Information Processing in the Mammalian Olfactory System

2005 ◽  
Vol 85 (1) ◽  
pp. 281-317 ◽  
Author(s):  
Pierre-Marie Lledo ◽  
Gilles Gheusi ◽  
Jean-Didier Vincent
Keyword(s):  
Olfactory System ◽  
Cellular Level ◽  
Adult Brain ◽  
Organizational Strategies ◽  
Cellular Mechanisms ◽  
Brain Functions ◽  
Olfactory Systems ◽  
And Behavior ◽  
High Degree ◽  
The Brain

Recently, modern neuroscience has made considerable progress in understanding how the brain perceives, discriminates, and recognizes odorant molecules. This growing knowledge took over when the sense of smell was no longer considered only as a matter for poetry or the perfume industry. Over the last decades, chemical senses captured the attention of scientists who started to investigate the different stages of olfactory pathways. Distinct fields such as genetic, biochemistry, cellular biology, neurophysiology, and behavior have contributed to provide a picture of how odor information is processed in the olfactory system as it moves from the periphery to higher areas of the brain. So far, the combination of these approaches has been most effective at the cellular level, but there are already signs, and even greater hope, that the same is gradually happening at the systems level. This review summarizes the current ideas concerning the cellular mechanisms and organizational strategies used by the olfactory system to process olfactory information. We present findings that exemplified the high degree of olfactory plasticity, with special emphasis on the first central relay of the olfactory system. Recent observations supporting the necessity of such plasticity for adult brain functions are also discussed. Due to space constraints, this review focuses mainly on the olfactory systems of vertebrates, and primarily those of mammals.

scholarly journals An architectonic type principle in the development of laminar patterns of cortico-cortical connections

2021 ◽  
Author(s):  
Sarah F. Beul ◽  
Alexandros Goulas ◽  
Claus C. Hilgetag
Keyword(s):  
Structural Connectivity ◽  
Macaque Monkey ◽  
Brain Regions ◽  
Adult Brain ◽  
Mammalian Brain ◽  
Cortical Connections ◽  
Cortical Projections ◽  
Structural Connections ◽  
High Degree ◽  
The Brain

AbstractStructural connections between cortical areas form an intricate network with a high degree of specificity. Many aspects of this complex network organization in the adult mammalian cortex are captured by an architectonic type principle, which relates structural connections to the architectonic differentiation of brain regions. In particular, the laminar patterns of projection origins are a prominent feature of structural connections that varies in a graded manner with the relative architectonic differentiation of connected areas in the adult brain. Here we show that the architectonic type principle is already apparent for the laminar origins of cortico-cortical projections in the immature cortex of the macaque monkey. We find that prenatal and neonatal laminar patterns correlate with cortical architectonic differentiation, and that the relation of laminar patterns to architectonic differences between connected areas is not substantially altered by the complete loss of visual input. Moreover, we find that the degree of change in laminar patterns that projections undergo during development varies in proportion to the relative architectonic differentiation of the connected areas. Hence, it appears that initial biases in laminar projection patterns become progressively strengthened by later developmental processes. These findings suggest that early neurogenetic processes during the formation of the brain are sufficient to establish the characteristic laminar projection patterns. This conclusion is in line with previously suggested mechanistic explanations underlying the emergence of the architectonic type principle and provides further constraints for exploring the fundamental factors that shape structural connectivity in the mammalian brain.

scholarly journals Entry of antiepileptic drugs (valproate and lamotrigine) into the developing rat brain

F1000Research ◽  
2021 ◽  
Vol 10 ◽  
pp. 384
Author(s):  
Samuel J. Toll ◽  
Fiona Qiu ◽  
Yifan Huang ◽  
Mark D. Habgood ◽  
Katarzyna M. Dziegielewska ◽  
...  
Keyword(s):  
Antiepileptic Drug ◽  
Placental Transfer ◽  
Rat Plasma ◽  
Developing Brain ◽  
Adult Brain ◽  
Cellular Mechanisms ◽  
Antiepileptic Drug Treatment ◽  
Dose Dependent ◽  
The Brain ◽  
Drug Entry

