156:
26:
314:. There are two molecular domains that exist within the CGE and closely resemble extensions of the caudal MGE and LGE. The CGE is distinct from the LGE and MGE in gene expression patterns and progeny produced. Unlike the cells from the MGE, the cells from the CGE were rarely parvalbumin-containing neurons. It seems that the majority of cells from the CGE were GABAergic interneurons, but depending on where they are located, CGE-derived cells are very diverse. CGE-derived cells include GABAergic interneurons, spiny interneurons, mossy cells, pyramidal and granule neurons, and even
129:. Tangential migration does not involve interactions with radial glial cells; instead the interneurons migrate perpendicularly through the radial glial cells to reach their final location. The characteristics and function of the cells that follow the tangential migration pathway seem to be closely related to the location and precise timing of their production, and the GEs contribute significantly to building up the GABAergic
570:
as further research is performed. The complexity of molecular steps needed to correctly place cells in a system as complicated as the brain is impressive, and as more pieces to this intricate puzzle arise, it will be easier to come up with strategies to remedy disorders associated with neuronal migration, and to potentially repair damage caused by trauma, stroke, maldevelopment, and aging.
294:. During the late stages of embryonic development, both the LGE and MGE guide cell migration to the cortex, specifically the proliferative regions of the cortex. Some studies have found that the LGE also contributes cells to the neocortex, but this remains an issue of debate. In vitro, cells migrating from the LGE travel at a rate of 100 ÎĽm per day, slower than the MGE cells.
199:
anterior entopeduncular region (AEP). The cells of the GEs are quite homogenous, with the MGE, LGE, and CGE all having small, dark, irregular nuclei and moderately dense cytoplasm, however, each eminence can be identified by the type of progeny that it produces. See the individual GE sections below for more information on the different types of progeny produced.
280:
of the basal ganglia and hippocampus. The MGE may also be a source of Cajal-Retzius cells, but this remains controversial. Early in embryonic development, the interneurons in the cortex stem primarily from the MGE and the AEP. In vitro experiments show that MGE cells migrate more than 300 ÎĽm per day,
159:
Coronal section in the forebrain of an embryonic mouse at 12.5 days of gestation (preplate stage), showing the lateral and medial ganglionic eminences (LGE, MGE) from which GABAergic interneurons tangentially migrate to the cortical anlage (left, yellow). Glutamatergic neurons destined for the cortex
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Further research could be done on the migration of cells from the basal ganglia to the neocortex. The molecular mechanisms in control of this are still not completely clarified. The number of known mutations that could interfere with neuronal migration is rapidly growing, and will continue to do so
458:
have been implicated in the migration as well. High GABA concentrations have been seen to cause random cell movement ("random walk migration"), while low concentrations promote directed migration. 5-HT has been tied to the process of incorporating interneurons into the cortical plate, as well as in
467:
The migration of cells from the ventricular zone to their intended destination and the success of their differentiation can be interrupted in many different ways, including interference with mechanical motors or an alteration of molecular signals that initiate movement, lead the cell in migration,
330:
Cells in the ganglionic eminence migrate tangentially to neocortex, giving rise to interneurons. A variety of molecular mechanisms cooperate to direct this process. Embryonic interneuronal migration to the cerebral cortex is mediated by an array of motogenic growth factors in the MGE, repulsive
289:
Compared to the early temporal frame of development in the MGE, the LGE aids in the tangential migration of cells later in the mid-embryogenic stage. Unlike the MGE, which guides most cell migration into the cortex during this stage, the LGE contributes less to cell migration to the cortex, and
198:
is required to determine the independent progenitor cell populations in the LGE and MGE. Interactions between these three genes define the boundaries between the different progenitor zones and mutations of these genes can cause abnormal expansion around the MGE, LGE, ventral pallium (VP), and
290:
instead guides many cells to the olfactory bulbs. In fact, the migration to the olfactory bulb is led by the LGE into adulthood. The route that newly generated neurons take from the anterior subventricular zone to the olfactory bulb is called the
371:. This directed migration is induced by differences in gene expression between these subpallial domains. An array of genes are involved in the differentiation and specification of interneurons and oligodendrocytes, including:
275:
zone. More specifically, performing a mechanical transection of the migratory route from the MGE to the neocortex causes a 33% decrease in GABAergic interneurons in the neocortex. The MGE also produces some of the neurons and
243:
interneurons in the striatum. Cells migrating along these pathways move at different rates. Some molecules that have been implicated in controlling the rate of the unidirectional movement of cells derived from the GEs are
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231:
These pathways are temporally and spatially distinct, and produce a variety of GABAergic, and non-GABAergic interneurons. One example of GABAergic interneurons that the GEs guide are
468:
and terminate its migration. The function of the molecules that affect migration are not confined to cell movement, overlapping considerably with the events associated with
419:
The induced migration of cells from the ganglionic eminence during development is directed by a variety of motogenic factors, molecules that increase cell motility, and
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852:
Lavdas, Grigoriou, Pachnis, & Parnavelas. (1999). The medial ganglionic eminence gives rise to a population of early neurons in the developing cerebral cortex.
