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85 Cards in this Set

  • Front
  • Back
Coloboma
defects in eye from failure of the choroid fissure to close
Peter’s anomaly
defects results from a lack of separation of the lens vesicle from the
corneal epithelium
during optic cup patterning, this regulates transcription factor expression in dorsal retina
BMP4
Upregulates tx5
Downregulates Vax and Pax2 in the dorsal retina

Tbx5
upregulates ephrin B1 & ephrin B2 dorsally

Lance: We have no Idea what we are tying to say about slide 40 from lecture 13
Ventroptin,
BMP4 inhibitory protein

prevents BMP4 from interacting w/cells of the Ventral retina
regulate transcription factor expression in ventral retina during optic cup patterning
Shh & RA
Upregulates Vax2
Downregulates BMP4
These genes for retina development are expressed early in the anterior neural plate
Pax6
Six3
Rx
Lhx2
Surface Ectoderm develops into
Lens

Corneal Epithelium
mesenchyme develops into
Corneal Stroma
Uvea: (choroid, iris, ciliary body)
Sclera
vitreous

CT, muscle (& vessels) come from cranial mesenchyme
Neural Ectoderm develops into
RPE
retina
optic nerve
these TF can cause ectopic eye formation
Pax6
Rx
Six3
if you KO these you will get cycloptic embryos
cyc
shh
retinal progenitor cells (RPCs)
E10.5, during lens placode invagenation

Undifferentiated, express common eye TF Pax6, Rx1, Six3, Six6, Lhx2, Hes1, chx10

multipotent & differentiate into ganglion cells, bipolar, amacrine, horizontal , photoreceptors and Müller cells
glia.
what are the dorsal regulators in Dorso-ventral axis of the retina
BMP4
Tbx5
what (TF) & where BMP4 in Dorso-ventral axis of retina
Dorsal
upregulates tx5
down regulates Vax & Pax2
what & where Tbx5 in Dorso-ventral axis of retina
Dorsal
upregulates ephrin B1, ephrin B2
down regulates EphBs
Ventral regulators in dorso-ventral axis of retina
Shh
Retinoic Acid
Shh & RA in Dorso-Ventral axis of retina
Ventral
Upregulate Vax2
Downregulates BMP4

Ventropin is found ventrally & binds BMP4 to further inhibit it
Vax2 in Dorso-Ventral axis of retina
Ventral
upregulates EphB2, EphB3
down regulates Ephrin Bs
Ephrin Bs and Eph Bs
control the lateral-medial axonal Targeting once the axons have reached the tectum
Optic Stalk from optic vesicle
Floor plate, prechordal plate releases Shh (& BMP7) --> induce Pax2
Pax2 down-regulates MITF & CHX10
Retina from optic vesicle
head ectoderm releases FGFs --> induces CHX10

chx10 down regulates Mitf & Pax2,
RPE from optic vesicle
TGF-beta from periocular mesenchym

upregulates MITF
downregulates Pax2, CHX10, & otx2
what causes the eye field to split
cyc controls expression of BMP7, Shh, twhh --> differentiation of the floorplate of the forebrain
Activates Pax2 (optic stalk)
Represses Pax6 & Rx (retina)
Lens placode does what for optic cup
secretes FGFs that turn on Chx10 & Lhx2
these are high medially in the naso-temporal axis of retina
BF2(foxd2)
SOHo1 (turns on EphrinAs)
GH6

--> high EphA
nasal TF of naso-temporal axis of retina
[high] BF1 (foxg1)
[low] BF2 (foxd2)
Tectum axis
EphA3 controls Anterior-posterior

Ephrin Bs and Eph Bs control the
lateral-medial
5 components to Chemoaffinity
1. neurons are different
2. different b/c retinal position
3. differences are biochemical & expressed on membrane
4. differences are present when in early development when connections are formed
5. pre/post synaptic have complementarty markers that are selectivly exclusive
Glu receptors 3 types
AMPA
NMDA
Metabotropic
AMPA
ionotropic: directly gates ion channels

binds agonist AMPA or kainate
Na+ & K+
NMDA receptor
ionotropic
Ca+, Na+, & K+
ligand AND voltage- ated channel

long term changes based on stimulation bursts from Pre

Enhances Occular dominace columns
NT4/5 & BDNF
causes loos of occular dominance columns
slave ossiclators
cerebral cortex
liver
kidney
Properties of Circadian rhythem
1. ubiquitus
2. generated by endogenous ossicaltors ~ 24hr
3. can be reset, phase shift by zeitgeburgs (external cues)
4. temp compensated (rate of clock genes, but not presents of clock)
5. genetically determined (tau)
6. clock based on molecular feed back loop
Entrainment
critical aspect is timing of light to relative to rhythm

phase shift sets the period of internal clock
Melatonin
released at night
Light Pulse at begingin, or end of dark cycle
phase delay
Light Pulse at end of dark cycle
phase advance
Superchiasmatic nucleus effectors
Temp
Adrenal Gland: Cortisol
Penial Gland: melationin
zeitoburg receptors
inner retina, glial cells

