Neuroanatomy Lectures #9 - 12: Development Of The Nervous System

Front 1

Structures that develope from neural tube and crest

Back 1

Neural tube: brain & spinal cord
Neural crest: PNS

Front 2

Role of BMP in ectoderm differenentiation

Back 2

BMP inhibits ectodermal cells from differentiating into neural cells, promoting the formation of epidermal tissue

Front 3

Different consequences from neural tube failing to close rostrally vs caudally

Back 3

Rostral: anencephaly
Caudal: spina bifida

Front 4

Relationship btwn the homeobox and Hox family of genes

Back 4

Hox genes encode txn factors that transcribe genes on/off. The homeobox is a conserved sequence of DNA inside the Hox gene that recognize and bind to DNA sequences on other genes.

Front 5

Retinoic Acid:
• Where it's produced
• What it activates
• What its concentration gradient contributes

Back 5

Retinoic Acid:
• Spemann organizer/Hensen's node
• txn of Hox genes
• an anterior-posterior sequence of Hox gene expression in the hindbrain

Front 6

Two general developmental mechanisms behind segmentation of the rhomencephalon

Also, name genes that are involved in segementation (3)

Back 6

1) Each segment of the rhombencephalon is called a rhombomere and each expresses its own set of genes as determined by homeobox genes

2) Cells within the region are restricted developmentally -
• first by Anterior-Posterior positioning through retinoic acid and Hox gene expression
• then by Dorso-Ventral through midline signals such as by shh protein

Kreisler, Krox-20 and Eph

Front 7

ssh Protein:
• its source (2)
• its influence on the neural tube
• its interaction with BMP

Back 7

ssh Protein:
• the neural tube, and later on by the floor plate
• it induces neural tube cells to become floor plate cells and ventrally located groups of cells to develop according to their prior hx
• Both shh and BMP serve to develop the NS but shh will devlop it ventrally and BMP, dorsally

Front 8

Overexpression of the eyeless gene in Drosophilia showed this

Back 8

Hox genes are examples of master control genes and can control the expression of other genes

Front 9

Genetic abnormalities of the emx gene show this in patients

Back 9

schizencephaly

Front 10

Genetic abnormalities of the otx gene show this in patients

Back 10

epilepsy

Front 11

Primary vesicles of the CNS w/ flexures

Back 11

Forebrain w/ optic vesicle (Midbrain flexure), Midbrain (Pontine flexure), Hindbrain

Front 12

Secondary vesicles

Back 12

Telencephalon, Diencephalon, Mesencephalon, Metencephalon, Myelencephalon

Front 13

Neuronal cell activity at the Ventricular and Pial surfaces

Back 13

Ventricular surface: cells are dividing
Pial surface: Direction where mature neurons migrate

Front 14

Marginal and Ventricular zones in Telencephalic vesicle

Back 14

Ventricular zone: the most proximal layer of neuroepithelial cells surrounding the notochord
Marginal zone: The outer layer of neuroepithelial cells, formed as the ventricular zone neuroepithelial cells mature

Front 15

Radial Glial cells:
• Fact about their connections during development
• The process of development they help mediate
• Two proteins that help with their fxn

Back 15

Radial Glial cells:
• They maintain their connections with both the ventricular and pial layers of the neural tube
• Neuronal migration
• astrotactin (glycoprotein) and an integrin isoform (ECM adhesion molecule)

Front 16

What reeler neurons showed about migration position and morphology

Back 16

Normal morphological appearance remained in tact despite aberrant positioning thus indicating that their identity was determined at birth and independent of position

Front 17

How layers of the cortex develop in an inside-out fashion

Back 17

neurons migrate along radial glia with younger neurons migrating past older ones in a inner to outer cortex direction

Front 18

Cajal-Reitzus cells:
• where they are located
• an important molecule it secretes and its classification
• what this molecule signals

Back 18

Cajal-Reitzus cells:
• in the marginal zone of the cortex
• reelin, a glycoprotein
• it signals the migrating neurons to get off the radial glia and take their final position in the cortex

Front 19

GnRH expressing neurons: '
• Where they migrate and btwn which two points
• The origin of their starting point of migration what it derives
• Syndrome that arises when GnRH cells fail to migrate and is sx (2)

Back 19

GnRH expressing neurons:
• Migrate into the CNS, btwn the olfactory pit and hypothalamus via a previously established axon tract
• olfactory pit - a derivative of the ectoderm that gives rise to the nasal
epithelium
• Kallmann's syndrome - anosmia and sterility

Front 20

The type of neurotransmitter released from neural crest cells that derive sensory and autonomic ganglia is dependent upon these factors (2)

Back 20

The final position of the neurons and the target cells/tissues with which they are matched

Front 21

How the Le Douarin experiments showed the environment influenced on cell maturation

Back 21

Transplanted quail neural crest cells (somites 18-24) that were originally programmed to released Ach were placed in the position of SCG somites in chicks switched to releasing catecholamines.

Similarly, SCG somites from chicks that were originally programmed to secrete catecholamines were transplanted to the position of somites 18-24 in quails and switched to releasing Ach.