Background: Women with epilepsy face difficult choices whether to continue antiepileptic drug treatment during pregnancy, as uncontrolled seizures carry great risk to mother and fetus but continuing treatment may have adverse effects on baby’s development. This study aimed at evaluating antiepileptic drug entry into developing brain. Methods: Anaesthetised pregnant, non-pregnant adult females, postnatal and fetal rats were injected intraperitoneally with different doses, single or in combinations, of valproate and lamotrigine, all within clinical range. Injectate included 3H-labelled drug. After 30min, CSF, blood and brain samples were obtained; radioactivity was measured using liquid scintillation counting. Some animals were also exposed to valproate in feed throughout pregnancy and into neonatal period. Drug levels were measured by liquid chromatography coupled to mass spectrometry (LC-MS). Results are given as CSF or tissue/plasma% as index of drug entry. Results: Entry of valproate into brain and CSF was higher at E19 and P4 compared to adult but was not dose-dependent;  placental transfer increased significantly at highest dose of 100mg/Kg. Lamotrigine entry into the brain was dose dependent only at E19. Chronic valproate treatment, or combination of valproate and lamotrigine had little effect on either drug entry, except for reduced valproate brain entry in adult brain with chronic treatment. Placental transfer decreased significantly after chronic valproate treatment. LC-MS measurement of valproate in adults confirmed that rat plasma values were within the clinical range and CSF/plasma and brain/plasma ratios for LC-MS and 3H-valproate were similar. Conclusion: Results suggest that entry of valproate may be higher in developing brain, the capacity of barrier mechanism is mostly unaffected by doses within the clinical range, with or without addition of lamotrigine. Chronic valproate exposure may result in upregulation in cellular mechanisms restricting its entry into the brain. Entry of lamotrigine was little different at different ages and was not dose dependent.

A Neuromarketing Perspective for Assessing the Role and Impact of Typefaces on Consumer Purchase Decision

2020 ◽  
pp. 208-228
Author(s):  
Nihal Toros Ntapiapis ◽  
Çağla Özkardeşler
Keyword(s):  
Consumer Behavior ◽  
Literature Review ◽  
Human Cognition ◽  
Purchase Decision ◽  
Consumer Behaviors ◽  
Brain Functions ◽  
New Methods ◽  
Consumer Neuroscience ◽  
And Behavior ◽  
The Brain

Given increasing knowledge about how consumers communicate with texts, our understanding of how brain processes information remains relatively limited. Besides that, in today's world, advancing neuroscience-related technology and developments have changed the understanding of consumer behavior. In this regard, in the 1990s, consumer neuroscience and neuromarketing concepts were revealed. This new concept has brought a multi-disciplinary approach and new perceptions of human cognition and behavior. For measuring consumer behaviors through a new alternative method, research has started combining traditional marketing researches with these new methods. This chapter explores how typeface knowledge from the brain functions using neuroscience technology and the importance neurosciences methodologies have for readability research. Moreover, this chapter will evaluate how typefaces affect the purchase decision of the consumers and offer an integrative literature review.

scholarly journals Diagnosis of brain death

2010 ◽  
Vol 2 (1) ◽  
pp. 2 ◽  
Author(s):  
Calixto Machado
Keyword(s):  
Brain Death ◽  
Perfusion Pressure ◽  
Cellular Level ◽  
Irreversible Loss ◽  
Clinical Expression ◽  
Neuronal Tissue ◽  
Brain Functions ◽  
The Mean ◽  
The Brain ◽  
Signs Of Death