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339:
factors in migratory corridors in the ganglionic eminence, and attractive factors in the cortex itself. Cells in the LGE migrate to the striatal domain (
281:
three times faster than the migration of LGE cells. See more about the time frame and function of MGE in comparison to the LGE in the following section.
310:, posterior to where the LGE and MGE fuse. The CGE is a fusion of the rostral medial and lateral ganglionic eminence, which begins at the mid to caudal
25:
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Hernández-Miranda, Parnavelas, & Chiara. (2010). Molecules & mechanisms involved in the generation and migration of cortical interneurons.
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435:, are a family of motogenic factors involved in directing migration. The cerebral cortex provides chemoattractant molecules (for example
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488:
155:
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Brazel, CY; Romanko, MJ; Rothstein, RP; Levison, SW (January 2003). "Roles of the mammalian subventricular zone in brain development".
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202:
Additionally, the subventricular zone is the starting point of multiple streams of tangentially migrating interneurons that express
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535:
143:
In humans, the GEs disappear by one year of age. During development, neuronal migration continues until the extinction of the
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enhances cell motility and directs cells away from subpallial regions and demarcates the routes followed by migrating cells.
472:. As a result, neuronal migration syndromes are difficult to classify. The largest class of neuronal migration syndromes is
1046:
122:
620:
MarĂn, O; Rubenstein, JL (November 2001). "A long, remarkable journey: tangential migration in the telencephalon".
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302:
The caudal ganglionic eminence is another subcortical structure that is essential to the generation of cortical
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Ghashghaei, HT; Lai, C; Anton, ES (February 2007). "Neuronal migration in the adult brain: are we there yet?".
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336:
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245:
49:
235:-containing interneurons in the neocortex. Some examples of non-GABAergic interneurons that the GEs guide are
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Ross, M. E., & Walsh, C. A. (2001). Human brain malformations and their lessons for neuronal migration.
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451:
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Purves, D., Augustine, G., Fitzpatrick, D., Hall, W., LaMantia, A.S., McNamara, J., and White, L. (2008).
61:
126:
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1041:
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Wonders, CP; Anderson, SA (September 2006). "The origin and specification of cortical interneurons".
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and assembly are rarely pure, but closely related to neuronal migration genes. This notably includes
95:
271:. The precursors of most GABAergic interneurons in the cerebral cortex migrate from the subcortical
165:
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type I and II in the cortex) while subpallial areas produce chemorepulsive molecules (for example
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209:. There are three main tangential migration pathways that have been identified in this region:
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Ganglionic eminences are categorized into three groups based on their location within the
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are generated locally in the cortical ventricular zone and migrate radially (right, red).
140:. The GEs also guide the axons growing from the thalamus into the cortex and vice versa.
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38:(red). The radially migrating interneurons travel parallel to the radial glial cells.
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A sulcus separates the medial and lateral ganglionic eminences. The expression of
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of cerebral and cerebellar cortex, occasionally with pachygyria surrounding the
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type III) in the migratory corridors are necessary for this process to occur.
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Interneurons (green) migrate tangentially from the ganglionic eminence to the
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443:) to direct cell migration. Additionally, some permissive factors (such as
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147:, at which point the remnants from the germ layer make up the eminences.
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34:. The tangentially migrating interneurons travel perpendicular to the
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597:
Encha-Razavi & Sonigo. (2003). Features of the developing brain.
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the medio-rostral migration (subpallial basal telencephalon to the
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and part of the septum. The CGE gives rise to interneurons in the
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The primary purpose of the MGE during development is to produce
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the latero-caudal migration (subpallial telencephalon to cortex)
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population. Another structure that the GEs contribute to is the
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925:
121:(a lateral, medial and caudal eminence), where they facilitate
541:
Disturbances in the genesis of neural elements can result in
476:. This includes a spectrum of simplified cortex ranging from
113:
The eminence is divided into three regions of the ventral
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the differentiation into subpopulations of interneurons.
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the latero-caudal migration (basal telencephalon to the
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Mis-migration of neurons can also result in bilateral
527:, and the failure of the olfactory bulb to develop.
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553:, and altered cell survival resulting in areas of
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484:(broadened gyri) with unusually thick cortex.
480:(a total absence of cortical convolutions) to
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757:: CS1 maint: multiple names: authors list (
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415:Molecular mechanisms for directed migration
351:. MGE cells follow a migratory path to the
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833:Development of the Nervous System. 3rd ed.
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248:/scattered factor (HGF/SF), and various
239:interneurons in the olfactory bulb, and
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737:. Sinauer Associates. pp. 555–8.