Front 22

How LIF is an example of a local peptide influencing phenotype

Back 22

LIF is secreted by muscle cells. When neural crest cells that are programmed to be adrenergic are co-cultured with heart muscle cells, the neural crest cells become cholinergic

Front 23

PMP-22:
• is essential for this type of glial cell to perform its fxn
• its normal fate when produced in tissue culture alone
• the fate of the protein in the presence of a tissue culture and developing neurons
• a disease of the protein and its molecular etiology

Back 23

PMP-22:
• is essential for Schwann cells to wrap tightly and seal themselves around the developing axon
• When Schwann cells are allowed to produce the protein, it is subsequently broken down
• The protein is allowed to be expressed in the membranes of Schwann cells which can then fuse to form myelin
• Charcot-Marie Tooth Disease, missense mutation, Gly --> Asp

Front 24

What experiments with 'Trembler' and Schwann cells showed

Back 24

The defect of myelination is not due to the axons but due to the Schwann cells

Front 25

Laminin:
• Where it's present
• Is synthesized by these cells
• What it promotes

Back 25

Laminin:
• Along the pathways that axons follow as they extend their processes (growth cone) in the developing NS
• Schwann cells, particulary after injury
• Neurite outgrowth

Front 26

Netrin:
• Where it is released
• What induces its release
• What it attracts
• Why it influences dorsal sensory but not ventral motor neuron growth

Back 26

Netrin:
• The floor plate of the notochord
• shh, released from the underlying notochord
• Developing nerves from the spinal tract are influenced to cross the anterior commissure
• Dorsal sensory neurons have the receptor for netrin

Front 27

Newborn mice injected w/ NGF antiserum:
• Effects on the Sympathetic NS, Parasympathetic NS and DRG
• Overall effect on animal life

Back 27

Newborn mice injected w/ NGF antiserum:
• Sympathetic NS - fails to develop; Parasympathetic NS - unaffected; DRG - Slightly smaller than normal
• animals lived normally but responded poorly to stress

Front 28

DRG neurons can be rescued from their natural pattern of neuronal cell death with this molecule

Back 28

BDNF

Front 29

NGF:
• enhances the outgrowth and survival of neurites from these regions
• radio-lebeling has shown this
• regulates the synthesis of this protein through the induction of two enzymes
• Earliest event following is binding to a high affinity receptor

Back 29

NGF:
• sensory and sympathetic neurons
• it is taken up into nerve terminals and actively transported back into the soma
• induces Tyr-hydroxylase and Dopamine beta-hydroxylase to stimulate synthesis of NorE
• an increase in Tyr-Plation of the receptors

Front 30

Apoptosis and its relationship to motor neurons and its targets

Back 30

Removal of motor neuron targets increases cell death while an increase in the number of targets prevents apoptosis of these motor neurons

Front 31

Name 3 members of the Trk family of proto-oncogene receptors and their respective ligands

Back 31

Trk A - NGF
Trk B - BDNF and NT-4/5
Trk C - NT-3

Front 32

The general results of retinal development & tectum innervation in the chick embryo

Back 32

The retinal ganglion cells grow based on the anterior-posterior axis. Temporal retina iNN the anterior tectum while Nasal retina iNN the posterior tectum and this preference/polarity is based on repulsive interactions.

Front 33

The Eph Family:
• class of molecules and where they are most concentrated
• their ligands and where they are concentrated

Back 33

The Eph Family:
• Receptor Tyr Kinases,most concentrated in the Temporal retina
• Eph-A2 and A5, with the gradient strongest/concentrated in posterior tectum

Front 34

Limitations regarding synaptic specificity and chemical matching (3):

Back 34

Limitations regarding synaptic specificity and chemical matching:

• A single directional gradient is not sufficient enough to enable neurons to reach target destinations. Other topographically graded distributions contribute

• Matching of axons to targets is not rigid, aeb removal of target tissue during development shows a shift in what neurons will iNN.

• Electrical activity is needed to fine tune connections, to provide fxn to the map

Front 35

Synapse elimination of polyneuronal innervated muscle fibers is mediated by this

Back 35

it's mediated by the muscle fibers themselves following the period of normal cell death in late embryonic development

Front 36

Def of critical period in relation to the visual projections from the LGN to the Visual/Striate cortex

Back 36

It is the time period of plasticity in the young animal during which certain characteristics of vision can be altered by activity/inactivity. These changes are reversible if the alterations occur during this period, or irreversible if the attempt to change occur after this period has closed.

Front 37

The effects of monocular deprivation on ocular dominance columns:
• Before the critical period
• After the critical period

Back 37

The effects of monocular deprivation on ocular dominance columns:

• Before the critical period - the working eye fails to retract its fibers and normal ocular column borders are not observed. This also leads to an absence of binocularly driven neurons.

• After the critical period, no deficits are seen.

Front 38

A histographical representation of monocular dominance during the critical period would show these results

Back 38

A high number of fxnal neuronal cells on the ipsilateral side of the normal eye, a great reduction of fxnal neuronal cells on the contralateral side as well as a great reduction of binocularly driven neurons