The olfactory system as a portal of entry for airborne polychlorinated biphenyls (PCBs) to the brain?

1998 ◽  
Vol 72 (5) ◽  
pp. 314-317 ◽  
Author(s):  
Raimund Apfelbach ◽  
Axel Engelhart ◽  
Peter Behnisch ◽  
Hanspaul Hagenmaier
Keyword(s):  
Polychlorinated Biphenyls ◽  
Olfactory System ◽  
Portal Of Entry ◽  
The Brain

The brain of the tree pangolin (Manis tricuspis ). II. The olfactory system

2018 ◽  
Vol 526 (16) ◽  
pp. 2548-2569 ◽  
Author(s):  
Aminu Imam ◽  
Adhil Bhagwandin ◽  
Moyosore S. Ajao ◽  
Muhammed A. Spocter ◽  
Amadi O. Ihunwo ◽  
...  
Keyword(s):  
Olfactory System ◽  
The Brain

Gene expression profiles in the brain of the neonate mouse perinatally exposed to methylmercury and/or polychlorinated biphenyls

2009 ◽  
Vol 84 (4) ◽  
pp. 271-286 ◽  
Author(s):  
Miyuki Shimada ◽  
Satomi Kameo ◽  
Norio Sugawara ◽  
Kozue Yaginuma-Sakurai ◽  
Naoyuki Kurokawa ◽  
...  
Keyword(s):  
Gene Expression ◽  
Polychlorinated Biphenyls ◽  
Expression Profiles ◽  
Gene Expression Profiles ◽  
The Brain

scholarly journals The cell biology of smell

2010 ◽  
Vol 191 (3) ◽  
pp. 443-452 ◽  
Author(s):  
Shannon DeMaria ◽  
John Ngai
Keyword(s):  
Olfactory System ◽  
Cell Biology ◽  
Odorant Receptor ◽  
Large Family ◽  
G Protein Coupled Receptors ◽  
Odorant Receptors ◽  
Chemical Structures ◽  
Wide Range ◽  
G Protein Coupled ◽  
The Brain

The olfactory system detects and discriminates myriad chemical structures across a wide range of concentrations. To meet this task, the system utilizes a large family of G protein–coupled receptors—the odorant receptors—which are the chemical sensors underlying the perception of smell. Interestingly, the odorant receptors are also involved in a number of developmental decisions, including the regulation of their own expression and the patterning of the olfactory sensory neurons' synaptic connections in the brain. This review will focus on the diverse roles of the odorant receptor in the function and development of the olfactory system.

Carnosine in the brain and olfactory system of amphibia and reptilia: A comparative study using immunocytochemical and biochemical methods

1991 ◽  
Vol 130 (2) ◽  
pp. 182-186 ◽  
Author(s):  
Cristina Artero ◽  
Elisa Martì ◽  
Stefano Biffo ◽  
Bruno Mulatero ◽  
Claudia Andreone ◽  
...  
Keyword(s):  
Comparative Study ◽  
Olfactory System ◽  
Biochemical Methods ◽  
The Brain

scholarly journals Functional integration of “undead” neurons in the olfactory system

2019 ◽  
Author(s):  
Lucia L. Prieto-Godino ◽  
Ana F. Silbering ◽  
Mohammed A. Khallaf ◽  
Steeve Cruchet ◽  
Karolina Bojkowska ◽  
...  
Keyword(s):  
Olfactory System ◽  
Functional Integration ◽  
Olfactory Receptors ◽  
Neural Pathways ◽  
Life Stages ◽  
Evoked Activity ◽  
Functional Neuron ◽  
Circuit Formation ◽  
The Brain ◽  
Chemosensory Organs

ABSTRACTProgrammed cell death (PCD) is widespread during neurodevelopment, typically eliminating the surpluses of neuronal production. Employing the Drosophila olfactory system, we examined the potential of cells fated to die to contribute to circuit evolution. Inhibition of PCD is sufficient to generate many new cells that express neural markers and exhibit odor-evoked activity. These “undead” neurons express a subset of olfactory receptors that, intriguingly, is enriched for recent receptor duplicates and include some normally found in other chemosensory organs and life-stages. Moreover, undead neuron axons integrate into the olfactory circuitry in the brain, forming novel receptor/glomerular couplings. Comparison of homologous olfactory lineages across drosophilids reveals natural examples of fate changes from death to a functional neuron. Finally, we provide evidence that PCD contributes to evolutionary differences in carbon dioxide-sensing circuit formation in Drosophila and mosquitoes. These results reveal the remarkable potential of alterations in PCD patterning to evolve new neural pathways.

From the periphery to the brain: Wiring the olfactory system

2011 ◽  
Vol 2 (4) ◽  
Author(s):  
Albert Blanchart ◽  
Laura López-Mascaraque
Keyword(s):  
Olfactory Bulb ◽  
Olfactory System ◽  
Neural Circuit ◽  
Critical Role ◽  
Precise Location ◽  
Reliable Transmission ◽  
Molecular Events ◽  
Perfect Model ◽  
Molecular Signals ◽  
The Brain

AbstractThe olfactory system represents a perfect model to study the interactions between the central and peripheral nervous systems in order to establish a neural circuit during early embryonic development. In addition, another important feature of this system is the capability to integrate new cells generated in two neurogenic zones: the olfactory epithelium in the periphery and the wall of the lateral ventricles in the CNS, both during development and adulthood. In all these processes the combination and sequence of specific molecular signals plays a critical role in the wiring of the olfactory axons, as well as the precise location of the incoming cell populations to the olfactory bulb. The purpose of this review is to summarize recent insights into the cellular and molecular events that dictate cell settling position and axonal trajectories from their origin in the olfactory placode to the formation of synapses in the olfactory bulb to ensure rapid and reliable transmission of olfactory information from the nose to the brain.