Brain death (BD) should be understood as the ultimate clinical expression of a brain catastrophe characterized by a complete and irreversible neurological stoppage, recognized by irreversible coma, absent brainstem reflexes, and apnea. The most common pattern is manifested by an elevation of intracranial pressure to a point beyond the mean arterial pressure, and hence cerebral perfusion pressure falls and, as a result, no net cerebral blood flow is present, in due course leading to permanent cytotoxic injury of the intracranial neuronal tissue. A second mechanism is an intrinsic injury affecting the nervous tissue at a cellular level which, if extensive and unremitting, can also lead to BD. We review here the methodology of diagnosing death, based on finding any of the signs of death. The irreversible loss of cardio-circulatory and respiratory functions can cause death only when ischemia and anoxia are prolonged enough to produce an irreversible destruction of the brain. The sign of such loss of brain functions, that is to say BD diagnosis, is fully reviewed.

scholarly journals Characteristics of Neural Network Changes in Normal Aging and Early Dementia

2021 ◽  
Vol 13 ◽  
Author(s):  
Hirohisa Watanabe ◽  
Epifanio Bagarinao ◽  
Satoshi Maesawa ◽  
Kazuhiro Hara ◽  
Kazuya Kawabata ◽  
...  
Keyword(s):  
Multisensory Integration ◽  
Resting State ◽  
Energy Supply ◽  
Healthy Aging ◽  
Supply And Demand ◽  
Cellular Level ◽  
Functional Network ◽  
Cellular Mechanisms ◽  
Atp Production ◽  
The Brain

To understand the mechanisms underlying preserved and impaired cognitive function in healthy aging and dementia, respectively, the spatial relationships of brain networks and mechanisms of their resilience should be understood. The hub regions of the brain, such as the multisensory integration and default mode networks, are critical for within- and between-network communication, remain well-preserved during aging, and play an essential role in compensatory processes. On the other hand, these brain hubs are the preferred sites for lesions in neurodegenerative dementias, such as Alzheimer’s disease. Disrupted primary information processing networks, such as the auditory, visual, and sensorimotor networks, may lead to overactivity of the multisensory integration networks and accumulation of pathological proteins that cause dementia. At the cellular level, the brain hub regions contain many synapses and require a large amount of energy. These regions are rich in ATP-related gene expression and had high glucose metabolism as demonstrated on positron emission tomography (PET). Importantly, the number and function of mitochondria, which are the center of ATP production, decline by about 8% every 10 years. Dementia patients often have dysfunction of the ubiquitin-proteasome and autophagy-lysosome systems, which require large amounts of ATP. If there is low energy supply but the demand is high, the risk of disease can be high. Imbalance between energy supply and demand may cause accumulation of pathological proteins and play an important role in the development of dementia. This energy imbalance may explain why brain hub regions are vulnerable to damage in different dementias. Here, we review (1) the characteristics of gray matter network, white matter network, and resting state functional network changes related to resilience in healthy aging, (2) the mode of resting state functional network disruption in neurodegenerative dementia, and (3) the cellular mechanisms associated with the disruption.

scholarly journals Interplay between Metabolism, Nutrition and Epigenetics in Shaping Brain DNA Methylation, Neural Function and Behavior

Genes ◽  
2020 ◽  
Vol 11 (7) ◽  
pp. 742 ◽  
Author(s):  
Tommaso Pizzorusso ◽  
Paola Tognini
Keyword(s):  
Dna Methylation ◽  
Cytosine Methylation ◽  
Maternal Nutrition ◽  
Adult Brain ◽  
Neural Function ◽  
Control Mechanisms ◽  
Dna Hydroxymethylation ◽  
And Behavior ◽  
The Impact ◽  
The Brain

