Expression of IGF-I and -II mRNA in the brain and craniofacial region of the rat fetus

Development ◽  
1991 ◽  
Vol 111 (1) ◽  
pp. 105-115 ◽  
Author(s):  
C. Ayer-le Lievre ◽  
P.A. Stahlbom ◽  
V.R. Sara

Insulin-like growth factors (IGF-I and -II) are present in the brain during development, with high levels of both being also found in the periphery particularly in the embryo. IGFs in the brain are believed to stimulate the proliferation of neuronal and glial precursors and their phenotypic differentiation. Using in situ hybridization, we have investigated the distribution of cells producing IGF-I and -II in the rat fetus during the second half of prenatal development with special emphasis on the peripheral and central nervous system. High levels of IGF-I mRNA were found in the olfactory bulb and in discrete neurons of the cranial sensory ganglia, notably in the trigeminal ganglion, as early as 13 days of gestation, in the pineal primordium of 18 day old fetuses, and in discrete groups of cells in the cochlear epithelium located laterally outside the forming spiral organ, in day 13 to 21 fetuses. High levels of IGF-II mRNA in the brain, besides the choroid plexus and the leptomeninges, were detected in hypothalamus, in the floor of the 3rd ventricle at all stages studied, in the pineal primordium at 18 days and in the pars intermedia of the pituitary or in the Rathke's pouch epithelium from which it is derived, with progressive fading towards the end of the gestation. In the peripheral nervous system the IGF-II mRNA was only found in association with the vascular endothelia of the ganglia. IGF-II mRNA in the nervous system was found in highly vascularized areas, meninges, blood vessels and choroid plexuses. It is thus associated with structures involved in the production of extracellular fluids and/or substrate transport and supply in the nervous tissues. A more specific role in the differentiation or fetal endocrine function should be considered for IGF-II in cells producing melatonin and melanocyte stimulating hormone (MSH) in the pineal and pituitary glands, respectively. The presence of IGF-I mRNA in the nervous system could be associated with fiber outgrowth and synaptogenesis in the cases of olfactory bulb and developing iris. The role of IGF-I in restricted populations of cells of the cochlear epithelium and in the pineal gland is unclear and requires further investigations including a search for IGF-I receptors in possible target cells. In the sensory ganglia, the presence of high levels of IGF-I mRNA eventually corresponds to the production, by post-translational processing, of the amino-terminal tripeptide of IGF-I, which might represent a neurotransmitter for these sensory neurons.

2017 ◽  
Vol 91 (22) ◽  
Author(s):  
D. Lori Wheeler ◽  
Jeremiah Athmer ◽  
David K. Meyerholz ◽  
Stanley Perlman

ABSTRACT Viral infection of the central nervous system (CNS) is complicated by the mostly irreplaceable nature of neurons, as the loss of neurons has the potential to result in permanent damage to brain function. However, whether neurons or other cells in the CNS sometimes survive infection and the effects of infection on neuronal function is largely unknown. To address this question, we used the rJHM strain (rJ) of mouse hepatitis virus (MHV), a neurotropic coronavirus that causes acute encephalitis in susceptible strains of mice. To determine whether neurons or other CNS cells survive acute infection with this virulent virus, we developed a recombinant JHMV that expresses Cre recombinase (rJ-Cre) and infected mice that universally expressed a silent (floxed) version of tdTomato. Infection of these mice with rJ-Cre resulted in expression of tdTomato in host cells. The results showed that some cells were able to survive the infection, as demonstrated by continued tdTomato expression after virus antigen could no longer be detected. Most notably, interneurons in the olfactory bulb, which are known to be inhibitory, represented a large fraction of the surviving cells. In conclusion, our results indicated that some neurons are resistant to virus-mediated cell death and provide a framework for studying the effects of prior coronavirus infection on neuron function. IMPORTANCE We developed a novel recombinant virus that allows the study of cells that survive an infection by a central nervous system-specific strain of murine coronavirus. Using this virus, we identified neurons and, to a lesser extent, nonneuronal cells in the brain that were infected during the acute phase of the infection and survived for approximately 2 weeks until the mice succumbed to the infection. We focused on neurons and glial cells within the olfactory bulb because the virus enters the brain at this site. Our results show that interneurons of the olfactory bulb were the primary cell type able to survive infection. Further, these results indicate that this system will be useful for functional and gene expression studies of cells in the brain that survive acute infection.


