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19 Cards in this Set

  • Front
  • Back

DETERMINANTS OF CORTICAL NEURONS

Morphology


Laminar position


Molecular markers


Projection patterns

CORTICAL PROJECTION PATTERNS

Corticofugal: (outside cortex) - deep layers


/Corticothalamic - to thalamus VI


/subcerebellar - beyond thalamus SC, pons and superior colliculus



CORTICAL PROJECTION NEURONS

CALLOSAL - connect two hemisphere of CC via corpus callosum (CONTRALATERAL)


Ipsi - same side


Columnar - local connectivity



Corticocortical: (within cortex, project through midline to contralateral hemisphere) LOCAL PROJECTIONS /Columnar - IV /CALLOSAL AND IPSILATERAL (LAYERS 2-3)

DENDRITE MORPHOLOGY CLASSES OF EXCITATORY NEURONS

Intratelencephalic


pyramidal tract neurons corticothalamic

LAYERS

Layer 1


No pyramidal neurons and few soma. Dense in dendrites and projections.


Layer 2 +3


Pyramidal neurons grouped together. Layer 2 has smallest somas.


Layer 3


Has pyramidal neurons whos somas are largest at lower surface and decrease in size on ascension



LAYERS II

Layer IV


Have pyramidal neurons and spiny stellate neurons.


Densest layers - most CBs


Layer V


Largest pyramidal neuron somas. Largest near bottom. Sparsely packed somas vs layer 6


Layer VI


Densely packed soma


UL VS LL

/UL has smaller soma size vs LL


/LL - more complex and elaborate dendritic treez


(morphology)



Connectivity


UL innervate NC and striatum


LL innervate subcerebral and subcortical regions. Give rise to associational and commisual



Genes


UL CDP, cux2


LL fezf2, otx1

SPECIFICATION OF NC

/Emx2 Pax6


/ Foxg1-


/Lhx2

SOX5

Controls sequential generation of corticofugal neuronal subtypes.


KO: PROBLEMS WITH LL


EXPRESSION IN CORTICOFUGAL PN



Axonal tracing. Retrograde transport. Subcerebral - both


Callosal - contra


SOX 5 KO

Only corticofugal PN affected


Cux 2(UL) not affected. Fexf2 was.



B11.5: misplaced and express L5 markers.


Morphology alteration.


Subplate cells misplaced, pyramidal and express CTIP2 (acquire characteristics of layer V prematurely)


Usually CTIP2 confined to lower region but in KO spread all over cortex

SOX5 MISEXPRESSION IN UL

Generates neurons that send axons through striatum. Subcerebral projections neurons accelerated.


CHANGE PROJECTION PATTERN

FEZF2 - CORTISPINAL PROJECTION NEURONS

Expressed in subcerebral PN.


KO- CORTISPINAL PN MISSING. LACK CSMN.


CTIP2 MISSING. NOT IN LAYER V.

MATURATION LAYER VI IMPAIRED IN FEZF2 MUTANT

Low levels CTIP2. POSITIVE TBR1.


SIGNAL MATURATION LOST.


V1 USUALLY COEXPRESS THE TWO.



LAYER 6 THICKNESS INCREASE. DISORGANISED SP.

UL DEVELOP NORMALLY IN FEZF2-/-

Layer V gone.

LAYER IV NEURONS EXPRESS LAYER V MARKERS AFTER FORCED FEZF2 EXPRESSION

ER81. Increased expression of L5 MARKERS.


/Some project subcerebrally after forced expression of fezf2.


+pyramidal +apical dendrites


/ULN express DLN change morphology and pattern projection


/reach cortical surface and extend tangentially


LONG AXON PROJECT TO STRIATUM


INDUCE CS fate on own

SATB2 - REGULATE identity of callosally projecting neurons

Expressed in subset of neurons in layers 2-5.


KO: PROJECT SUBCEREBRAL NO LONGER VIA CORPUS CALLOSUM


PROJECT THROUGH IC AND EXTN CAPSULE (REDISTRIBUTION)


CHANGE PROJECTION PATTERNS OF B-GALACTOSIDASE

SATB2

Wt: CC, AC, IC/CP



Ko: AC, IC/CP NO CC

UL IN SATB2 KO

CTIP2 expression in UL increases.


Tbr normal


Cuz2 normal but mashed migration

LACK OF SATB2

Disappearance of CS TRACT BEYOND CEREBRAL PEDUNCLE.


SATB2 ROLE IN MATURATION of CS PN.


No alkaline phosphatase in BS


PYRAMIDAL DECUSSATION MASHED