Talk:Neural - Ventricular System Development

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Cite this page: Hill, M.A. (2021, June 21) Embryology Neural - Ventricular System Development. Retrieved from

Four ventricles and foramina

foramina - openings that connect ventricular spaces

  • 2 lateral ventricles (right and left)
    • interventricular foramina (foramina of Monro)
  • third ventricle
    • cerebral aqueduct (Sylvius)
  • fourth ventricle
    • median aperture (Magendie) subarachnoid space via the cisterna magna
    • right and left lateral aperture (Luschka) subarachnoid space via the cistern of great cerebral vein

Spinal cord

  • central canal



Sainz LV, Zipfel J, Kerscher SR, Weichselbaum A, Bevot A & Schuhmann MU. (2019). Cerebro-venous hypertension: a frequent cause of so-called "external hydrocephalus" in infants. Childs Nerv Syst , 35, 251-256. PMID: 30474714 DOI. Cerebro-venous hypertension: a frequent cause of so-called "external hydrocephalus" in infants External hydrocephalus (eHC) is commonly defined as a subtype of infant "hydrocephalus" consisting of macrocepahly associated with enlarged subarachnoid space and no or mild ventriculomegaly. This status is thought to be related to impaired CSF absorption because of arachnoid villi immaturity. However, other factors like the venous system might be involved in the development of the clinical picture. METHODS: All patients diagnosed with eHC received prospectively contrast-enhanced 3D MR phlebography. Venous sis abnormalities were graded depending on the number of affected sinus segments and type. External CSF space volume was quantified planimetrically. RESULTS: Seventeen patients with the typical clinical feature of eHC were included. In 15, venous sinus abnormalities were found. There was a significant correlation between the volume of the widened cortical subarachnoid space (CSAS) and the number of venous sinus segments affected. Conversely, ventricular volume was not correlated. CONCLUSION: These results support the hypothesis that impaired venous outflow plays a major role in external hydrocephalus development. Raised venous pressure increases intracranial pressure accelerating head growth, resulting in an enlargement of the cortical subarachnoid space. Increased venous pressure increases the capillary bed pressure and brain turgor preventing ventricular space to enlarge forcing displacement of ventricular CSF to the subarachnoid space. As a result, ventriculomegaly is rarely found. The descriptive term "external hydrocephalus" implying a primary etiology within the CSF system is misleading and this work supports the notion that venous hypertension is the leading cause of the clinical picture. KEYWORDS: Benign idiopathic macrocephaly; MR phlebography; Subarachnoid space; Venous sinuses DOI: 10.1007/s00381-018-4007-3


Floor plate descendants in the ependyma of the adult mouse Central Nervous System

Khazanov S, Paz Y, Hefetz A, Gonzales BJ, Netser Y, Mansour AA & Ben-Arie N. (2017). Floor plate descendants in the ependyma of the adult mouse Central Nervous System. Int. J. Dev. Biol. , 61, 257-265. PMID: 27528042 DOI.

Khazanov S1, Paz Y, Hefetz A, Gonzales BJ, Netser Y, Mansour AA, Ben-Arie N. Author information Abstract During embryonic development of the Central Nervous System (CNS), the expression of the bHLH transcription factor Nato3 (Ferd3l) is unique and restricted to the floor plate of the neural tube. In mice lacking Nato3 the floor plate cells of the spinal cord do not fully mature, whereas in the midbrain floor plate, progenitors lose some neurogenic activity, giving rise to a reduced population of dopaminergic neurons. Since the floor plate is considered to be disintegrated at the time of birth, Nato3 expression was never tested postnatally and in adult mice. Here, we utilized a Nato3 knockout mouse model in which a LacZ reporter precisely replaced the coding region under the endogenous regulatory elements, so that its expression recapitulates the spatiotemporal pattern of Nato3 expression. Nato3 was found to be expressed in the CNS throughout life in a highly restricted manner along the medial cavities: in subpopulations of cells in the IIIrd ventricle, the cerebral aqueduct, the IVth ventricle, the central canal of the spinal cord, and the subcommissural organ, a gland located in the midbrain. A few unifying themes are shared among all Nato3-positive cells: all are positioned in the midline, are of an ependymal type, and contact the cerebrospinal fluid (CSF) similarly to the embryonic position of the floor plate bordering the lumen of the neural tube. Taken together, Nato3 defines an unrecognized subpopulation of medial cells positioned at only one side of circular ependymal structures, and it may affect their regulatory activities and neuronal stem cell function. PMID: 27528042 DOI: 10.1387/ijdb.160232nb

MafB is required for development of the hindbrain choroid plexus

Koshida R, Oishi H, Hamada M, Takei Y & Takahashi S. (2017). MafB is required for development of the hindbrain choroid plexus. Biochem. Biophys. Res. Commun. , 483, 288-293. PMID: 28025141 DOI.

Koshida R1, Oishi H2, Hamada M2, Takei Y3, Takahashi S2. Author information Abstract The choroid plexus (ChP) is a non-neural epithelial tissue that produces cerebrospinal fluid (CSF). The ChP differentiates from the roof plate, a dorsal midline structure of the neural tube. However, molecular mechanisms underlying ChP development are poorly understood compared to neural development. MafB is a bZip transcription factor that is known to be expressed in the roof plate. Here we investigated the role of MafB in embryonic development of the hindbrain ChP (hChP) using Mafb-deficient mice. Immunohistochemical analyses revealed that MafB is expressed in the roof plate and early hChP epithelial cells but its expression disappears at a later embryonic stage. We also found that the Mafb-deficient hChP exhibits delayed differentiation and results in hypoplasia compared to the wild-type hChP. Furthermore, the Mafb-deficient hChP exhibits increased apoptotic cell death and decreased proliferating cells at E12.5, an early stage of hChP development. Collectively, our findings reveal that MafB play an important role in promoting hChP development during embryogenesis. KEYWORDS: Hindbrain choroid plexus; Lmx1a; MafB; Roof plate PMID: 28025141 DOI: 10.1016/j.bbrc.2016.12.150


Development of the choroid plexus and blood-CSF barrier

Front Neurosci. 2015 Mar 3;9:32. doi: 10.3389/fnins.2015.00032. eCollection 2015.

Liddelow SA1.


Well-known as one of the main sources of cerebrospinal fluid (CSF), the choroid plexuses have been, and still remain, a relatively understudied tissue in neuroscience. The choroid plexus and CSF (along with the blood-brain barrier proper) are recognized to provide a robust protective effort for the brain: a physical barrier to impede entrance of toxic metabolites to the brain; a "biochemical" barrier that facilitates removal of moieties that circumvent this physical barrier; and buoyant physical protection by CSF itself. In addition, the choroid plexus-CSF system has been shown to be integral for normal brain development, central nervous system (CNS) homeostasis, and repair after disease and trauma. It has been suggested to provide a stem-cell like repository for neuronal and astrocyte glial cell progenitors. By far, the most widely recognized choroid plexus role is as the site of the blood-CSF barrier, controller of the internal CNS microenvironment. Mechanisms involved combine structural diffusion restraint from tight junctions between plexus epithelial cells (physical barrier) and specific exchange mechanisms across the interface (enzymatic barrier). The current hypothesis states that early in development this interface is functional and more specific than in the adult, with differences historically termed as "immaturity" actually correctly reflecting developmental specialization. The advanced knowledge of the choroid plexus-CSF system proves itself imperative to understand a range of neurological diseases, from those caused by plexus or CSF drainage dysfunction (e.g., hydrocephalus) to more complicated late-stage diseases (e.g., Alzheimer's) and failure of CNS regeneration. This review will focus on choroid plexus development, outlining how early specializations may be exploited clinically. KEYWORDS: blood-CSF barrier; brain patterning; cerebrospinal fluid; choroid plexus; development; epithelia; neuroependyma

PMID 25784848


Open fourth ventricle prior to 20 weeks' gestation: a benign finding?

