The Brain, Cranial Nerves, and Sensory and Motor Pathways
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Spatially Heterogeneous Choroid Plexus Transcriptomes Encode Positional Identity and Contribute to Regional CSF Production
The Journal of Neuroscience, March 25, 2015 • 35(12):4903–4916 • 4903 Development/Plasticity/Repair Spatially Heterogeneous Choroid Plexus Transcriptomes Encode Positional Identity and Contribute to Regional CSF Production Melody P. Lun,1,3 XMatthew B. Johnson,2 Kevin G. Broadbelt,1 Momoko Watanabe,4 Young-jin Kang,4 Kevin F. Chau,1 Mark W. Springel,1 Alexandra Malesz,1 Andre´ M.M. Sousa,5 XMihovil Pletikos,5 XTais Adelita,1,6 Monica L. Calicchio,1 Yong Zhang,7 Michael J. Holtzman,7 Hart G.W. Lidov,1 XNenad Sestan,5 Hanno Steen,1 XEdwin S. Monuki,4 and Maria K. Lehtinen1 1Department of Pathology, and 2Division of Genetics, Boston Children’s Hospital, Boston, Massachusetts 02115, 3Department of Pathology and Laboratory Medicine, Boston University School of Medicine, Boston, Massachusetts 02118, 4Department of Pathology and Laboratory Medicine, University of California Irvine School of Medicine, Irvine, California 92697, 5Department of Neurobiology and Kavli Institute for Neuroscience, Yale School of Medicine, New Haven, Connecticut 06510, 6Department of Biochemistry, Federal University of Sa˜o Paulo, Sa˜o Paulo 04039, Brazil, and 7Pulmonary and Critical Care Medicine, Department of Medicine, Washington University, St Louis, Missouri 63110 A sheet of choroid plexus epithelial cells extends into each cerebral ventricle and secretes signaling factors into the CSF. To evaluate whether differences in the CSF proteome across ventricles arise, in part, from regional differences in choroid plexus gene expression, we defined the transcriptome of lateral ventricle (telencephalic) versus fourth ventricle (hindbrain) choroid plexus. We find that positional identitiesofmouse,macaque,andhumanchoroidplexiderivefromgeneexpressiondomainsthatparalleltheiraxialtissuesoforigin.We thenshowthatmolecularheterogeneitybetweentelencephalicandhindbrainchoroidplexicontributestoregion-specific,age-dependent protein secretion in vitro. -
Human Cerebrospinal Fluid Induces Neuronal Excitability Changes in Resected Human Neocortical and Hippocampal Brain Slices
bioRxiv preprint doi: https://doi.org/10.1101/730036; this version posted August 8, 2019. The copyright holder for this preprint (which was not certified by peer review) is the author/funder, who has granted bioRxiv a license to display the preprint in perpetuity. It is made available under aCC-BY-ND 4.0 International license. Human cerebrospinal fluid induces neuronal excitability changes in resected human neocortical and hippocampal brain slices Jenny Wickham*†1, Andrea Corna†1,2,3, Niklas Schwarz4, Betül Uysal 2,4, Nikolas Layer4, Thomas V. Wuttke4,5, Henner Koch4, Günther Zeck1 1 Neurophysics, Natural and Medical Science Institute (NMI) at the University of Tübingen, Reutlingen, Germany 2 Graduate Training Centre of Neuroscience/International Max Planck Research School, Tübingen, Germany. 3 Institute for Ophthalmic Research, University of Tübingen, Tübingen, Germany 4 Department of Neurology and Epileptology, Hertie-Institute for Clinical Brain Research, University of Tübingen, Tübingen, Germany 5 Department of Neurosurgery, University of Tübingen, Tübingen, Germany * Communicating author: Jenny Wickham ([email protected]) and Günther Zeck ([email protected]) † shared first author, Shared last author Acknowledgments: This work was supported by the German Ministry of Science and Education (BMBF, FKZ 031L0059A) and by the German Research Foundation (KO-4877/2-1 and KO 4877/3- 1) Author contribution: JW and AC performed micro-electrode array recordings, NS, BU, NL, TW, HK and JW did tissue preparation and culturing, JW, AC, GZ did data analysis and writing. Proof reading and study design: all. Conflict of interest: None Keywords: Human tissue, human cerebrospinal fluid, Microelectrode array, CMOS-MEA, hippocampus, cortex, tissue slice 1 bioRxiv preprint doi: https://doi.org/10.1101/730036; this version posted August 8, 2019. -
Cranial Nerve Palsy
