scholarly journals Running Changes the Brain: the Long and the Short of It

Physiology ◽  
2017 ◽  
Vol 32 (6) ◽  
pp. 410-424 ◽  
Author(s):  
Carmen Vivar ◽  
Henriette van Praag

Exercise is a simple intervention that profoundly benefits cognition. In rodents, running increases neurogenesis in the hippocampus, a brain area important for memory. We describe the dynamic changes in new neuron number and afferent connections throughout their maturation. We highlight the effects of exercise on the neurotransmitter systems involved, with a focus on the role of glutamate and acetylcholine in the initial development of new neurons in the adult brain.

2015 ◽  
Vol 28 (3-4) ◽  
pp. 253-283 ◽  
Author(s):  
Irene Sperandio ◽  
Irene Sperandio ◽  
Philippe A. Chouinard

Size constancy is the result of cognitive scaling operations that enable us to perceive an object as having the same size when presented at different viewing distances. In this article, we review the literature on size and distance perception to form an overarching synthesis of how the brain might combine retinal images and distance cues of retinal and extra-retinal origin to produce a perceptual visual experience of a world where objects have a constant size. A convergence of evidence from visual psychophysics, neurophysiology, neuropsychology, electrophysiology and neuroimaging highlight the primary visual cortex (V1) as an important node in mediating size–distance scaling. It is now evident that this brain area is involved in the integration of multiple signals for the purposes of size perception and does much more than fulfil the role of an entry position in a series of hierarchical cortical events. We also discuss how information from other sensory modalities can also contribute to size–distance scaling and shape our perceptual visual experience.


2019 ◽  
Vol 23 (4) ◽  
pp. 448-455
Author(s):  
U. S. Drozd ◽  
E. V. Shaburova ◽  
N. N. Dygalo

The serotonergic system is one of the most important neurotransmitter systems that take part in the regulation of vital CNS functions. The understanding of its mechanisms will help scientists create new therapeutic approaches to the treatment of mental and neurodegenerative diseases and find out how this neurotransmitter system interacts with other parts of the brain and regulates their activity. Since the serotonergic system anatomy and functionality are heterogeneous and complex, the best tools for studying them are based on manipulation of individual types of neurons without affecting neurons of other neurotransmitter systems. The selective cell control is possible due to the genetic determinism of their functions. Proteins that determine the uniqueness of the cell type are expressed under the regulation of cell-specific promoters. By using promoters that are specific for genes of the serotonin system, one can control the expression of a gene of interest in serotonergic neurons. Here we review approaches based on such promoters. The genetic models to be discussed in the article have already shed the light on the role of the serotonergic system in modulating behavior and processing sensory information. In particular, genetic knockouts of serotonin genes sert, pet1, and tph2 promoted the determination of their contribution to the development and functioning of the brain. In addition, the review describes inducible models that allow gene expression to be controlled at various developmental stages. Finally, the application of these genetic approaches in optogenetics and chemogenetics provided a new resource for studying the functions, discharge activity, and signal transduction of serotonergic neurons. Nevertheless, the advantages and limitations of the discussed genetic approaches should be taken into consideration in the course of creating models of pathological conditions and developing pharmacological treatments for their correction.


2021 ◽  
Vol 12 ◽  
Author(s):  
Katrina V. Good ◽  
John B. Vincent ◽  
Juan Ausió

Mutations in methyl CpG binding protein 2 (MeCP2) are the major cause of Rett syndrome (RTT), a rare neurodevelopmental disorder with a notable period of developmental regression following apparently normal initial development. Such MeCP2 alterations often result in changes to DNA binding and chromatin clustering ability, and in the stability of this protein. Among other functions, MeCP2 binds to methylated genomic DNA, which represents an important epigenetic mark with broad physiological implications, including neuronal development. In this review, we will summarize the genetic foundations behind RTT, and the variable degrees of protein stability exhibited by MeCP2 and its mutated versions. Also, past and emerging relationships that MeCP2 has with mRNA splicing, miRNA processing, and other non-coding RNAs (ncRNA) will be explored, and we suggest that these molecules could be missing links in understanding the epigenetic consequences incurred from genetic ablation of this important chromatin modifier. Importantly, although MeCP2 is highly expressed in the brain, where it has been most extensively studied, the role of this protein and its alterations in other tissues cannot be ignored and will also be discussed. Finally, the additional complexity to RTT pathology introduced by structural and functional implications of the two MeCP2 isoforms (MeCP2-E1 and MeCP2-E2) will be described. Epigenetic therapeutics are gaining clinical popularity, yet treatment for Rett syndrome is more complicated than would be anticipated for a purely epigenetic disorder, which should be taken into account in future clinical contexts.