Author(s):  
Mark Walterfang ◽  
Ramon Mocellin ◽  
Dennis Velakoulis

This chapter examines the role of neurometabolic, neuroendocrine, and mitochondrial disorders in causing neuropsychiatric syndromes. It examines how disorders of cellular metabolic processes, particularly those that affect the brain, can result in major psychiatric syndromes and the over-representation of some neurometabolic disorders in psychiatric illness. It also discusses a range of endocrine disorders, particularly disorders of increased or reduced endocrine function and endocrine tumours, in producing psychiatric syndromes. The chapter also reviews the role of mitochondrial disorders in disrupting central nervous system processes and metabolism, and how some mitochondrial disorders result in psychiatric illness.


2016 ◽  
Vol 90 (20) ◽  
pp. 9285-9292 ◽  
Author(s):  
Akiko Takenaka ◽  
Hiroki Sato ◽  
Fusako Ikeda ◽  
Misako Yoneda ◽  
Chieko Kai

ABSTRACTIn the current study, we generated recombinant chimeric canine distemper viruses (CDVs) by replacing the hemagglutinin (H) and/or phosphoprotein (P) gene in an avirulent strain expressing enhanced green fluorescent protein (EGFP) with those of a mouse-adapted neurovirulent strain. Anin vitroexperimental infection indicated that the chimeric CDVs possessing the H gene derived from the mouse-adapted CDV acquired infectivity for neural cells. These cells lack the CDV receptors that have been identified to date (SLAM and nectin-4), indicating that the H protein defines infectivity in various cell lines. The recombinant viruses were administered intracerebrally to 1-week-old mice. Fatal neurological signs of disease were observed only with a recombinant CDV that possessed both the H and P genes of the mouse-adapted strain, similar to the parental mouse-adapted strain, suggesting that both genes are important to drive virulence of CDV in mice. Using this recombinant CDV, we traced the intracerebral propagation of CDV by detecting EGFP. Widespread infection was observed in the cerebral hemispheres and brainstems of the infected mice. In addition, EGFP fluorescence in the brain slices demonstrated a sequential infectious progression in the central nervous system: CDV primarily infected the neuroependymal cells lining the ventricular wall and the neurons of the hippocampus and cortex adjacent to the ventricle, and it then progressed to an extensive infection of the brain surface, followed by the parenchyma and cortex. In the hippocampal formation, CDV spread in a unidirectional retrograde pattern along neuronal processes in the hippocampal formation from the CA1 region to the CA3 region and the dentate gyrus. Our mouse model demonstrated that the main target cells of CDV are neurons in the acute phase and that the virus spreads via neuronal transmission pathways in the hippocampal formation.IMPORTANCECDV is the etiological agent of distemper in dogs and other carnivores, and in many respects, the pathogenesis of CDV infection in animals resembles that of measles virus infection in humans. We successfully generated a recombinant CDV containing the H and P genes from a mouse-adapted neurovirulent strain and expressing EGFP. The recombinant CDV exhibited severe neurovirulence with high mortality, comparable to the parental mouse-adapted strain. The mouse-infectious model could become a useful tool for analyzing CDV infection of the central nervous system subsequent to passing through the blood-cerebrospinal fluid barrier and infectious progression in the target cells in acute disease.


2013 ◽  
Vol 37 (1) ◽  
pp. 53-60 ◽  
Author(s):  
Denovan P. Begg ◽  
Stephen C. Woods

The endocrine pancreas is richly innervated with sympathetic and parasympathetic projections from the brain. In the mid-20th century, it was established that α-adrenergic activation inhibits, whereas cholinergic stimulation promotes, insulin secretion; this demonstrated the importance of the sympathetic and parasympathetic systems in pancreatic endocrine function. It was later established that insulin injected peripherally could act within the brain, leading to the discovery of insulin and insulin receptors within the brain and the receptor-mediated transport of insulin into the central nervous system from endothelial cells. The insulin receptor within the central nervous system is widely distributed, reflecting insulin's diverse range of actions, including acting as an adiposity signal to reduce food intake and increase energy expenditure, regulation of systemic glucose responses, altering sympathetic activity, and involvement in cognitive function. As observed with central insulin administration, the pancreatic hormones glucagon, somatostatin, pancreatic polypeptide, and amylin can each also reduce food intake. Pancreatic and also gut hormones are released cephalically, in what is an important mechanism to prepare the body for a meal and prevent excessive postprandial hyperglycemia.