Ultrasound Obstet Gynecol. 2014 Feb;43(2):154-8. doi: 10.1002/uog.13227.

Contro E1, Volpe P, De Musso F, Muto B, Ghi T, De Robertis V, Pilu G.


OBJECTIVE: To evaluate the role of the brainstem-vermis (BV) angle in the diagnosis of fetal posterior fossa abnormalities at 15-18 weeks' gestation. METHODS: We examined retrospectively three-dimensional (3D) ultrasound volumes acquired at 15-18 gestational weeks in fetuses with normal posterior fossa (controls) and in those with cystic posterior fossa. Whether the fourth ventricle appeared open posteriorly in axial views was noted and the BV angle was measured. A detailed follow-up was obtained in all cases. RESULTS: Of the 139 controls, 46 cases were excluded because of inadequate quality of the 3D volumes. Of the 93 remaining normal fetuses, 84 (90.3%) had a closed fourth ventricle and a BV angle < 20°, whereas 9/93 (9.7%) had an open fourth ventricle and a BV angle between 20° and 37°. The study group of 11 fetuses included seven with Dandy-Walker malformation and four with Blake's pouch cyst. In abnormal cases as a whole, the BV angle was significantly increased compared with that in controls (P < 0.0001). However, fetuses with Blake's pouch cyst and normal fetuses with an open fourth ventricle had strikingly similar sonograms: the BV angle was between 20° and 37° and the fourth ventricle appeared open only when viewed using a more steeply angulated scanning plane than that of the standard transcerebellar plane; in fetuses with Dandy-Walker malformation the fourth ventricle was widely open posteriorly, even in the standard transcerebellar view, and the BV angle was > 45°, significantly increased compared both with that in normal fetuses (P < 0.0001) and with that in fetuses with Blake's pouch cyst (P = 0.004). CONCLUSION: An open fourth ventricle is found in about 10% of normal fetuses at 15-18 weeks' gestation. Measurement of the BV angle is useful in such cases, as a value ≥ 45° is associated with a very high risk of severe posterior fossa malformation. Copyright © 2013 ISUOG. Published by John Wiley & Sons Ltd. KEYWORDS: Dandy-Walker malformation; brainstem-vermis angle; congenital anomalies; fetus; prenatal diagnosis; ultrasound PMID 24151160

Conditional N-WASP knockout in mouse brain implicates actin cytoskeleton regulation in hydrocephalus pathology

Exp Neurol. 2014 Jan 23. pii: S0014-4886(14)00024-7. doi: 10.1016/j.expneurol.2014.01.011. [Epub ahead of print] Jain N1, Lim LW1, Tan WT1, George B1, Makeyev E1, Thanabalu T2. Author information


Cerebrospinal fluid (CSF) is produced by the choroid plexus and moved by multi-ciliated ependymal cells through the ventricular system of the vertebrate brain. Defects in the ependymal layer functionality are a common cause of hydrocephalus. N-WASP (Neural-Wiskott Aldrich Syndrome Protein) is a brain-enriched regulator of actin cytoskeleton and N-WASP knockout caused embryonic lethality in mice with neural tube and cardiac abnormalities. To shed light on the role of N-WASP in mouse brain development, we generated N-WASP conditional knockout mouse model N-WASPfl/fl; Nestin-Cre (NKO-Nes). NKO-Nes mice were born with Mendelian ratios but exhibited reduced growth characteristics compared to their littermates containing functional N-WASP alleles. Importantly, all NKO-Nes mice developed cranial deformities due to excessive CSF accumulation and did not survive past weaning. Coronal brain sections of these animals revealed dilated lateral ventricles, defects in ciliogenesis, loss of ependymal layer integrity, reduced thickness of cerebral cortex and aqueductal stenosis. Immunostaining for N-cadherin suggests that ependymal integrity in NKO-Nes mice is lost as compared to normal morphology in the wild-type controls. Moreover, scanning electron microscopy and immunofluorescence analyses of coronal brain sections with anti-acetylated tubulin antibodies revealed the absence of cilia in ventricular walls of NKO-Nes mice indicative of ciliogenesis defects. N-WASP deficiency does not lead to altered expression of N-WASP regulatory proteins, Fyn and Cdc42, which have been previously implicated in hydrocephalus pathology. Taken together, our results suggest that N-WASP plays a critical role in normal brain development and implicate actin cytoskeleton regulation as a vulnerable axis frequently deregulated in hydrocephalus. Copyright © 2014. Published by Elsevier Inc. KEYWORDS: Actin cytoskeleton, Astrogliosis, Cerebral ventricles, Cilia, Hydrocephalus, N-WASP

PMID 24462670


Planar polarity of ependymal cilia

Differentiation. 2012 Feb;83(2):S86-90. Epub 2011 Nov 17.

Kishimoto N, Sawamoto K. Source Department of Developmental and Regenerative Biology, Nagoya City University, Graduate School of Medical Sciences, Nagoya 467-8601, Japan.


Ependymal cells, epithelial cells that line the cerebral ventricles of the adult brain in various animals, extend multiple motile cilia from their apical surface into the ventricles. These cilia move rapidly, beating in a direction determined by the ependymal planar cell polarity (PCP). Ciliary dysfunction interferes with cerebrospinal fluid circulation and alters neuronal migration. In this review, we summarize recent studies on the cellular and molecular mechanisms underlying two distinct types of ependymal PCP. Ciliary beating in the direction of fluid flow is established by a combination of hydrodynamic forces and intracellular planar polarity signaling. The ciliary basal bodies' anterior position on the apical surface of the cell is determined in the embryonic radial glial cells, inherited by ependymal cells, and established by non-muscle myosin II in early postnatal development. Copyright © 2011 International Society of Differentiation. Published by Elsevier B.V. All rights reserved.

PMID 2210106

The human brain intracerebral microvascular system: development and structure

Front Neuroanat. 2012 Sep 13;6:38. eCollection 2012.

Marín-Padilla M1.