2021 ◽  
Vol 22 (18) ◽  
pp. 9806
Author(s):  
Martyna Bayassi-Jakowicka ◽  
Grazyna Lietzau ◽  
Ewelina Czuba ◽  
Aleksandra Steliga ◽  
Monika Waśkow ◽  
...  

A growing body of evidence suggests that nucleus accumbens (NAc) plays a significant role not only in the physiological processes associated with reward and satisfaction but also in many diseases of the central nervous system. Summary of the current state of knowledge on the morphological and functional basis of such a diverse function of this structure may be a good starting point for further basic and clinical research. The NAc is a part of the brain reward system (BRS) characterized by multilevel organization, extensive connections, and several neurotransmitter systems. The unique role of NAc in the BRS is a result of: (1) hierarchical connections with the other brain areas, (2) a well-developed morphological and functional plasticity regulating short- and long-term synaptic potentiation and signalling pathways, (3) cooperation among several neurotransmitter systems, and (4) a supportive role of neuroglia involved in both physiological and pathological processes. Understanding the complex function of NAc is possible by combining the results of morphological studies with molecular, genetic, and behavioral data. In this review, we present the current views on the NAc function in physiological conditions, emphasizing the role of its connections, neuroplasticity processes, and neurotransmitter systems.


Author(s):  
Hamideh Abotalebi ◽  
Babak Ebrahimi ◽  
Raziyeh Shahriyari ◽  
Reyhaneh Shafieian

Abstract Adult neurogenesis is the production of new nerve cells in the adult brain. Neurogenesis is a clear example of the neuroplasticity phenomenon which can be observed in most of mammalian species, including human beings. This phenomenon occurs, at least, in two regions of the brain: the subgranular zone of the dentate gyrus in hippocampus and the ventricular zone of lateral ventricles. Numerous studies have investigated the relationship between sex steroid hormones and neurogenesis of adult brain; of which, mostly concentrated on the role of estradiol. It has been shown that estrogen plays a significant role in this process through both classic and non-classic mechanisms, including a variety of different growth factors. Therefore, the objective of this review is to investigate the role of female sex steroids with an emphasis on estradiol and also its potential implications for regulating the neurogenesis in the adult brain.


Endocrinology ◽  
2003 ◽  
Vol 144 (2) ◽  
pp. 594-598 ◽  
Author(s):  
Daniel J. Selvage ◽  
Catherine Rivier

We previously reported that in adult male rats, the intracerebroventricular (icv) injection of corticotropin-releasing factor (CRF) or the β-adrenergic agonist isoproterenol (ISO) significantly inhibited the ability of human chorionic gonadotropin (hCG) to stimulate testosterone (T) secretion. The finding that this phenomenon also took place when LH release had been blocked with an LHRH antagonist suggested that icv CRF and ISO did not alter Leydig cell function by influencing the activity of pituitary gonadotrophs. We therefore proposed the existence of a neural pathway connecting the brain to the testes, whose activation by icv CRF or ISO interfered with T secretion. Based on the intratesticular injection of the transganglionic tracer pseudorabies virus, we recently identified the paraventricular nucleus (PVN) of the hypothalamus as a component of this neural link. The aim of the present work was to investigate the functional role of this brain area in mediating the ability of CRF and ISO to inhibit the ability of hCG to stimulate T secretion. We first demonstrated that local microinfusion of CRF or ISO directly into the PVN mimicked the effect of their icv injection, suggesting that the PVN does indeed represent a site of action of ISO and CRF in altering Leydig cell responsiveness to gonadotropin. In contrast, neither CRF nor ISO microinfusion into the central amygdala or the frontal cortex influenced hCG-stimulated T secretion. To further investigate the role of the PVN in ISO- and CRF-induced blunting of hCG stimulation of T, we determined the effect of icv CRF or ISO on testicular activity of rats with electrolytic lesions of the PVN. These lesions, which did not in themselves influence Leydig cell responsiveness to hCG, blocked the effect of both icv ISO and CRF on hCG-induced T release. Collectively, these results support the hypothesis that CRF- and ISO-induced activation of cells in the area of the PVN decreases the ability of gonadotropin to release T and suggests that this nucleus represents an important site of the proposed neural connection between the brain and the testes.