2018 ◽  
Vol 2 (1) ◽  
pp. 385-400
Author(s):  
Ángel Rodríguez ◽  
Susana Domínguez ◽  
Mario Cantín ◽  
Mariana Rojas

This study briefly reviews the main events and processes that lead to the formation of the nervous system in mammals. At the end of gastrulation, they begin a series of fundamental morphogenetic processes with the formation of the neural plate (start of neurulation) culminating in the attainment of a normal nervous system. Embryological ectodermal primordia involved in the formation of the nervous system are the neuroectoblast, the neural crest cells and placodes that will evolve based on inductive phenomena, mainly from the notochord, prechordal plate and ectoderm. During the embryonic period consolidates the final development plan of the nervous system: 1) it comes complete neural tube formation when closing the rostral and caudal neuropores, 2) the different placodes invaginate to help form the organs of senses and sensory ganglia of the head, 3) the neural crest cells migrate to give rise to sensory and autonomic constituents of the peripheral nervous system and 4) developing brain vesicles, which will derive all the constituents of the brain. In the fetal period nervous system increases its mass and ultimately strengthens their functional organization.


Author(s):  
S.S. Spicer ◽  
B.A. Schulte

Generation of monoclonal antibodies (MAbs) against tissue antigens has yielded several (VC1.1, HNK- 1, L2, 4F4 and anti-leu 7) which recognize the unique sugar epitope, glucuronyl 3-sulfate (Glc A3- SO4). In the central nervous system, these MAbs have demonstrated Glc A3-SO4 at the surface of neurons in the cerebral cortex, the cerebellum, the retina and other widespread regions of the brain.Here we describe the distribution of Glc A3-SO4 in the peripheral nervous system as determined by immunostaining with a MAb (VC 1.1) developed against antigen in the cat visual cortex. Outside the central nervous system, immunoreactivity was observed only in peripheral terminals of selected sensory nerves conducting transduction signals for touch, hearing, balance and taste. On the glassy membrane of the sinus hair in murine nasal skin, just deep to the ringwurt, VC 1.1 delineated an intensely stained, plaque-like area (Fig. 1). This previously unrecognized structure of the nasal vibrissae presumably serves as a tactile end organ and to our knowledge is not demonstrable by means other than its selective immunopositivity with VC1.1 and its appearance as a densely fibrillar area in H&E stained sections.


Author(s):  
Grazia Tagliafierro ◽  
Cristiana Crosa ◽  
Marco Canepa ◽  
Tiziano Zanin

Barnacles are very specialized Crustacea, with strongly reduced head and abdomen. Their nervous system is rather simple: the brain or supra-oesophageal ganglion (SG) is a small bilobed structure and the toracic ganglia are fused into a single ventral mass, the suboesophageal ganglion (VG). Neurosecretion was shown in barnacle nervous system by histochemical methods and numerous putative hormonal substances were extracted and tested. Recently six different types of dense-core granules were visualized in the median ocellar nerve of Balanus hameri and serotonin and FMRF-amide like substances were immunocytochemically detected in the nervous system of Balanus amphitrite. The aim of the present work is to localize and characterize at ultrastructural level, neurosecretory neuron cell bodies in the VG of Balanus amphitrite.Specimens of Balanus amphitrite were collected in the port of Genova. The central nervous system were Karnovsky fixed, osmium postfixed, ethanol dehydrated and Durcupan ACM embedded. Ultrathin sections were stained with uranyl acetate and lead citrate. Ultrastructural observations were made on a Philips M 202 and Zeiss 109 T electron microscopy.


2012 ◽  
Vol 13 (2) ◽  
pp. 32-42 ◽  
Author(s):  
Yvette D. Hyter

Abstract Complex trauma resulting from chronic maltreatment and prenatal alcohol exposure can significantly affect child development and academic outcomes. Children with histories of maltreatment and those with prenatal alcohol exposure exhibit remarkably similar central nervous system impairments. In this article, I will review the effects of each on the brain and discuss clinical implications for these populations of children.


2018 ◽  
Vol 23 (1) ◽  
pp. 10-13
Author(s):  
James B. Talmage ◽  
Jay Blaisdell

Abstract Injuries that affect the central nervous system (CNS) can be catastrophic because they involve the brain or spinal cord, and determining the underlying clinical cause of impairment is essential in using the AMA Guides to the Evaluation of Permanent Impairment (AMA Guides), in part because the AMA Guides addresses neurological impairment in several chapters. Unlike the musculoskeletal chapters, Chapter 13, The Central and Peripheral Nervous System, does not use grades, grade modifiers, and a net adjustment formula; rather the chapter uses an approach that is similar to that in prior editions of the AMA Guides. The following steps can be used to perform a CNS rating: 1) evaluate all four major categories of cerebral impairment, and choose the one that is most severe; 2) rate the single most severe cerebral impairment of the four major categories; 3) rate all other impairments that are due to neurogenic problems; and 4) combine the rating of the single most severe category of cerebral impairment with the ratings of all other impairments. Because some neurological dysfunctions are rated elsewhere in the AMA Guides, Sixth Edition, the evaluator may consult Table 13-1 to verify the appropriate chapter to use.


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