The capillary from the meningeal inner pial lamella play a crucial role in the development and structural organization of the cerebral cortex extrinsic and intrinsic microvascular compartments. Only pial capillaries are capable of perforating through the cortex external glial limiting membrane (EGLM) to enter into the nervous tissue, although incapable of perforating the membrane to exit the brain. Circulatory dynamics and functional demands determine which capillaries become arterial and which capillaries become venous. The perforation of the cortex EGLM by pial capillaries is a complex process characterized by three fundamental stages: (1) pial capillary contact with the EGLM with fusion of vascular and glial basal laminae at the contact site, (2) endothelial cell filopodium penetration through the fussed laminae with the formation of a funnel between them that accompanies it into the nervous tissue while remaining open to the meningeal interstitium and, (3) penetration of the whole capillary carrying the open funnel with it and establishing an extravascular Virchow-Robin Compartment (V-RC) that maintains the perforating vessel extrinsic (outside) the nervous tissue through its entire length. The V-RC is walled internally by the vascular basal lamina and externally by the basal lamina of joined glial cells endfeet. The VRC outer glial wall appear as an extension of the cortex superficial EGLM. All the perforating vessels within the V-RCs constitute the cerebral cortex extrinsic microvascular compartment. These perforating vessels are the only one capable of responding to inflammatory insults. The V-RC remains open (for life) to the meningeal interstitium permitting the exchanges of fluid and of cells between brain and meninges. The V-RC function as the brain sole drainage (prelymphatic) system in both physiological as well as pathological situations. During cortical development, capillaries emerge from the perforating vessels, by endothelial cells growing sprouts analogous to their angiogenesis, entering into their corresponding V-RCs. These new capillaries to enter into the nervous tissue must perforate through the V-RC outer glial wall, a process analogous to the original perforation of the cortex EGLM by pial capillaries. These emerging capillaries are incapable of reentering the V-RCs and/or perforating vessels. As the new capillary enters into the nervous tissue, it becomes surrounded by glial endfeet and carries a single basal lamina (possibly glial). Capillaries emerging from contiguous perforators establish an anastomotic plexus between them, by mechanisms still poorly understood. The capillaries of this anastomotic plexus constitute the cerebral cortex intrinsic microvascular compartment and together constitute the so-called blood-brain-barrier. The intrinsic capillaries are changing and readapting continuously, by both active angiogenesis and reabsorption, to the gray matter neurons developmental and functional needs. The brain intrinsic capillaries are among the most active microvessels of the human body. Unresolved developmental and functional aspects concerning the cerebral cortex intrinsic capillary plexus need to be further investigated. KEYWORDS: EGLM; endothelial cell filopodium; human brain; intracerebral microvascular system; meningeal inner pial lamella

PMID 22993505

Why the embryo still matters: CSF and the neuroepithelium as interdependent regulators of embryonic brain growth, morphogenesis and histiogenesis

Dev Biol. 2009 Mar 15;327(2):263-72. Epub 2009 Jan 3.

Gato A, Desmond ME. Source Departamento de Anatomía y Radiologia, Facultad de Medicina, Universidad de Valladolid, Avda Ramón y Cajal 7, 47005 Valladolid, España. Abstract The key focus of this review is that both the neuroepithelium and embryonic cerebrospinal fluid (CSF) work in an integrated way to promote embryonic brain growth, morphogenesis and histiogenesis. The CSF generates pressure and also contains many biologically powerful trophic factors; both play key roles in early brain development. Accumulation of fluid via an osmotic gradient creates pressure that promotes rapid expansion of the early brain in a developmental regulated way, since the rates of growth differ between the vesicles and for different species. The neuroepithelium and ventricles both contribute to this growth but by different and coordinated mechanisms. The neuroepithelium grows primarily by cell proliferation and at the same time the ventricle expands via hydrostatic pressure generated by active transport of Na(+) and transport or secretion of proteins and proteoglycans that create an osmotic gradient which contribute to the accumulation of fluid inside the sealed brain cavity. Recent evidence shows that the CSF regulates relevant aspects of neuroepithelial behavior such as cell survival, replication and neurogenesis by means of growth factors and morphogens. Here we try to highlight that early brain development requires the coordinated interplay of the CSF contained in the brain cavity with the surrounding neuroepithelium. The information presented is essential in order to understand the earliest phases of brain development and also how neuronal precursor behavior is regulated.

PMID 19154733


Molecularly and temporally separable lineages form the hindbrain roof plate and contribute differentially to the choroid plexus

Development. 2007 Oct;134(19):3449-60. Epub 2007 Aug 29.

Hunter NL1, Dymecki SM.


Both hindbrain roof plate epithelium (hRPe) and hindbrain choroid plexus epithelium (hCPe) produce morphogens and growth factors essential for proper hindbrain development. Despite their importance, little is known about how these essential structures develop. Recent genetic fate maps indicate that hRPe and hCPe descend from the same pool of dorsal neuroectodermal progenitor cells of the rhombic lip. A linear developmental progression has been assumed, with the rhombic lip producing non-mitotic hRPe, and seemingly uniform hRPe transforming into hCPe. Here, we show that hRPe is not uniform but rather comprises three spatiotemporal fields, which differ in organization, proliferative state, order of emergence from the rhombic lip, and molecular profile of either the constituent hRPe cells themselves and/or their parental progenitors. Only two fields contribute to hCPe. We also present evidence for an hCPe contribution directly by the rhombic lip at late embryonic stages when hRPe is no longer present; indeed, the production interval for hCPe by the rhombic lip is surprisingly extensive. Further, we show that the hCPe lineage appears to be unique among the varied rhombic lip-derived lineages in its proliferative response to constitutively active Notch1 signaling. Collectively, these findings provide a new platform for investigating hRPe and hCPe as neural organizing centers and provide support for the model that they are themselves patterned structures that might be capable of influencing neural development along multiple spatial and temporal axes.

PMID 17728348


The blood-CSF barrier explained: when development is not immaturity

Bioessays. 2008 Mar;30(3):237-48.

Johansson PA, Dziegielewska KM, Liddelow SA, Saunders NR. Source Department of Pharmacology, University of Melbourne, Parkville, Vic, Australia.


It is often suggested that during development the brain barriers are immature. This argument stems from teleological interpretations and experimental observations of the high protein concentrations in fetal cerebrospinal fluid (CSF) and decreases in apparent permeability of passive markers during development. We argue that the developmental blood-CSF barrier restricts the passage of lipid-insoluble molecules by the same mechanism as in the adult (tight junctions) rendering the paracellular pathway an unlikely route of entry. Instead, we suggest that both protein and passive markers are transferred across the epithelium through a transcellular route. We propose that changes in volume of distribution can largely explain the decrease in apparent permeability for passive markers and that developmentally regulated cellular transfer explains changes in CSF protein concentrations. The blood-CSF tight junctions are functionally mature from very early in development, and it appears that transfer from blood into embryonic brain occurs predominately via CSF rather than the vasculature. PMID 18293362


Internal luminal pressure during early chick embryonic brain growth: descriptive and empirical observations

Anat Rec A Discov Mol Cell Evol Biol. 2005 Aug;285(2):737-47.

Desmond ME, Levitan ML, Haas AR. Source Department of Biology, Villanova University, Villanova, PA 19085, USA.


If the intraluminal pressure of the brain is decreased for 24 hr, the brain and neuroepithelium volumes are both reduced in half. The current study measured the intraluminal pressure throughout the period of rapid brain growth using a servo-null micropressure monitoring system. From 613 measurements made on 55 embryos, we show that the intraluminal pressure over this time period is appropriately described by a linear model with correlation coefficient of 0.752. To assess whether sustained hyperpressure would increase mitosis, elevated intraluminal pressure was induced in 10 embryos for 1-hr duration via a gravity-fed drip. The mitotic density and index of the mesencephalon were measured for the 10 embryos. Those embryos, in which the colchicine solution was added to the intraluminal cerebrospinal fluid creating a sustained hyperpressure, exhibited at least a 2.5-fold increase in both the mitotic density and index compared with control embryos. Based on the small sample size, we cautiously conclude that sustained hyper-intraluminal pressure does stimulate mitosis. (c) 2005 Wiley-Liss, Inc.