The Effects of Thyroid Hormone Level and Action in Developing Brain: Are These Targets for the Actions of Polychlorinated Biphenyls and Dioxins?

1998 ◽  
Vol 14 (1-2) ◽  
pp. 121-158 ◽  
Author(s):  
Ellen S. Sher ◽  
Xiao Ming Xu ◽  
Perrie M. Adams ◽  
Cheryl M. Craft ◽  
Stuart A. Stein
Keyword(s):  
Thyroid Hormone ◽  
Animal Models ◽  
Polychlorinated Biphenyls ◽  
Hormone Level ◽  
Motor Behavior ◽  
Endocrine Disrupting Compounds ◽  
Mitochondrial Genes ◽  
Thyroid Hormone Level ◽  
Neuronal Maintenance ◽  
The Brain

Alterations in thyroid hormone level or responsivity to thyroid hormone have significant neurologic sequelae throughout the life cycle. Duringfetal and early neonatal periods, disorders of thyroid hormone may lead to the development of motor and cognitive disorders. During childhood and adult life, thyroid hormone is required for neuronal maintenance as well as normal metabolic function. Those with an underlying disorder of thyroid hormone homeostasis or mitochondrial function may be at greater risk for developing cognitive, motor, or metabolic dysfunction upon exposure to substances which alter thyroid hormone economy. Polychlorinated biphenyls (PCBs) and dioxins have been argued to interfere with thyroid hormone action and thus may affect the developing and mature brain. Animal models provide useful tools for studying the effects of thyroid hormone disorders and the effects of environmental endocrine disruptors. The congenitally hypothyroid, hyt/hyt, mouse exhibits abnormalities in both the cognitive and motor systems. In this mouse and other animal models of thyroid hormone disorders, delayed somatic and reflexive development are noted, as are permanent deficits in hearing and locomotor and adaptive motor behavior. This animal's behavioral abnormalities are predicated on anatomic abnormalities in the nervous system. In turn, these abnormalities are correlated with differences in neuronal structural proteins. In normal mice, the expression of mRNAs coding for these proteins occurs temporally with the onset of autonomous thyroid hormone production. The hyt/hyt mouse has a mutation in the thyroid stimulating hormone receptor (TSHr) gene which renders it incapable of transducing the TSH signal in the thyrocyte to produce thyroid hormone. Some behavioral and possibly some biochemical abnormalities in mice exposed to PCBs are similar to those seen in the hyt/hyt mouse. In addition to direct effects on brain development and neuronal maintenance, thyroid hormone is necessary for maintaining metabolic functioning through its influence on mitochondria. Because the brain is particularly sensitive to inadequate energy generation, disorders of thyroid hormone economy also indirectly impair brain functioning. Alterations in thyroid hormone level result in differing expression of mitochondrial genes. Mutations in these mitochondrial genes lead to well-recognized syndromes of encephalomyopathy, myopathy, and multisystem disorder. Hence, PCBs and dioxins, by possibly altering the thyroid hormone milieu, may alter thefunctioning of mitochondria in the generation of adenosine triphosphate (ATP). The use of animal models of thyroid hormone deficiency for behavioral, anatomic, histologic, and molecular comparison will help elucidate the mechanisms of action of these putative endocrine-disrupting compounds. The study of thyroid hormone disorders provides a template for relating thyroid hormone mediated effects on the brain to these compounds.

scholarly journals Olfactory System Involvement in Natural Scrapie Disease

2009 ◽  
Vol 83 (8) ◽  
pp. 3657-3667 ◽  
Author(s):  
Cristiano Corona ◽  
Chiara Porcario ◽  
Francesca Martucci ◽  
Barbara Iulini ◽  
Barbara Manea ◽  
...  
Keyword(s):  
Nasal Mucosa ◽  
Olfactory System ◽  
Olfactory Nerve ◽  
Nerve Fibers ◽  
Transmissible Spongiform Encephalopathies ◽  
Brain Areas ◽  
Spongiform Encephalopathies ◽  
Prion Infection ◽  
Natural Scrapie ◽  
The Brain

ABSTRACT The olfactory system (OS) is involved in many infectious and neurodegenerative diseases, both human and animal, and it has recently been investigated in regard to transmissible spongiform encephalopathies. Previous assessments of nasal mucosa infection by prions following intracerebral challenge suggested a potential centrifugal spread along the olfactory nerve fibers of the pathological prion protein (PrPSc). Whether the nasal cavity may be a route for centripetal prion infection to the brain has also been experimentally studied. With the present study, we wanted to determine whether prion deposition in the OS occurs also under field conditions and what type of anatomical localization PrPSc might display there. We report here on detection by different techniques of PrPSc in the nasal mucosa and in the OS-related brain areas of sheep affected by natural scrapie. PrPSc was detected in the perineurium of the olfactory nerve bundles in the medial nasal concha and in nasal-associated lymphoid tissue. Olfactory receptor neurons did not show PrPSc immunostaining. PrPSc deposition was found in the brain areas of olfactory fiber projection, chiefly in the olfactory bulb and the olfactory cortex. The prevalent PrPSc deposition patterns were subependymal, perivascular, and submeningeal. This finding, together with the discovery of an intense PrPSc immunostaining in the meningeal layer of the olfactory nerve perineurium, at the border with the subdural space extension surrounding the nerve rootlets, strongly suggests a probable role of cerebrospinal fluid in conveying prion infectivity to the nasal submucosa.

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