visual neuro final cards !! Flashcards
(32 cards)
diabetes
haemorrhage
ischemia -> leaky vessels
basement membrane thickness increase
loss of pericytes -> increased vascular perm.
microaneurisms
stroke
blood vessel diameter can be a predictor
parkinsons
OPL thickening -> a-syn deposits
RNFL thinning and decreased macular thickness
alzheimers
b amyloid plaques can be seen using hyperspectral imaging
rnfl thinning bc decreased GCs
MS
loss of GCs
hypertension
ratio between art : vein thickness alters
art narrowing = increased pressure = squishes veins
blood retinal barrier breakdown
pupillary light reflex pathways - dilation
absence of light
sympathetic NS
sphincter muscles relax
dilate for emotion too
pupillary light reflex pathways - constriction
presence of light
parasympathetic NS
activate sphincter muscles
constrict for near vision
pupillary light reflex pathways - 3 neuron model
- hypothalamus -> thoracic s.c.
- thoracic sympathetic trunk -> long ciliary
- dilator muscle (release NA to a1 rec)
horner’s syndrome
pupillary light reflex pathways 3 neuron pathway disrupted
can’t dilate eye
lid droops
no sweating
blood vessel dilation in this area
accessory optic system
birds & fish -> main visual area
mammals -> large field motion
optokinesis & vestibular connections
nystagmus = involuntary eye movements
accessory optic system - inputs
MT/MST and V1
super colliculus
directing eye based on attention (and maintaining gaze on something)
humans -> in cortex
birds -> ventral and dorsal streams
bimodal and tri modal neurons
suprachiasmatic nucleus
input from: intrinsically photosensitive GCs
circadian rhythm
pulvinar nucleus of the thalamus - input and output
input -> both layers of SC
output -> wide to cortical visual areas & parietal cortex
pulvinar role
lesion =?
combine different pieces of information
lesion = facial rec. issues
activation for angry (closed mouth) and surprised facial expressions
simple vs complex cells (huber and wiesel)
simple -> small r.f., separate on and off, L4 and 6
complex -> large r.f., overlapping on and off, outside L4
issues with hubel and wiesel
- remove inhibition to striate cell = no orientation sel
- complex often respond to stimuli simple cells don’t -> so how can complex get input from simple?
- both complex and hypercomplex can be monosynaptically excited from LGN
- simple and complex distinction doesn’t apply at low contrast or after adaptation
saccades: FEF, PPC, DLPFC
fef: voluntary
ppc: reflex
dlpfc: inhib reflex
latency: vor vs okn
okn - 80ms
vor - 7ms
endogenous attention can be split into two types - what are they
spatial (attend to road while driving)
feature based (alll red cars in car park)
____ rf along ventral steam
increased
v1 v4 teo te
when do critical periods end?
- axonal growth stops = can’t change arbor length
- synaptic transmission fully matures
- neuromodulator activity decrease
why critical periods?
adapt developing ns to enviro, fine tune and calibrate cells