Cranial Nerve Palsy What is a cranial nerve? Cranial nerves are nerves that lead directly from the brain to parts of our head, face, and trunk. There are 12 pairs of cranial nerves and some are involved in special senses (sight, smell, hearing, taste, feeling) while others control muscles and glands. Which cranial nerves pertain to the eyes? The second cranial nerve is called the optic nerve. It sends visual information from the eye to the brain. The third cranial nerve is called the oculomotor nerve. It is involved with eye movement, eyelid movement, and the function of the pupil and lens inside the eye. The fourth cranial nerve is called the trochlear nerve and the sixth cranial nerve is called the abducens nerve. They each innervate an eye muscle involved in eye movement. The fifth cranial nerve is called the trigeminal nerve. It provides facial touch sensation (including sensation on the eye). What is a cranial nerve palsy? A palsy is a lack of function of a nerve. A cranial nerve palsy may cause a complete or partial weakness or paralysis of the areas served by the affected nerve. In the case of a cranial nerve that has multiple functions (such as the oculomotor nerve), it is possible for a palsy to affect all of the various functions or only some of the functions of that nerve. What are some causes of a cranial nerve palsy? A cranial nerve palsy can occur due to a variety of causes. It can be congenital (present at birth), traumatic, or due to blood vessel disease (hypertension, diabetes, strokes, aneurysms, etc). -
Thalamus and Limbic System
Prof. Saeed Abuel Makarem 1 Objectives By the end of the lecture, you should be able to: Describe the anatomy and main functions of the thalamus. Name and identify different nuclei of the thalamus. Describe the main connections and functions of thalamic nuclei. Name and identify different parts of the limbic system. Describe main functions of the limbic system. Describe the effects of lesions of the limbic system. It is the largest nuclear mass of Thalamus the whole body. It is the largest part of the THALAMUS diencephalon It is formed of two oval masses Corpus callosum of grey matter. It is the gateway to the Midbrain cortex. Resemble a PONS small hen. Together with the hypothalamus they form the lateral wall of the 3rd ventricle. 3 It sends received Thalamus information to the cerebral cortex from different brain regions. Axons from every sensory system (except olfaction) synapse in the thalamus as the last relay site 'last pit stop' before the information reaches the cerebral cortex. There are some thalamic nuclei that receive input from: 1. Cerebellar nuclei, 2. Basal ganglia- and 3. Limbic-related brain regions. 4 It has 4 surfaces & 2 ends. Relations Surfaces Lateral:(L) Posterior limb of the internal capsule. Medial: (3) The 3rd ventricle. In some people the 2 thalami are connected to ach other by interthalamic adhesion S (connexus,) or Massa intermedia, which crosses L through the 3rd ventricle. 3 Superior: (s) I Lateral ventricle and fornix. Inferior: Hypothalamus, anteriorly & Subthalamus posteriorly. 5 Anterior end: Forms a projection, called the anterior tubercle. It lies just behind the interventricular foramen. -
A Cyclops and a Synotus by K
J Neurol Psychopathol: first published as 10.1136/jnnp.s1-17.65.48 on 1 July 1936. Downloaded from 48 ORIGINAL PAPERS A CYCLOPS AND A SYNOTUS BY K. H. BOUMAN, AMSTERDAM, AND V. W. D. SCHENK, TiH HAGUE INTRODUCTION ONLY a small number of cases of cyclopia in human beings and mammals have been minutely examined. The number becomes still smaller if a more or less complete microscopic investigation of the central nervous system is stipulated. It is really only the cases of Davidson Black and Winkler and perhaps that of Naegli which answer this requirement. In contrast therewith there is an abundance of experimental studies in this field in urodela and other lower classes of animals. For all that, unanimity does not by any means prevail here, although the Protected by copyright. views of Stockard and his followers-who held that the first determination of the eye lay unpaired in the median line-and those of Spemann-who pointed to a paired rudiment from the outset, which views were originally diametrically opposed-appear to have drawn somewhat nearer to each other in recent years. Woerdeman, for instance, found that the paired rudiment of the eye shifts its position laterally downwards very early (when the folds of the medullary plate become visible) and he rightly says that this is not the same as Stockard's lateral growth of an unpaired eye rudiment. Yet, by saying this, he admits certain changes and growth conditions to which Fischel, for instance, did not do full justice. E. Manchot, on the other hand, who defends Stockard's views, admits that between the two regions of the eye http://jnnp.bmj.com/ rudiment there must be a tract of brain tissue (lamina terminalis and regio chiasmatica). -