511:, and focal/subependymal heterotopia.
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15:
7:
491:, a disease recognized by neuronal
489:periventricular nodular heterotopia
86:) is a transitory structure in the
831:Sanes, Reh, & Harris. (2012).
267:and direct their migration to the
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913:Annual Review of Neuroscience, 24
285:Lateral ganglionic eminence (LGE)
175:Lateral ganglionic eminence (LGE)
88:development of the nervous system
423:molecules. The motogenic factor
298:Caudal ganglionic eminence (CGE)
256:Medial ganglionic eminence (MGE)
178:Caudal ganglionic eminence (CGE)
172:Medial ganglionic eminence (MGE)
94:migration. It is present in the
854:The Journal of Neuroscience, 99
536:agenesis of the corpus callosum
499:is characterized by a cortical
495:lining the lateral ventricles.
347:) and parts of the septum and
1:
803:10.1016/s0301-0082(03)00002-9
367:, and specific nuclei in the
1047:Cardiac neural crest complex
868:Nature Reviews. Neuroscience
670:Nature Reviews. Neuroscience
622:Nature Reviews. Neuroscience
306:. It is located next to the
835:Academic Press. pp. 62–63.
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1219:Developmental neuroscience
96:embryonic and fetal stages
359:, the bed nucleus of the
123:tangential cell migration
60:
23:
791:Progress in Neurobiology
292:rostral migratory stream
246:hepatocyte growth factor
599:Child's Nervous System
450:The neurotransmitters
161:
62:Anatomical terminology
158:
127:embryonic development
90:that guides cell and
1054:Truncal neural crest
1042:Cranial neural crest
856:(19). pp. 7881–7888.
735:Neuroscience. 4th ed
547:ectopic neurogenesis
463:Associated disorders
250:neurotrophic factors
952:Development of the
561:, and heterotopia.
545:. Examples include
166:subventricular zone
80:ganglionic eminence
19:Ganglionic eminence
1024:Adult neurogenesis
977:Neural development
543:cortical dysplasia
521:mental retardation
497:Zellweger Syndrome
162:
102:found between the
100:neural development
36:radial glial cells
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1205:
1129:
1128:
1072:Rostral neuropore
841:978-0-12-374539-2
744:978-0-87893-697-7
532:axonal projection
515:is recognized by
513:Kallmann syndrome
357:nucleus accumbens
308:lateral ventricle
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1163:Surface ectoderm
1091:Cervical flexure
1086:Cephalic flexure
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565:Further research
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68:edit on Wikidata
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1196:Otic vesicle
1186:Otic placode
1168:Lens placode
1034:Neural crest
1019:Neuropoiesis
1002:Neural plate
962:Neurogenesis
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797:(1): 49–69.
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1153:Optic stalk
1143:Neural tube
1106:Basal plate
1064:Neural tube
1007:Neural fold
982:Neurulation
555:hyperplasia
503:similar to
493:heterotopia
421:chemotactic
365:hippocampus
241:cholinergic
233:parvalbumin
44:Identifiers
1116:Neuroblast
1101:Alar plate
1081:Rhombomere
574:References
557:, reduced
482:pachygyria
431:, such as
337:permissive
273:progenitor
145:germ layer
55:D000097803
1158:Optic cup
1111:Glioblast
1077:Neuromere
992:Notochord
753:cite book
559:apoptosis
501:dysplasia
335:and LGE,
320:astrocyte
269:neocortex
262:GABAergic
1213:Category
1191:Otic pit
888:16883309
819:24001139
811:12637172
690:17237805
642:11715055
369:amygdala
349:amygdala
333:striatum
312:thalamus
225:striatum
131:cortical
104:thalamus
987:Neurula
970:General
896:3329713
698:9322780
650:5604192
517:anosmia
345:putamen
125:during
117:of the
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478:agyria
425:HGF/SF
397:Nkx5.1
393:Nkx2.1
363:, the
192:, and
184:Nkx2-1
892:S2CID
815:S2CID
694:S2CID
646:S2CID
385:Mash1
207:genes
66:[
884:PMID
837:ISBN
807:PMID
759:link
739:ISBN
686:PMID
638:PMID
456:5-HT
454:and
452:GABA
445:NRG1
441:Slit
437:NRG1
433:BDNF
409:Vax1
407:and
405:Six3
401:Isl1
389:Gsh2
381:Gsh1
377:Dlx2
373:Dlx1
343:and
318:and
278:glia
195:Pax6
189:Gsx2
134:cell
106:and
92:axon
78:The
50:MeSH
1179:Ear
1135:Eye
876:doi
799:doi
678:doi
630:doi
205:Dlx
98:of
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399:,
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391:,
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383:,
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821:.
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700:.
680::
674:8
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70:]
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