Gene expression in the brain is dramatically regulated by a variety of stimuli. While the role of neural activity has been extensively studied, less is known about the effects of metabolism and nutrition on transcriptional control mechanisms in the brain. Extracellular signals are integrated at the chromatin level through dynamic modifications of epigenetic marks, which in turn fine-tune gene transcription. In the last twenty years, it has become clear that epigenetics plays a crucial role in modulating central nervous system functions and finally behavior. Here, we will focus on the effect of metabolic signals in shaping brain DNA methylation, both during development and adulthood. We will provide an overview of maternal nutrition effects on brain methylation and behavior in offspring. In addition, the impact of different diet challenges on cytosine methylation dynamics in the adult brain will be discussed. Finally, the possible role played by the metabolic status in modulating DNA hydroxymethylation, which is particularly abundant in neural tissue, will be considered.

scholarly journals Insight from animal models of environmentally driven epigenetic changes in the developing and adult brain

2016 ◽  
Vol 28 (4pt2) ◽  
pp. 1229-1243 ◽  
Author(s):  
Tiffany S. Doherty ◽  
Tania L. Roth
Keyword(s):  
Central Nervous System ◽  
Animal Models ◽  
Behavioral Outcomes ◽  
Adult Brain ◽  
Epigenetic Changes ◽  
Behavioral Deficits ◽  
The Central Nervous System ◽  
Brain And Behavior ◽  
And Behavior ◽  
The Brain

AbstractThe efforts of many neuroscientists are directed toward understanding the appreciable plasticity of the brain and behavior. In recent years, epigenetics has become a core of this focus as a prime mechanistic candidate for behavioral modifications. Animal models have been instrumental in advancing our understanding of environmentally driven changes to the epigenome in the developing and adult brain. This review focuses mainly on such discoveries driven by adverse environments along with their associated behavioral outcomes. While much of the evidence discussed focuses on epigenetics within the central nervous system, several peripheral studies in humans who have experienced significant adversity are also highlighted. As we continue to unravel the link between epigenetics and phenotype, discerning the complexity and specificity of epigenetic changes induced by environments is an important step toward understanding optimal development and how to prevent or ameliorate behavioral deficits bred by disruptive environments.

scholarly journals Neurobiological After-Effects of Low Intensity Transcranial Electric Stimulation of the Human Nervous System: From Basic Mechanisms to Metaplasticity

2021 ◽  
Vol 12 ◽  
Author(s):  
Sohaib Ali Korai ◽  
Federico Ranieri ◽  
Vincenzo Di Lazzaro ◽  
Michele Papa ◽  
Giovanni Cirillo
Keyword(s):  
Transcranial Electrical Stimulation ◽  
Cellular Mechanisms ◽  
After Effects ◽  
Brain Functions ◽  
Non Invasive ◽  
Low Intensity ◽  
The Brain ◽  
Human Nervous System

Non-invasive low-intensity transcranial electrical stimulation (tES) of the brain is an evolving field that has brought remarkable attention in the past few decades for its ability to directly modulate specific brain functions. Neurobiological after-effects of tES seems to be related to changes in neuronal and synaptic excitability and plasticity, however mechanisms are still far from being elucidated. We aim to review recent results from in vitro and in vivo studies that highlight molecular and cellular mechanisms of transcranial direct (tDCS) and alternating (tACS) current stimulation. Changes in membrane potential and neural synchronization explain the ongoing and short-lasting effects of tES, while changes induced in existing proteins and new protein synthesis is required for long-lasting plastic changes (LTP/LTD). Glial cells, for decades supporting elements, are now considered constitutive part of the synapse and might contribute to the mechanisms of synaptic plasticity. This review brings into focus the neurobiological mechanisms and after-effects of tDCS and tACS from in vitro and in vivo studies, in both animals and humans, highlighting possible pathways for the development of targeted therapeutic applications.

scholarly journals Dehydroepiandrosterone Metabolism by 3β-Hydroxysteroid Dehydrogenase/Δ5-Δ4 Isomerase in Adult Zebra Finch Brain: Sex Difference and Rapid Effect of Stress