PMID 15977221


The development of the epidural space in human embryos

Folia Morphol (Warsz). 2004 Aug;63(3):273-9.

Patelska-Banaszewska M, Woźniak W. Source Department of Anatomy, University School of Medical Sciences, Poznań, Poland.


The epidural space is seen in embryos at stage 17 (41 days) on the periphery of the primary meninx. During stage 18 (44 days) the dura mater proper appears and the epidural space is located between this meninx and the perichondrium and contains blood vessels. During the last week of the embryonic period (stages 20-23) the epidural space is evident around the circumference of the spinal cord. On the posterior surface it is found between the dura mater and the mesoderm of the dorsal body wall.

PMID 15478101


Development of the cerebrospinal fluid pathway in the normal and abnormal human embryos

Childs Brain. 1980;6(1):26-38.

Osaka K, Handa H, Matsumoto S, Yasuda M.


The subarachnoid space, the chorioid plexus and the arachnoid villi are microscopically studied in 60 normal human embryos and in 3 abnormal human embryos with rhombencephaloschisis and cervical myeloschisis. The subarachnoid space has been generally considered to be developed by outflow of cerebrospinal fluid (CSF) of the choroid-plexus origin from the IVth ventricle. This generally accepted concept does not meet with our findings: (1) cavity formation in the meninx primitiva is seen before appearance of the choroid plexus; (2) the primitive subarachnoid space is developed earlier in the prepontine region than in the area dorsal to the rhombic roof, and (3) the primitive subarachnoid space is formed in the embryos with dysraphism where the perineural subarachnoid space is separated from the ventricles. Apparently the embryonic pattern of CSF circulation should be much different from the generally believed pattern of adult, since the arachnoid villi are absent in the embryos and the ability of production of CSF in the embryonic choroid plexus is questionable. It is suggested that such embryonic pattern of CSF production and absorption may partly persist in adult human being.

PMID 7351160


Embryonic and fetal development of structures associated with the cerebro-spinal fluid in man and other species. Part I: The ventricular system, meninges and choroid plexuses

Arch Anat Cytol Pathol. 1998;46(3):153-69.

Catala M. Source Service d'Histologie-Embryologie et Cytogénétique, Groupe Hospitalier Pitié-Salpêtrière, Paris, France.


Little is known about the development of the central nervous system (CNS) in humans. Ethical considerations preclude experimental studies in this field, and as a result most available data on human ontogenesis are descriptive. Comparative anatomic and embryologic studies have demonstrated that the main developmental milestones are conserved across species, and their results can be used to suggest a likely scenario for human development. The development of the ventricles, meninges, and choroid plexuses are discussed in this article. The central cavity of the neural tube is formed during neurulation, which occurs during the fourth gestational week. The first milestone is occlusion of the spinal neurocele (the central canal in the neural tube) shortly after neurulation. This prevents free communication between the ventricular system and the amniotic cavity. The second milestone is development of the meninges, which separate the central nervous system from the rest of the body. The embryonic origin of the meninges varies across species. In birds (and probably in mammals), the spinal meninges are derived from the somitic mesoderm, the brainstem meninges from the cephalic mesoderm, and the telencephalic meninges from the neural crest. Differentiation of the meninges, which involves formation of the subarachnoid space, occurs early, before the cerebrospinal fluid (CSF) begins to flow around the CNS. During ontogenesis, the meninges play a key role in regulating the growth of underlying nervous structures. They induce the formation of the superficial glial limiting layer and stimulate the growth of precursors located in the superficial blastemas of the cerebellum and hippocampus. The choroid plexuses are complex specialized structures that produce most of the CSF. Their epithelium derives from the neural tube epithelium and their mesenchyma from the meninges. Of the many enzymes produced in the choroid plexuses, some reflect the pivotal metabolic role of these structures (alkaline and acid phosphatases, magnesium-dependent ATPase, glucose-6-phosphatase, thiamine pyrophosphatase, adenylate cyclase, oxidoreductase, esterases, hydrolases, cathepsin D, and glutathion S-transferase). The two enzymes that are crucial to the production of CSF are Na+/K+ ATPase and carbonic anhydrase. Inactivation of catecholamines is mediated by catechol-O-methyltransferase and by the monoamine oxidases A and B. The morphology and synthesis profile of the choroid plexuses changes during development, although little is known about these changes in humans.

PMID 9754371


The development of cerebro-spinal fluid pathway in human embryos

No Shinkei Geka. 1977 Sep;5(10):1047-55. Japanese (author's transl)

Osaka K, Matsumoto S, Yasuda M.


The early development of the subarachnoid space, the choroid plexus, and the arachnoid villi was studied in 60 normal human embryos ranging from Carnegie stage 12 to 23. The embryos were fixed in Bouin's fluid, paraffin-embedded, serially sectioned and stained with hematoxylin-eosin and Azan. One abnormal human embryo with exencephaly and myeloschisis in the high cervical cord was added for the study. A primitive subarachnoid space (future subarachnoid space) is first distinguishable as cavity formation within the meninx primitiva in the areas ventral to the middle brain vesicle at stage 14. The development of the primitive subarachnoid space precedes the appearance of the choroid plexus. The primitive subarachnoid space appears earlier in the region ventral to the rhombencephalon than in the region posterior to the fourth ventricle. By stage 20, a primitive subarachnoid space almost completely surrounds the neural tube. A fairly-well developed primitive subarachnoid space was observed in the abnormal human embryo, in which the fourth ventricle was open to the amniotic cavity and the ventricular system was completely separated from the primitive subarachoid space. These findings imply that the extraventricular spread of fluid of choroid plexus origin is not an essential factors, and that probably it is not even an important factor, for the development of the subarachnoid space. The arachnoid villi dose not appear even at the end of the embryonal stage. Absorption of the cerebrospinal fluid in an embryo should be done by the way other than the arachnoid villi.

PMID 909616

Historic Articles

  • The development of the human cerebrospinal fluid pathway with particular reference to the roof of the fourth ventricle. Brocklehurst G. J Anat. 1969 Nov;105(Pt 3):467-75. No abstract available. PMID: 4187088

  • Fetal fourth ventricle: US appearance and frequency of depiction. Baumeister LA, Hertzberg BS, McNally PJ, Kliewer MA, Bowie JD. Radiology. 1994 Aug;192(2):333-6. PMID: 8029392
"PURPOSE: To define the normal appearance of the fetal fourth ventricle throughout gestation and ascertain an expected frequency of depiction at different gestational ages. MATERIALS AND METHODS: Three hundred ten consecutive second- and third-trimester fetuses were studied with ultrasound. The posterior fossa was examined to document the size and appearance of the fourth ventricle. RESULTS: The fourth ventricle was seen in 221 of the 310 fetuses (71.3%) and was most consistently demonstrated in the middle of the second trimester. At this stage of gestation, the fourth ventricle was almost always seen when the anatomic features of the posterior fossa were identified. The mean anteroposterior dimension of the fourth ventricle was 3.5 mm +/- 1.3 (standard deviation), and the mean width was 3.9 mm +/- 1.7. CONCLUSION: The fetal fourth ventricle can be seen in most fetuses beginning in the middle of the second trimester and increases in size with advancing gestation. It can be difficult to depict before the middle of the second trimester and late in the third trimester."
Notice - Mark Hill
Currently this page is only a template and will be updated (this notice removed when completed).


