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Transcript
Nolte – Chapter 2 (Development of the Nervous System) and all Class-Notes
tagged with Chapter 2.

Gastrulation is what gives rise to three different germ layers by going from
symmetrical to asymmetrical.
o Ectoderm
 Leads to the nervous system, epidermis, and nervous system
 These cells all have an affinity to become neurons (since the
express bone morphogenetic proteins)
 The organizer has a BMP inhibitor.
o Endoderm
 Yields the gut
o Mesoderm
 Muscle and tissues
o A neural plate initially forms as a longitudinal band of ectoderm
 This neural plate, by way of the organizer begins to hold from
the outside in to approach the dorsal midline. As cells come in
an move under the ectoderm that got pinched, the cells on top
get inhibited, while the other ones begin to express their
calling of becoming neurons. The hinhibited ones become
epidermis.
 The dorsal blastopore lip forms.
o A full fusing results in the neural tube, that is
separate from the ectoderm.
o The segments of the plate that touched first will
drop off and break below as the neural crest,
which will sit on top of the tube.
 Neural crest cells will be used for many
purposes, but mainly becoming parts of
the PNS and Enteric nervous system.
 This process is known as primary neurulation
 If a new organizer is introduced, a new axis will be
created.
 This neural tub develops into virtually the entire CNS
 The cavity becomes the ventricular system.
o Concentration gradients cause the dorsal to become separated from
ventral
 The ectoderm is responsible for dorsal and notochord for
ventral.
 A groove will appear marking this sepeartion
 Its known as the sulcus limitans
 Formal name for dorsal is alar. Basal for ventral.
 Sensory in alar, motor with basal.
The notochord remains in close proximity to the floor plate
and motor neurons flank the floor plate.
 Sonic Hedghod protein is expressed here and directy
ventral identity.
Neural Tube has rostral to caudal enlargements in its cylinder.
o Prosencephalon (fore)
 Develops into cerebrum
 Gives rise to the Telencephalon
 Becomes the cerebral hemisphere
 There is a thin membrane that connects the two
swellings on either side of the neural tube known as the
lamina terminalis
o Become the anterior commissure and the CC.
 Basal part thickens and becomes the basal ganglia.
 The rest of telencephalon proliferates and hangs down
(off of lamina terminalis?) and folds down to the
diencephalon.
o Where tel and dien meet is the insula.
o The hanging creates the ventricular system.
 Gives rise to the Diencephelon
 Becomes the thalamus, hypothalamus, and retina.
 There is a bit of fusion to form the hypothalamic sulcus.
o Mesencephelaon(mid)
 Becomes the midbrain
 Has a bending known as the cephalic flexure
 Ends up being the bend between the axes of the
brainstem and cerebrum.
o Rhombencephalon(hind)
 Rest of brainstem and cerebellum
 Gives rise to the metencephalon
 Becomes the Pons
 Gives rise to the Myelencephalon
 Becomes the medulla
 Between met and myelencephalon there is a pontine flexure
 This gives rise to the fourth ventricle (remember this
looks like a rhombus  rhombencephalon)
 This flexure shoves the dorsal (alar) to the side of the
basal in this region.
o So now its lateral medial relationship. So the
lateral is more sensory and the medial is more
motor.
o The lateral portions of this alar plate thicken to
form the rhombic lips which continue to enlarge,
and fuse in the midline and form the cerebellum




This seems a little strange since alar was
sensory?
o Spinal Cord
 Separated from Rhombencephalon by the cervical fissure.
Defects
o Complete failure to close the neural tube
 Craniorachischisis
 Just the caudal end
 Spina bifida (myelomeningocele)
 Just the rostral end
 Anencephaly
o Most of cerebral hemisphere is lost.
 Sufficient levels of folic acid seem to help against neural tube
closer problems
 We can detect problems by elevated levels of alpha fetoprotein
that the open neural tub allows to leak out into maternal
circulation.
o Abnormal Development
 Disrupting the signaling molecules can cause
holoprosencephaly (can be evoked by mutations in SHH)
 Failure of prosencephalon to separate into the
diencephalon and telencephalon.