Melanopsin
Crytpochrome/B2 cofactor
Crytpochrome
1 & 2
1 more important
xpressed in INL & Ganglion cells, & in the SCN
Melanopsin:
TM protein
in small group of RGC dendrites
clock genes
Per – period
Tim – timeless
Dbt – doubletime
Cry - cryptochrome
Clock molecular mech
Per & Tim are inhibit Clk & Cyc at night, but Clk & Cyc inhibit Per & Tim during the day from entering the nucleus

complex with clk & Cyc, & Bma! affect gene transcription
Clock mid day
CLK and CYC active (+ PER and TIM)

• PER unstable - DBT (doubletime)
phosphorylates PER

• CRY degrades TIM as long as light is present
Clock dusk
Tim accumulates & displaces DBT

Tim (nuclear signal)
Clock midnight
Per & Tim in nucleus, bind Clk & Cyc
--> Per & Tim mRNA decreases,
--> Clk mRNA increases
Dawn Clock
Perception of light by CRY
• Degradation of TIM
• Phoshorylation and degradation of PER
Phase advance mech
light near end of dark cycle will destroy Tim
Phase delay mech
Light after dusk by postponing production of Tim
Melatonin regulation pathway
Retinohypothalmic tract
RGC ->
RHT Retinohypothalmic Tract -->
SCN -->
PVH) PeriVentricular nucleus
(IML) Interomediolateral cell column of spinal cord -->
SCG superior cervical Ganglion
Pineal gland
mealatonin feeds back to hypo
Melanopsin:
TM protein
in small group of RGC dendrites
clock genes
Per – period
Tim – timeless
Dbt – doubletime
Cry - cryptochrome
Clock molecular mech
Per & Tim are inhibit Clk & Cyc at night, but Clk & Cyc inhibit Per & Tim during the day from entering the nucleus

complex with clk & Cyc, & Bma! affect gene transcription
Clock mid day
CLK and CYC active (+ PER and TIM)

• PER unstable - DBT (doubletime)
phosphorylates PER

• CRY degrades TIM as long as light is present
Clock dusk
Tim accumulates & displaces DBT

Tim (nuclear signal)
Clock midnight
Per & Tim in nucleus, bind Clk & Cyc
--> Per & Tim mRNA decreases,
--> Clk mRNA increases
Dawn Clock
Perception of light by CRY
• Degradation of TIM
• Phoshorylation and degradation of PER
Phase advance mech
light near end of dark cycle will destroy Tim
Phase delay mech
Light after dusk by postponing production of Tim
Melatonin regulation pathway
RGC ->
RHT Retinohypothalmic Tract -->
SCN -->
PVH) PeriVentricular nucleus
(IML) Interomediolateral cell column of spinal cord -->
SCG superior cervical Ganglion
Pineal gland
Geniculo-hypothalamic tract- melatonin pathway
RGC
LGN [IGL=Intergeniculate Leaflet]
hypothalamus
NPY & GABA
Features of Circadian Imbalance
Sleep Disturbances
2. Carbohydrate Cravings
3. Confusion/Poor coordination
4. Malaise/Blues
5. Susceptibility to Infectious Disease
inner ear
Vestibule - vestibular system
2. Semicircular canals - vestibular system
3. Cochlea auditory organ
Scala tympani and scala vestibuli
perilymph
Scala media
endolymph, K+
Inner hair cells
Linear
supported by pillar cells
Outer hair cells
V-shaped palisade
supported by Dieter cells (phalangeal cells)
hair cell innervation
Afferent- spiral ganaglion cells

Efferent: reguates sensititivy
bass
Excites near apex
high pitch
excites near base
Hair cell transduction
movement-> intake Ca 7 K+
Voltage change --> K+
Glu released in graded to afferent & efferent
phase locking
phase @ nerve fires the same
compression

as freq rises, nerve can't fire as fast, but keeps phase
population
# of nerves firing, increases w/sound level
CNS gets info about freq
place code
where on basilar membrane
hair stereocilia differ in length & stifness
differ ion channels
Temporal code
phase locking- sync w/part of wave but not whole
Volley Principle; get many different parts to get full wave
Place Code & Temporal code interact
Place codes cant do bass, eaiser to phase lock lower freq

Temporal cant do pitch
hair cell adapt
intersital plaque holds hairs together
hairs move -> Ca & K in
Calmodulin active & releases myosin
plaque slides down & hairs separate
conduction deafness
vibrations cant get to inner ear

wax
ruptured drum
ossification
Sensorineural deafness
damaged hair cels or auditory pathway

result of age & loudness
Chochlear implant
electrodes implanted in Scala tympani

directly stimulates nerve fibers on basilar membrane
Otits MEdia
ear infection
upper respriatory viral
swollen Eustachian tubes

Effusion of middle ear provides nice medium for bacterial growth
Retino-tectal mapping
Nasal has this & looks for
nasal has low EphA
looks for High EphrinA in Posterior
Temporal looks for
Retio-Tectal mapping
Has high EphA
looks for low EphrinA in Anterior Tectum
Dorsal
Retio Tetctum mapping
Has Low EphB
looks for High EphrinB in Medial tectum
Ventral
retina tectum mapping
has high EphB
Looks for low EphrinB in lateral tectum