Cerebrospinal fluid (CSF) is produced mainly by the choroid plexus which is a structure lining the floor of the lateral ventricle and the roof of the third and fourth ventricles.

In development and the space within the spinal cord (central canal) and the brain (ventricles) was derived from the same space within the neural tube. In the adult these 2 spaces remain connected containing the same CSF.

Early in development the cavity within the neural tube (which will form the ventricular space) is filled with amniotic fluid. As the brain and spinal cord grow, this fluid filled space makes up the majority of the nervous system (by volume). Upon closure of the neuropores and development of the embryonic vasculature, this fluid is then synthesized by the choroid plexus, a specialized vascular epithelium. In mammals, the choroid plexuses develop at four sites in the roof of the neural tube shortly after its closure, in the order forth (IV, lateral, and third (III) ventricles.

Choroid Plexus in lateral ventricle (Week 10 fetus)

The choroid plexuses form one region of the blood-brain barrier that regulates the brain's internal environment.

In adult humans, the total production of CSF is about 400-600 millilitres of fluid a day. This is more than 4 times the overall fluid spaces of the nervous system. Note that some additional fluid also arises from leaking of fluid by the brain into the ventricles.

CSF contains high amount of: salts, sugars and lipids. The total amount of protein in normal CSF is relatively low (0.3-0.7 microg/microL), though there appears to be 60+ proteins as identified by 2D gel. Presence of some protein in the CSF can be indicative of disruption of or incomplete blood/brain barrier.

Some Recent Findings

Heep A, Bartmann P, Stoffel-Wagner B, Bos A, Hoving E, Brouwer O, Teelken A, Schaller C, Sival D. Cerebrospinal fluid obstruction and malabsorption in human neonatal hydrocephaly. Childs Nerv Syst. 2006 Oct;22(10):1249-55.

"In neonatal posthaemorrhagic high-pressure hydrocephalus (HC), high concentrations of malabsorption-related biomarkers contrast with lower concentrations in spina bifida and non-haemorrhagic triventricular HC. During the early development of high pressure HC in spina bifida neonates, CSF biomarkers strongly indicate that CSF obstruction contributes more to the development of HC than malabsorption."


Development Overview

Ventricles and Central Canal

22 days - neural groove begins to close to form the neural tube which remains open to the amniotic space at either end at the neuropores (cranial and caudal). The neural tube space is therefore initially filled with amniotic fluid.

24 days - cranial neuropore closes.

26 days - caudal neuropore closes.

Week 4 - neural tube space will generate both the ventricular space within the brain and the central canal of the spinal cord.

Choroid Plexus Development

Epithelium from the neural tube epithelium.

Mesenchyma from the meninges.

Enzymes required for CSF production are Na+/K+ ATPase and carbonic anhydrase.

Subarachnoid Space Development

Stage 14 (33 days) - initially as irregular spaces on the ventral surface of the spinal cord.

Stage 18 (44 days) - dura mater is formed and spaces surround the circumference of the spinal cord, which coalesce and contain many blood vessels.

(Data from: [#16228957 Patelska-Banaszewska M, Wozniak W., 2005])

There are also several good research articles and reviews from the 1980's and 1990's on CSF development.


<ref><pubmed>9754371&dopt=Abstract Catala M.] Embryonic and fetal development of structures associated with the cerebro-spinal fluid in man and other species. Part I: The ventricular system, meninges and choroid plexuses. Arch Anat Cytol Pathol. 1998;46(3):153-69.

<ref><pubmed>7351160&dopt=Abstract Osaka K, Handa H, Matsumoto S, Yasuda M] Development of the cerebrospinal fluid pathway in the normal and abnormal human embryos. Childs Brain. 1980;6(1):26-38.


<ref><pubmed>2285038&dopt=Abstract O'Rahilly R, Muller F.] Ventricular system and choroid plexuses of the human brain during the embryonic period proper. Am J Anat. 1990 Dec;189(4):285-302.

<ref><pubmed>7351160&dopt=Abstract Osaka K, Handa H, Matsumoto S, Yasuda M] Development of the cerebrospinal fluid pathway in the normal and abnormal human embryos. Childs Brain. 1980;6(1):26-38.

Stage 22 Embryo

File:Chroidplex sm2.jpg

Head Stage 22- blue box (lower right) shown in image below
File:Choroidplex sm.jpg
Chorid plexus in the Stage 22 Human Brain
Chorid plexus

See also: A section of [../wwwhuman/hipower/HumB/B3L.htm Stage 22 human head], and a [../wwwhuman/hipower/HumB/B4L.htm high power image of choroid plexus] from this same section.

CSF Production

Cerebrospinal fluid (CSF) is produced by both choroid plexus (a structure lining the floor of the lateral ventricle (ventricle=the brain's interior fluid spaces) and the roof of the third and fourth ventricles) and weeping of tissue fluid by the brain into the ventricles. These structures are capable of producing 400-600 cc's of fluid a day which is enough to completely fill the fluid spaces of the nervous system 4 times over.

Once produced, the CSF circulates from these ventricles to the subarachoid fluid space (a fluid space investing the brain and spinal cord) outside the brain. The CSF then reaches structures (arachoidal villi) along the superior, midline surface of the brain where it is reabsorbed back into the bloodvessels (the sagital sinus). There are several key passage ways through which the CSF must past to exit the ventricular spaces to reach the subarachnoid spaces. First, each of the two lateral ventricles have an outlet into the third ventricle called the foramen of Monroe. The third ventricle in turn has an outlet, the aqueduct of Sylvius or aqueduct, to the fourth ventricle. Finally, the fourth ventricle has three outlets, the foramen of Magendie and the paired foramena of Luschka. Additionally, the subarachnoid space has a potential point for blockage of flow of CSF to the arachnoidal villi at an opening in the tent like structure which divides the upper and lower parts of the brain (the tentorial notch). Distortion or enlargement of the brain in the region of this opening can compress the subarachnoid space preventing fluid from flowing up to the arachnoidal villi.

(text from: CSF Production and Hydrocephalus Institute for Neurology and Neurosurgery at the Beth Israel Nedical Center New York)

CSF Synthesis

Two key enzymes are required to produce CSF they are the Na+/K+ ATPase and carbonic anhydrase.

Other known chorid plexus enzymes include: alkaline and acid phosphatases, magnesium-dependent ATPase, glucose-6-phosphatase, thiamine pyrophosphatase, adenylate cyclase, oxidoreductase, esterases, hydrolases, cathepsin D, and glutathion S-transferase. (More? [#9754371 Catala M., 1998])

"The epithelial cells of the choroid plexus secrete cerebrospinal fluid (CSF), by a process that involves the movement of Na(+), Cl(-) and HCO(3)(-) from the blood to the ventricles of the brain. This creates the osmotic gradient, which drives the secretion of H(2)O. The unidirectional movement of the ions is achieved due to the polarity of the epithelium, i.e., the ion transport proteins in the blood-facing (basolateral) are different to those in the ventricular (apical) membranes."