Endocrinology ◽  
2004 ◽  
Vol 145 (4) ◽  
pp. 1668-1677 ◽  
Author(s):  
Kiran K. Soma ◽  
Noel A. Alday ◽  
Michaela Hau ◽  
Barney A. Schlinger
Keyword(s):  
Sex Differences ◽  
Sex Difference ◽  
Zebra Finch ◽  
Sex Steroids ◽  
Hydroxysteroid Dehydrogenase ◽  
Adult Brain ◽  
Brain And Behavior ◽  
Rapid Modulation ◽  
And Behavior ◽  
The Brain

Abstract Dehydroepiandrosterone (DHEA) is a precursor to sex steroids such as androstenedione (AE), testosterone (T), and estrogens. DHEA has potent effects on brain and behavior, although the mechanisms remain unclear. One possible mechanism of action is that DHEA is converted within the brain to sex steroids. 3β-Hydroxysteroid dehydrogenase/Δ5-Δ4 isomerase (3β-HSD) catalyzes the conversion of DHEA to AE. AE can then be converted to T and estrogen within the brain. We test the hypothesis that 3β-HSD is expressed in the adult brain in a region- and sex-specific manner using the zebra finch (Taeniopygia guttata), a songbird with robust sex differences in song behavior and telencephalic song nuclei. In zebra finch brain, DHEA is converted by 3β-HSD to AE and subsequently to estrogens and 5α- and 5β-reduced androgens. 3β-HSD activity is highest in the diencephalon and telencephalon. In animals killed within 2–3 min of disturbance, baseline 3β-HSD activity in portions of the telencephalon is higher in females than males. Acute restraint stress (10 min) decreases 3β-HSD activity in females but not in males, and in stressed animals, telencephalic 3β-HSD activity is greater in males than in females. Thus, the baseline sex difference is rapidly reversed by stress. To our knowledge, this is the first demonstration of 1) brain region differences in DHEA metabolism by 3β-HSD, 2) rapid modulation of 3β-HSD activity, and 3) sex differences in brain 3β-HSD and regulation by stress. Songbirds are good animal models for studying the regulation and functions of DHEA and neurosteroids in the nervous system.

scholarly journals What Do Microglia Really Do in Healthy Adult Brain?

Cells ◽  
2019 ◽  
Vol 8 (10) ◽  
pp. 1293 ◽  
Author(s):  
Marcus Augusto-Oliveira ◽  
Gabriela P. Arrifano ◽  
Amanda Lopes-Araújo ◽  
Leticia Santos-Sacramento ◽  
Priscila Y. Takeda ◽  
...  
Keyword(s):  
Healthy Adult ◽  
Cellular Level ◽  
Adult Brain ◽  
Neuronal Function ◽  
Learning Deficits ◽  
Neuroinflammatory Response ◽  
Circulating Cells ◽  
Cognition And Learning ◽  
And Behavior ◽  
Brain Homeostasis

Microglia originate from yolk sac-primitive macrophages and auto-proliferate into adulthood without replacement by bone marrow-derived circulating cells. In inflammation, stroke, aging, or infection, microglia have been shown to contribute to brain pathology in both deleterious and beneficial ways, which have been studied extensively. However, less is known about their role in the healthy adult brain. Astrocytes and oligodendrocytes are widely accepted to strongly contribute to the maintenance of brain homeostasis and to modulate neuronal function. On the other hand, contribution of microglia to cognition and behavior is only beginning to be understood. The ability to probe their function has become possible using microglial depletion assays and conditional mutants. Studies have shown that the absence of microglia results in cognitive and learning deficits in rodents during development, but this effect is less pronounced in adults. However, evidence suggests that microglia play a role in cognition and learning in adulthood and, at a cellular level, may modulate adult neurogenesis. This review presents the case for repositioning microglia as key contributors to the maintenance of homeostasis and cognitive processes in the healthy adult brain, in addition to their classical role as sentinels coordinating the neuroinflammatory response to tissue damage and disease.

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