Hamburger Hamilton Stages
UNSW Embryology- Chicken Development Stages http://embryology.med.unsw.edu.au/OtherEmb/chick1.htm Hamburger Hamilton Stages Hamburger Identification of Hamilton Age Stages Stages Before Laying Shell membrane of 3.5-4.5 Early egg formed in hr cleavage isthmus of oviduct Germ wall formed During from marginal cleavage periblast 4.5-24.0 Shell of egg Late cleavage hr formed in uterus After Laying Preprimitive streak 1 (embryonic shield) Initial primitive 2 6-7 hr streak, 0.3-0.5 mm long Intermediate 12-13 hr 3 primitive streak Definitive primitive 4 18-19 hr streak, ±1.88 mm long Head process 19-22 hr 5 (notochord) 6 23-25 hr Head fold 1 somite; neural 23-26 hr 7 folds ca. 1-3 somites; 7 to 8- 23-26 hr coelom 1 / 5 2007/03/20 9:05 UNSW Embryology- Chicken Development Stages http://embryology.med.unsw.edu.au/OtherEmb/chick1.htm 4 somites; blood 26-29 hr 8 islands 7 somites; primary 29-33 hr 9 optic vesicles 8-9 somites; 9+ to 10- ca. 33 hr anterior amniotic fold 10 somites; 3 10 33-38 hr primary brain vesicles 13 somites; 5 11 40-45 hr neuromeres of hindbrain 16 somites; 45-49 hr 12 telencephalon 19 somites; 13 48-52 hr atrioventricular canal ca. 20-21 somites; tail 13+ to 14- 50-52 hr bud 22 somites; trunk flexure; visceral 50-53 hr 14 arches I and II, clefts 1 and 2 23 somites; ca. premandibular 14+ to 15- 50-54 hr head cavities 24-27 somites; 15 50-55 hr visceral arch III, cleft 3 26-28 somites; 16 51-56 hr wing bud; posterior 2 / 5 2007/03/20 9:05 UNSW Embryology- Chicken Development Stages http://embryology.med.unsw.edu.au/OtherEmb/chick1.htm -
Basic Brain Anatomy
Chapter 2 Basic Brain Anatomy Where this icon appears, visit The Brain http://go.jblearning.com/ManascoCWS to view the corresponding video. The average weight of an adult human brain is about 3 pounds. That is about the weight of a single small To understand how a part of the brain is disordered by cantaloupe or six grapefruits. If a human brain was damage or disease, speech-language pathologists must placed on a tray, it would look like a pretty unim- first know a few facts about the anatomy of the brain pressive mass of gray lumpy tissue (Luria, 1973). In in general and how a normal and healthy brain func- fact, for most of history the brain was thought to be tions. Readers can use the anatomy presented here as an utterly useless piece of flesh housed in the skull. a reference, review, and jumping off point to under- The Egyptians believed that the heart was the seat standing the consequences of damage to the structures of human intelligence, and as such, the brain was discussed. This chapter begins with the big picture promptly removed during mummification. In his and works down into the specifics of brain anatomy. essay On Sleep and Sleeplessness, Aristotle argued that the brain is a complex cooling mechanism for our bodies that works primarily to help cool and The Central Nervous condense water vapors rising in our bodies (Aristo- tle, republished 2011). He also established a strong System argument in this same essay for why infants should not drink wine. The basis for this argument was that The nervous system is divided into two major sec- infants already have Central nervous tions: the central nervous system and the peripheral too much moisture system The brain and nervous system. -
What to Expect After Having a Subarachnoid Hemorrhage (SAH) Information for Patients and Families Table of Contents