(text from: <ref><pubmed>11135448&dopt=Abstract Speake T, Whitwell C, Kajita H, Majid A, Brown PD]. Mechanisms of CSF secretion by the choroid plexus. Microsc Res Tech. 2001 Jan 1;52(1):49-59. Review.)

CSF Reabsorption

File:CSF arachnoid granulation2.jpg
Arachnoid Granulation (image: Gray's Anatomy)

CSF drainage (absorption or reabsorption) into the venous system is through arachnoid granulations.

CSF in the subarachnoid space extends into the arachnoid granulations, which then project through the dura into the superior sagittal sinus.

See also note in CSF Circulation section, point 3.

Alpha-Fetoprotein (AFP)

"AFP is produced by both the yolk sack and fetal liver. At around 12 weeks of gestation, the yolk sack degenerates and the fetal liver becomes the main site of AFP synthesis. Concentration of this protein in the fetus is very high (1-10 mg/ml), but it decreases abruptly soon after the birth (by the end of second month postpartum, only a trace amount of AFP can be detected), and it is almost completely substituted by serum albumin. It has been also established that variation in the AFP content during pregnancy can be of use for the detection of fetal abnormalities, including Down's syndrome and open neural tube, defects, such as spina bifida."

(text from:<ref><pubmed>11004554&dopt=Abstract GillespieJR, Uversky VN]. Structure and function of alpha-fetoprotein: a biophysical overview. Biochim Biophys Acta. 2000 Jul 14;1480(1-2):41-56.)

Adult CSF Normal Values (Lumbar CSF)

Opening pressure: 50–200 mm H2O CSF

Color: Colorless

Turbidity: Crystal clear

Mononuclear cells: less than 5 / mm3

Polymorphonuclear leukocytes: 0

Total protein: 22–38 mg/dl Range 9–58 mg/dl (mean ± 2.0 SD)

Glucose: 60–80% of blood glucose

(Data from: Clinical Methods, 3rd ed, Table 74.1)

CSF Circulation

Greitz D. Cerebrospinal fluid circulation and associated intracranial dynamics. A radiologic investigation using MR imaging and radionuclide cisternography. Acta Radiol Suppl. 1993;386:1-23. (modified text below from this reference abstract)

  1. CSF-circulation is propelled by a pulsating flow, which causes an effective mixing. Flow is produced by the alternating pressure gradient, which is a consequence of the systolic expansion of the intracranial arteries causing expulsion of CSF into the compliant and contractable spinal subarachnoid space.
  2. No bulk flow is necessary to explain the transport of tracers in the subarachnoid space.
  3. Main absorption of the CSF is not through the Pacchionian granulations (arachnoid granulations), but a major part of the CSF transportation to the blood-stream is likely to occur via the paravascular and extracellular spaces of the central nervous system. (MH- Note this statement conflicts with previous CSF Reabsorption in literature)
  4. The intracranial dynamics may be regarded as the result of an interplay between the demands for space by the four components of the intracranial content (arterial blood, brain volume, venous blood and CSF). Interaction has a time offset within the cerebral hemispheres in a fronto-occipital direction during the cardiac cycle (the fronto-occipital "volume wave").
  5. Outflow from the cranial cavity to the cervical subarachnoid space (SAS) is dependent in size and timing on the intracranial arterial expansion during systole.

CSF Abnormalities


Hydrocephalus is the result of an imbalance between the rate at which the CSF is being formed and the rate at which the CSF is passing through the arachnoidal villi back into the blood (hydrocephalus rate is a function of the degree of imbalance in these two).

very small imbalance exhibit subtle, if any, symptoms.

large imbalances will have rapidly evolving symptoms of unmistakable import.

Obstructive Hydrocephalus

Obstruction of the CSF pathways within the interior of the brain or at the tentorial notch (the opening in the tentorium cerebelli fold of dura mater for the brainstem).

File:Tentorium cerebelli sm.jpg
Tentorium cerebelli, viewed from above (image: Gray's Anatomy)

Communication Hydrocephalus

Inability of the CSF to pass through the arachnoidal villi to get back into the blood stream. This can result when the arachnoidal villi become inflamed by infection or blood with the inflammatory process blocking the microscopic pores through which the CSF must pass from the subarachoidal space into the blood.

Congenital Hydrocephalus

Present at birth and can be due to blockage at the aqueduct (aqueductal stenosis), congenital anomalies such as an [neuron2.htm#Chiari Chiari malformation] or [neuron2.htm#dws Dandy-Walker malformation] (malformations at the base of the brain resulting in obstruction of outflow of CSF from the brain's interior) or it can be due to an inflammatory process when premature birth has resulted in bleeding within the brain.

Acquired Hydrocephalus - arises later in postnatal life.

(text modified from: CSF Production and Hydrocephalus Institute for Neurology and Neurosurgery at the Beth Israel Nedical Center New York)

Hydrocephalus - treated by endoscopic third vetriculostomy (ETV) surgery.


Represents about 0.4 - 0.6% of all intracranial, 2 - 3% of pediatric neoplasms.

Plexus papillomas outnumber choroid plexus carcinomas (by a ratio of 5:1). Choroid plexus carcinomas 80% arise in children.

Plexus tumors are most common in the lateral (80% of lateral ventricle tumors in children) and fourth ventricles (evenly distributed all age groups). (More? text modified from: <ref><pubmed>11135453&dopt=Abstract Rickert] )



Cerebrospinal Fluid Research ISSN: 17438454 Papers on all aspects of cerebrospinal fluid in health and disease.

Online Textbooks

Clinical Methods Third Edition Walker, H.K.; Hall, W.D.; Hurst, J.W.; editors Stoneham (MA): Butterworth Publishers; c1990 Cerebrospinal Fluid

Neuroscience Purves, Dale; Augustine, George.J.; Fitzpatrick, David; Katz, Lawrence.C.; LaMantia, Anthony-Samuel.; McNamara, James.O.; Williams, S. Mark, editors. Sunderland (MA): Sinauer Associates, Inc. c2001. The Ventricular System

Basic Neurochemistry, Molecular, Cellular, and Medical Aspects 6th ed. Siegal, George J.; Agranoff, Bernard W.; Albers, R. Wayne; Fisher, Stephen K.; Uhler, Michael D., editors. Philadelphia: Lippincott, Williams & Wilkins; c1999.ale; Augustine, George.J.; Fitzpatrick, David; Katz, Lawrence.C.; LaMantia, Anthony-Samuel.; McNamara, James.O.; Williams, S. Mark, editors. Sunderland (MA): Sinauer Associates, Inc. c2001. Blood—Cerebrospinal Fluid Barrier



<ref><pubmed>17091274&dopt=Abstract Beni-Adani L, Biani N, Ben-Sirah L, Constantini S.] The occurrence of obstructive vs absorptive hydrocephalus in newborns and infants: relevance to treatment choices. Childs Nerv Syst. 2006 Dec;22(12):1543-63.

<ref><pubmed>16685545&dopt=Abstract Oi S, Di Rocco C.] Proposal of "evolution theory in cerebrospinal fluid dynamics" and minor pathway hydrocephalus in developing immature brain. Childs Nerv Syst. 2006 Jul;22(7):662-9.

