia ◽  
Luis Martí-Bonmatí ◽  
...  

Introduction: There is growing scientific interest in understanding the biological mechanisms affecting and/or underlying violent behaviors in order to develop effective treatment and prevention programs. In recent years, neuroscientific research has tried to demonstrate whether the intrinsic activity within the brain at rest in the absence of any external stimulation (resting-state functional connectivity; RSFC) could be employed as a reliable marker for several cognitive abilities and personality traits that are important in behavior regulation, particularly, proneness to violence. Aims: This review aims to highlight the association between the RSFC among specific brain structures and the predisposition to experiencing anger and/or responding to stressful and distressing situations with anger in several populations. Methods: The scientific literature was reviewed following the PRISMA quality criteria for reviews, using the following digital databases: PubMed, PsycINFO, Psicodoc, and Dialnet. Results: The identification of 181 abstracts and retrieval of 34 full texts led to the inclusion of 17 papers. The results described in our study offer a better understanding of the brain networks that might explain the tendency to experience anger. The majority of the studies highlighted that diminished RSFC between the prefrontal cortex and the amygdala might make people prone to reactive violence, but that it is also necessary to contemplate additional cortical (i.e. insula, gyrus [angular, supramarginal, temporal, fusiform, superior, and middle frontal], anterior and posterior cingulated cortex) and subcortical brain structures (i.e. hippocampus, cerebellum, ventral striatum, and nucleus centralis superior) in order to explain a phenomenon as complex as violence. Moreover, we also described the neural pathways that might underlie proactive violence and feelings of revenge, highlighting the RSFC between the OFC, ventral striatal, angular gyrus, mid-occipital cortex, and cerebellum. Conclusions. The results from this synthesis and critical analysis of RSFC findings in several populations offer guidelines for future research and for developing a more accurate model of proneness to violence, in order to create effective treatment and prevention programs.


Biomedicines ◽  
2021 ◽  
Vol 9 (7) ◽  
pp. 823
Author(s):  
Ekaterina A. Rudnitskaya ◽  
Tatiana A. Kozlova ◽  
Alena O. Burnyasheva ◽  
Natalia A. Stefanova ◽  
Nataliya G. Kolosova

Sporadic Alzheimer’s disease (AD) is a severe disorder of unknown etiology with no definite time frame of onset. Recent studies suggest that middle age is a critical period for the relevant pathological processes of AD. Nonetheless, sufficient data have accumulated supporting the hypothesis of “neurodevelopmental origin of neurodegenerative disorders”: prerequisites for neurodegeneration may occur during early brain development. Therefore, we investigated the development of the most AD-affected brain structures (hippocampus and prefrontal cortex) using an immunohistochemical approach in senescence-accelerated OXYS rats, which are considered a suitable model of the most common—sporadic—type of AD. We noticed an additional peak of neurogenesis, which coincides in time with the peak of apoptosis in the hippocampus of OXYS rats on postnatal day three. Besides, we showed signs of delayed migration of neurons to the prefrontal cortex as well as disturbances in astrocytic and microglial support of the hippocampus and prefrontal cortex during the first postnatal week. Altogether, our results point to dysmaturation during early development of the brain—especially insufficient glial support—as a possible “first hit” leading to neurodegenerative processes and AD pathology manifestation later in life.


Author(s):  
Hans Liljenström

AbstractWhat is the role of consciousness in volition and decision-making? Are our actions fully determined by brain activity preceding our decisions to act, or can consciousness instead affect the brain activity leading to action? This has been much debated in philosophy, but also in science since the famous experiments by Libet in the 1980s, where the current most common interpretation is that conscious free will is an illusion. It seems that the brain knows, up to several seconds in advance what “you” decide to do. These studies have, however, been criticized, and alternative interpretations of the experiments can be given, some of which are discussed in this paper. In an attempt to elucidate the processes involved in decision-making (DM), as an essential part of volition, we have developed a computational model of relevant brain structures and their neurodynamics. While DM is a complex process, we have particularly focused on the amygdala and orbitofrontal cortex (OFC) for its emotional, and the lateral prefrontal cortex (LPFC) for its cognitive aspects. In this paper, we present a stochastic population model representing the neural information processing of DM. Simulation results seem to confirm the notion that if decisions have to be made fast, emotional processes and aspects dominate, while rational processes are more time consuming and may result in a delayed decision. Finally, some limitations of current science and computational modeling will be discussed, hinting at a future development of science, where consciousness and free will may add to chance and necessity as explanation for what happens in the world.


1997 ◽  
Vol 9 (6) ◽  
pp. 699-713 ◽  
Author(s):  
Stephan B. Hamann ◽  
Larry R. Squire

Recent studies have challenged the notion that priming for ostensibly novel stimuli such as pseudowords (REAB) reflects the creation of new representations. Priming for such stimuli could instead reflect the activation of familiar memory representations that are orthographically similar (READ) and/or the activation of subparts of stimuli (RE, EX, AR), which are familar because they occur commonly in English. We addressed this issue in three experiments that assessed perceptual identification priming and recognition memory for novel and familiar letter strings in amnesic patients and control subjects. Priming for words, pseudowords, and orthographically illegal nonwords was fully intact in the amnesic patients following a single exposure, whereas recognition memory was impaired for the same items. Thus, priming can occur for stimuli that are unlikely to have preexisting representations. Words and pseudowords exhibited twice as much priming as illegal nonwords, suggesting that activation may contribute to priming for words and wordlike stimuli. Additional results showed that priming for illegal nonwords resulted from the formation of new perceptual associations among the component letters of each nonword rather than the activation of individual letter representations. In summary, the results demonstrate that priming following a single exposure can depend on the creation of new perceptual representations and that such priming is independent of the brain structures essential for declarative memory.


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