What to expect after having a subarachnoid hemorrhage (SAH) Information for patients and families Table of contents What is a subarachnoid hemorrhage (SAH)? .......................................... 3 What are the signs that I may have had an SAH? .................................. 4 How did I get this aneurysm? ..................................................................... 4 Why do aneurysms need to be treated?.................................................... 4 What is an angiogram? .................................................................................. 5 How are aneurysms repaired? ..................................................................... 6 What are common complications after having an SAH? ..................... 8 What is vasospasm? ...................................................................................... 8 What is hydrocephalus? ............................................................................... 10 What is hyponatremia? ................................................................................ 12 What happens as I begin to get better? .................................................... 13 What can I expect after I leave the hospital? .......................................... 13 How will the SAH change my health? ........................................................ 14 Will the SAH cause any long-term effects? ............................................. 14 How will my emotions be affected? .......................................................... 15 When should -
Mir-124 Regulates Early Neurogenesis in the Optic Vesicle and Forebrain, Targeting Neurod1
Published online 3 December 2010 Nucleic Acids Research, 2011, Vol. 39, No. 7 2869–2879 doi:10.1093/nar/gkq904 MiR-124 regulates early neurogenesis in the optic vesicle and forebrain, targeting NeuroD1 Kaili Liu1,2,3, Ying Liu1,2,*, Weichuan Mo1,3, Rong Qiu1, Xiumei Wang1,2, Jane Y. Wu1,4 and Rongqiao He1,3,5,* 1The State Key Laboratory of Brain and Cognitive Science, 2Key Laboratory of Noncoding RNA, Institute of Biophysics, Chinese Academy of Sciences, 15 Datun Road, Chaoyang District, Beijing 100101, 3Graduate University of Chinese Academy of Sciences, Beijing 100049, China, 4Department of Neurology, Lurie Comprehensive Cancer Center, Center for Genetic Medicine, Northwestern University Feinberg School of Medicine, Chicago, IL 60611, USA and 5Key Laboratory of Mental Health, Chinese Academy of Sciences, Beijing 100101, China Received April 23, 2010; Revised September 5, 2010; Accepted September 23, 2010 ABSTRACT post-transcriptional mechanisms controlling their expres- sion are poorly understood. In recent years, systematic MicroRNAs (miRNAs) are involved in the fine control studies in zebrafish and mouse have determined specific of cell proliferation and differentiation during the microRNAs (miRNAs) expressed in the developing eye development of the nervous system. MiR-124, a and brain (1,2). MiR-7 and let-7 have been shown to be neural specific miRNA, is expressed from the begin- involved in Drosophila eye development (3,4). In Xenopus, ning of eye development in Xenopus, and has been miR-24a has been reported to play an essential role in shown to repress cell proliferation in the optic cup, repressing apoptosis in the developing neural retina (5). -
Sylvian Aqueduct Syndrome and Global Rostral Midbrain Dysfunction Associated with Shunt Malfunction
Sylvian aqueduct syndrome and global rostral midbrain dysfunction associated with shunt malfunction Giuseppe Cinalli, M.D., Christian Sainte-Rose, M.D., Isabelle Simon, M.D., Guillaume Lot, M.D., and Spiros Sgouros, M.D. Department of Pediatric Neurosurgery and Pediatric Radiology, Hôpital Necker•Enfants Malades, Université René Decartes; and Department of Neurosurgery, Hôpital Lariboisiere, Paris, France Object. This study is a retrospective analysis of clinical data obtained in 28 patients affected by obstructive hydrocephalus who presented with signs of midbrain dysfunction during episodes of shunt malfunction. Methods. All patients presented with an upward gaze palsy, sometimes associated with other signs of oculomotor dysfunction. In seven cases the ocular signs remained isolated and resolved rapidly after shunt revision. In 21 cases the ocular signs were variably associated with other clinical manifestations such as pyramidal and extrapyramidal deficits, memory disturbances, mutism, or alterations in consciousness. Resolution of these symptoms after shunt revision was usually slow. In four cases a transient paradoxical aggravation was observed at the time of shunt revision. In 11 cases ventriculocisternostomy allowed resolution of the symptoms and withdrawal of the shunt. Simultaneous supratentorial and infratentorial intracranial pressure recordings performed in seven of the patients showed a pressure gradient between the supratentorial and infratentorial compartments with a higher supratentorial pressure before shunt revision. Inversion of this pressure gradient was observed after shunt revision and resolution of the gradient was observed in one case after third ventriculostomy. In six recent cases, a focal midbrain hyperintensity was evidenced on T2-weighted magnetic resonance imaging sequences at the time of shunt malfunction. This rapidly resolved after the patient underwent third ventriculostomy. -