<<ref><pubmed>9754371&dopt=Abstract Catala M.] Embryonic and fetal development of structures associated with the cerebro-spinal fluid in man and other species. Part I: The ventricular system, meninges and choroid plexuses. Arch Anat Cytol Pathol. 1998;46(3):153-69.

<ref><pubmed>7351160&dopt=Abstract Osaka K, Handa H, Matsumoto S, Yasuda M] Development of the cerebrospinal fluid pathway in the normal and abnormal human embryos. Childs Brain. 1980;6(1):26-38.


Killer HE, Jaggi GP, Flammer J, Miller NR, Huber AR, Mironov A. Cerebrospinal fluid dynamics between the intracranial and the subarachnoid space of the optic nerve. Is it always bidirectional? Brain. 2007 Feb;130(Pt 2):514-20. Epub 2006 Nov 17. PMID: 17114796 [PubMed - indexed for MEDLINE]

Killer HE, Jaggi GP, Flammer J, Miller NR, Huber AR. The optic nerve: a new window into cerebrospinal fluid composition? Brain. 2006 Apr;129(Pt 4):1027-30.

Heep A, Bartmann P, Stoffel-Wagner B, Bos A, Hoving E, Brouwer O, Teelken A, Schaller C, Sival D. Cerebrospinal fluid obstruction and malabsorption in human neonatal hydrocephaly. Childs Nerv Syst. 2006 Oct;22(10):1249-55.

<ref><pubmed>16228957&dopt=Abstract Patelska-Banaszewska M, Wozniak W.] The subarachnoid space develops early in the human embryonic period. Folia Morphol (Warsz). 2005 Aug;64(3):212-6.

<ref><pubmed>11135444&dopt=Abstract Dziegielewska KM, Ek J, Habgood MD, Saunders NR]. Development of the choroid plexus. Microsc Res Tech. 2001 Jan 1;52(1):5-20.

<ref><pubmed>11135448&dopt=Abstract Speake T, Whitwell C, Kajita H, Majid A, Brown PD]. Mechanisms of CSF secretion by the choroid plexus. Microsc Res Tech. 2001 Jan 1;52(1):49-59.

<ref><pubmed>11135453&dopt=Abstract Rickert CH, Paulus W.] Tumors of the choroid plexus. Microsc Res Tech. 2001 Jan 1;52(1):104-11.

<ref><pubmed>10924373&dopt=Abstract Guermazi A, De Kerviler E, Zagdanski AM, Frija J.] Diagnostic imaging of choroid plexus disease. Clin Radiol. 2000 Jul;55(7):503-16.

<ref><pubmed>10696509&dopt=Abstract Segal MB]. The choroid plexuses and the barriers between the blood and the cerebrospinal fluid. Cell Mol Neurobiol. 2000 Apr;20(2):183-96.

<ref><pubmed>2230809&dopt=Abstract Weisgerber C, Husmann M, Frosch M, Rheinheimer C, Peuckert W, Gorgen I, Bitter-Suermann D.] Embryonic neural cell adhesion molecule in cerebrospinal fluid of younger children: age-dependent decrease during the first year. J Neurochem. 1990 Dec;55(6):2063-71.

<ref><pubmed>2285038&dopt=Abstract O'Rahilly R, Muller F.] Ventricular system and choroid plexuses of the human brain during the embryonic period proper. Am J Anat. 1990 Dec;189(4):285-302.

<ref><pubmed>7351160&dopt=Abstract Osaka K, Handa H, Matsumoto S, Yasuda M] Development of the cerebrospinal fluid pathway in the normal and abnormal human embryos. Childs Brain. 1980;6(1):26-38.

Search PubMed: term= cerebrospinal fluid development | choroid plexus development | brain ventricular development | fetal cerebrospinal fluid |

WWW Links

Institute for Neurology (NY)