2016 ◽  
Vol 2016 ◽  
pp. 1-11 ◽  
Author(s):  
Marta Vicente-Rodríguez ◽  
Rosalía Fernández-Calle ◽  
Esther Gramage ◽  
Carmen Pérez-García ◽  
María P. Ramos ◽  
...  

Midkine (MK) is a cytokine that modulates amphetamine-induced striatal astrogliosis, suggesting a possible role of MK in neuroinflammation induced by amphetamine. To test this hypothesis, we studied astrogliosis and microglial response induced by amphetamine (10 mg/kg i.p. four times, every 2 h) in different brain areas of MK−/− mice and wild type (WT) mice. We found that amphetamine-induced microgliosis and astrocytosis are enhanced in the striatum of MK−/− mice in a region-specific manner. Surprisingly, LPS-induced astrogliosis in the striatum was blocked in MK−/− mice. Since striatal neuroinflammation induced by amphetamine-type stimulants correlates with the cognitive deficits induced by these drugs, we also tested the long-term effects of periadolescent amphetamine treatment (3 mg/kg i.p. daily for 10 days) in a memory task in MK−/− and WT mice. Significant deficits in the Y-maze test were only observed in amphetamine-pretreated MK−/− mice. The data demonstrate for the first time that MK is a novel modulator of neuroinflammation depending on the inflammatory stimulus and the brain area considered. The data indicate that MK limits amphetamine-induced striatal neuroinflammation. In addition, our data demonstrate that periadolescent amphetamine treatment in mice results in transient disruption of learning and memory processes in absence of endogenous MK.


1990 ◽  
Vol 24 (1) ◽  
pp. 113-132 ◽  
Author(s):  
Janice D. Russell ◽  
Milton G. Roxanas

The frontal lobes of the brain have long been regarded as enigmatic in their function and perhaps should be considered even more so in states of dysfunction. Observed associations between structural lesions and psychiatric symptoms and the demonstration of disturbed function and morphology in the frontal lobes of individuals suffering from major psychiatric disorders have led to increased interest in this brain area. Psychiatrists have been particularly concerned with seeking the aetiogenesis of common diagnostic entities and this article attempts to synthesize the available facts. A brief overview of relevant biological data precedes a description of methods of neuropsychological testing and the clinical features arising from frontal lobe damage. A discussion of the role of the frontal lobes in some aspects of personality function follows. Neuropsychiatric features associated with known frontal lobe pathology are described, prefacing a discussion of those psychiatric conditions where an aetiological role for frontal lobe dysfunction has been proposed.


2021 ◽  
Author(s):  
Chitose Orikasa

Sexual dimorphism of the adult brain regulates sex-dependent functions including reproductive and neuroendocrine activities in rodents. It is determined by sex steroid hormones during a critical perinatal period in female and male rodents. Sex steroids act on each nuclear receptor in the brain and control different physiological and neuroendocrine functions and behaviors. Several regions of the brain show evident morphological sex differences that are involved in their physiological functions. This review addresses and focuses largely on the role of sex-dependent differences in the brain, and their crucial functions in animal models. Particularly, recent intriguing data concerning the diversity of neuronal functions and sexual dimorphism are discussed.


Mind Shift ◽  
2021 ◽  
pp. 63-79
Author(s):  
John Parrington

This chapter evaluates the basic unit of the human brain: the nerve cell, or neuron. These cells are also the main units of the peripheral nervous system, which sends messages from the brain to the other tissues and organs that make up our bodies. Neurons are the most well-known cells in the brain but they are not the only type of cell in this organ. The other main types are the glial cells, also known as neuroglia. Recent studies of the role of glial cells in the brain are revealing potentially important differences between humans and other species in the functions of these cells. The chapter then turns to the large-scale structure of the brain. The most dramatic changes in brain size and structure occurred in the final phase of human evolutionary change. Indeed, Neanderthals had brains similar in size to those of modern humans. An important feature of the human brain is that a larger fraction of its growth occurs outside the womb. Although humans reach adult brain size in childhood, brain development continues for decades afterwards.


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