Differentiation of the Cerebellum 2463
Development 128, 2461-2469 (2001) 2461 Printed in Great Britain © The Company of Biologists Limited 2001 DEV1660 Inductive signal and tissue responsiveness defining the tectum and the cerebellum Tatsuya Sato, Isato Araki‡ and Harukazu Nakamura* Department of Molecular Neurobiology, Institute of Development, Aging and Cancer, Seiryo-machi 4-1, Aoba-ku, Sendai 980- 8575, Japan ‡Present address: Department of Neurobiology, University of Heidelberg, Im Neuenheimer Feld 364, D-69120 Heidelberg, Germany *Author for correspondence (e-mail: [email protected]) Accepted 11 April 2001 SUMMARY The mes/metencephalic boundary (isthmus) has an Fgf8b repressed Otx2 expression, but upregulated Gbx2 and organizing activity for mesencephalon and metencephalon. Irx2 expression in the mesencephalon. As a result, Fgf8b The candidate signaling molecule is Fgf8 whose mRNA is completely changed the fate of the mesencephalic alar plate localized in the region where the cerebellum differentiates. to cerebellum. Quantitative analysis showed that Fgf8b Responding to this signal, the cerebellum differentiates in signal is 100 times stronger than Fgf8a signal. Co- the metencephalon and the tectum differentiates in the transfection of Fgf8b with Otx2 indicates that Otx2 is a key mesencephalon. Based on the assumption that strong Fgf8 molecule in mesencephalic generation. We have shown by signal induces the cerebellum and that the Fgf8b signal is RT-PCR that both Fgf8a and Fgf8b are expressed, Fgf8b stronger than that of Fgf8a, we carried out experiments to expression prevailing in the isthmic region. The results all misexpress Fgf8b and Fgf8a in chick embryos. Fgf8a did not support our working hypothesis that the strong Fgf8 signal affect the expression pattern of Otx2, Gbx2 or Irx2. -
Anatomy of Cerebellum Rajasekhar Sajja Srinivasa Siva Naga
Chapter Anatomy of Cerebellum Rajasekhar Sajja Srinivasa Siva Naga Abstract The cerebellum receives inputs from spinal cord, cerebrum, brainstem, and sensory systems of the body and controls the motor system of the body. The Cerebellum harmonizes the voluntary motor activities such as maintenance of posture and equilibrium, and coordination of voluntary muscular activity including learning of the motor behaviours. Cerebellum occupies posterior cranial fossa, and it is relatively a small part of the brain. It weighs about one tenth of the total brain. Cerebellar lesions do not cause motor or cognitive impairment. However, they cause slowing of movements, tremors, lack of equilibrium/balance. Complex motor action becomes shaky and faltering. Keywords: Cerebellum, Spinocerebellar ataxia, Cortex, Medulla, Peduncles, Nuclei 1. Introduction The Cerebellum is the largest part of the hindbrain and develops from the alar plates (rhombic lips) of the metencephalon. It lies between the temporal and occipital lobes of cerebrum and the brainstem in the posterior cranial fossa. It is attached to the posterior surface of the brainstem by three large white fibre bundles. It is attached to the midbrain by superior cerebel- lar peduncle, pons by middle cerebellar peduncle, and medulla by inferior cerebellar peduncle. Cerebellum is concerned with three primary functions: a) coordination of voluntary motor functions of the body initiated by the cerebral cortex at an uncon- scious level, b) maintenance of balance, and posture, c) Maintenance of muscle tone. It receives and integrates the sensory inputs from the cerebrum and the spinal cord necessary for a planning and smooth coordination of the movements [1]. Cerebellar lesions result in irregular and uncoordinated, awkward intentional muscle movements.