  • 3rd ventricle- ventricular cavity within the [#diencephalon diencephalon].
  • 4th ventricle- ventricular cavity within the [#rhombencephalon rhombencephalon].
  • accessory nerve-
  • adenohypophysis- anterior pituitary= 3 parts pars distalis, pars intermedia, pars tuberalis
  • alar plate- afferent, dorsal horns
  • anlage- (Ger. ) primordium, structure or cells which will form a future structure.
  • arachnoid- (G.) spider web-like
  • basal ganglia-
  • basal plate- efferent, ventral horns
  • brachial plexus- mixed spinal nerves innervating the upper limb form a complex meshwork (crossing).
  • brain- general term for the central nervous system formed from 3 primary vesicles.
  • buccopharyngeal membrane- (=oral membrane) at cranial (mouth) end of gastrointestinal tract (GIT) where surface ectoderm and GIT endoderm meet. (see also [#cloacal membrane cloacal membrane])
  • cauda equina- (=horse's tail) caudal extension of the mature spinal cord.
  • central canal- lumen, cavity of neural tube within the spinal cord. Space is continuous with ventricular system of the brain.
  • cerebral aqueduct- ventricular cavity within the [#mesencephalon mesencephalon].
  • cervical flexure- most caudal brain flexure (of 3) between spinal cord and rhompencephalon.
    • ( sc-^V^ )
  • choroid plexus- specialized vascular plexus responsible for secreting ventricular fluid that with further additions becomes cerebrospinal fluid (CSF).
  • cloacal membrane- at caudal (anal) end of gastrointestinal tract (GIT) where surface ectoderm and GIT endoderm meet forms the openings for GIT, urinary, reproductive tracts. (see also [#buccopharyngeal membrane buccopharyngeal membrane])
  • cortex-
  • cortical plate- outer neural tube region which post-mitotic neuroblasts migrate too along radial glia to form adult cortical layers.
  • cranial flexure- (=midbrain flexure) most cranial brain flexure (of 3) between mesencephalon and prosencephalon.
    • ( sc-^V^ )
  • diencephalon- the caudal portion of forebrain after it divides into 2 parts in the 5 secondary vesicle brain (week 5). (cavity- 3rd ventricle) Forms the thalmus and other nuclei in the adult brain.
    • (sc-My-Met-Mes-Di-Tel)
  • dorsal root ganglia- (=spinal ganglia) sensory ganglia derived from the neural crest lying laterally paired and dorsally to the spinal cord (in the embryo found ventral to the spinal cord). Connects centrally with the dorsal horn of the spinal cord.
  • dura mater-
  • ectoderm- the germ layer which form the nervous system from the neural tube and neural crest.
  • ependyma- epithelia of remnant cells after neurons and glia have been generated and left the ventricular zone
  • floorplate- early forming thin region of neural tube closest to the notochord.
  • ganglia- (pl. of ganglion) specialized neural cluster.
  • glia- supporting, non-neuronal cells of the nervous system. Generated from neuroepithelial stem cells in ventricular zone of neural tube. Form astrocytes, oligodendrocytes.
  • glossopharyngeal ganglion-
  • grey matter- neural regions containing cell bodies (somas) of neurons. In the brain it is the outer layer, in the spinal cord it is inner layer. (see [#white matter white matter])
  • growth factor- usually a protein or peptide that will bind a cell membrane receptor and then activates an intracellular signaling pathway. The function of the pathway will be to alter the cell directly or indirectly by changing gene expression. (eg shh)
  • hox- (=homeobox) family of transcription factors that bind DNA and activate gene expression. Expression of different Hox genes along neural tube defines rostral-caudal axis and segmental levels.
  • intervertebral foramina-
  • isthmus- (G. narrow passage)
  • lamina terminalis- anterior region of brain where cranial neuropore closes.
  • lumbar plexus- mixed spinal nerves innervating the lower limb form a complex meshwork (crossing).
  • mantle layer- layer of cells generated by first neuroblasts migrating from the ventricular zone of the neural tube. Layers are rearranged during development of the brain and spinal cord.
    • (Ven-Man-Mar-CP)
  • marginal zone- layer of processes from neuroblasts in mantle layer.
    • (Ven-Man-Mar-CP)
  • mater- (L. mother)
  • meninges- mesenchyme surrounding neural tube forms 3 layer (Dura-, pia-, arachnoid- mater) connective tissue sheath of nervous system.
    • (D-P-A-cns)
  • mesencephalon- (=midbrain), the middle portion of the 3 primary vesicle brain (week 4).
    • (sc-R-M-P)
  • metencephalon- the cranial portion of hindbrain after it divides into 2 parts in the 5 secondary vesicle brain (week 5). Forms the pons and cerebellum in the adult brain.
    • (sc-My-Met-Mes-Di-Tel)
  • myelencephalon- the caudal portion of hindbrain after it divides into 2 parts in the 5 secondary vesicle brain (week 5). Forms the medulla in the adult brain.
    • (sc-My-Met-Mes-Di-Tel)
  • neural tube- neural plate region of ectoderm pinched off to form hollow ectodermal tube above notochord in mesoderm.
  • neural tube defect- (NTD) any developmental abnormality that affects neural tube development. Commonly failure of neural tube closure.
  • neuroblast- undifferentiated neuron found in ventricular layer of neural tube.
  • neurohypophysis- (=posterior pituitary=pas nervosa)
  • neuron- The cellur "unit" of the nervous system, transmitting signals between neurons and other cells. The post-mitotic cells generated from neuroepithelial stem cells (neuroblasts) in ventricular zone of neural tube.
  • neuropore- opening at either end of neural tube: cranial=rostral=anterior, caudal=posterior. The cranial neuropore closes (day 25) approx. 2 days (human) before caudal.
  • notochord- rod of cells lying in mesoderm layer ventral to the neural tube, induces neural tube and secretes sonic hedgehog which "ventralizes" the neural tube.
  • olfactory bulb- (=cranial nerve I, CN I) bipolar neurons from nasal epithelium project axons through cribiform palate into olfactory bulb of the brain.
  • optic cup-
  • optic nerve- (=cranial nerve II, CN II) retinal ganglion neurons project from the retina as a tract into the brain (at the level of the diencephalon).
  • otocyst- (=otic vesicle) sensory [#placode placode] which sinks into mesoderm to form spherical vesicle (stage 13/14 embryo) that will form components of the inner ear.
  • pars- (L. part of)
  • pharyngeal arches- (=branchial arches, Gk. gill) form structures of the head. Six arches form but only 4 form any structures. Each arch has a pouch, membrane and cleft.
  • pharynx- uppermost end of GIT, beginning at the buccopharyngeal membrane and at the level of the pharyngeal arches.
  • pia mater-
  • placode- specialized regions of ectoderm which form components of the sensory apparatus.
  • pontine flexure- middle brain flexure (of 3) between cervical and cranial flexure in opposite direction, also generates thin roof of rhombencephalon and divides it into myelencephalon and metencephalon. ( sc-^V^ )
  • prosencephalon- (=forebrain), the most cranial portion of the 3 primary vesicle brain (week 4).
    • (sc-R-M-P)
  • Rathke's pouch- a portion of the roof of the pharynx pushes upward towards the floor of the brain forming the anterior pituirary (adenohypophysis, pars distalis, pars tuberalis pars intermedia). Where it meets a portion of the brain pushing downward forming the posterior pituitary (neurohypophysis, pars nervosa). Rathke's pouch eventually looses its connection with the pharynx.
    • [Martin Heinrich Rathke 1973-1860, embryologist and anatomist]
  • rhombencephalon- (=hindbrain), the most caudal portion of the 3 primary vesicle brain (week 4).
    • (sc-R-M-P)
  • roofplate- early forming thin region of neural tube closest to the overlying ectoderm.
  • spinal cord- caudal end of neural tube that does not contribute to brain. Note: the process of secondary neuralation contributes the caudal end of the spinal cord.
  • spinal ganglia- (=dorsal root ganglia, drg) sensory ganglia derived from the neural crest lying laterally paired and dorsally to the spinal cord (in the embryo found ventral to the spinal cord). Connects centrally with the dorsal horn of the spinal cord.
  • spinal nerve- mixed nerve (motor and sensory) arising as latera pairs at each vertebral segmental level.
  • sonic hedgehog- (=shh) secreted growth factor that binds patched (ptc) receptor on cell membrane. SHH function is different for different tissues in the embryo. In the nervous system, it is secreted by the notochord, ventralizes the neural tube, inducing the floor plate and motor neurons.
  • sulcus- (L. furrow) groove
  • sulcus limitans- longitudinal lateral groove in neural tube approx. midway between roofplate and floorplate. Groove divides alar (dorsal) and basal (ventral) plate regions.
  • sympathetic ganglia-
  • telencephalon- the cranial portion of forebrain after it divides into 2 parts in the 5 secondary vesicle brain (week 5). (cavity- lateral ventricles and some of 3rd ventricle) Forms the cerebral hemispheres in the adult brain.
    • (sc-My-Met-Mes-Di-Tel)
  • thalamus- (G. thalamos= bedchamber) cns nucleus, lateral to 3rd ventricle, paired (pl thalami).
  • transcription factor- a factor (protein or protein with steroid) that binds to DNA to alter gene expression, usually to activate. (eg steroid hormone+receptor, Retinoic acid+Receptor, Hox, Pax, Lim, Nkx-2.2)
  • trigeminal ganglion- (=cranial nerve V, CN V) first arch ganglion, very large and has 3 portions.
  • vagal ganglion- (=cranial nerve X, CN X) fourth and sixth arch ganglion, innervates the viscera and heart.
  • ventricles- the fluid-filled interconnected cavity system with the brain. Fluid (cerebrospinal fluid, CSF) is generated by the specialized vascular network, the choroid plexus. The ventricles are directly connected to the spinal canal (within the spinal cord).
  • ventricular zone- Neuroepithelial cell layer of neural tube closest to lumen. Neuroepithelial cells generate neurons, glia and ependymal cells.
    • (Ven-Man-Mar-CP)
  • vestibulocochlear nerve- (=cranial nerve VIII, CN VIII, also called statoacoustic)
  • white matter- neural regions containing processes (axons) of neurons. In the brain it is the inner layer, in the spinal cord it is outer layer. (see [#grey matter grey matter])


Use these notes as an introduction to CSF, its production, role and components.

Also look at the selected highpower images of Stage 22 Brain showing the choroid plexus.

Then look also at the later Week 10 embryo sagittal sections which show choroid plexus distribution within the ventricles.

Note: the acronym "CSF" is also used in the literature for Colony Stimulating Factor, a growth factor, which is not related to cerebrospinal fluid.