visual plasticity Flashcards
what is long-term potentiation?
what neurotransmitter is released onto those cells from presynpses?
how many inputs does it take generally to depolarise that cell?
the ability of synapses to change their strength ( the persistent strengthening of synaptic connections caused by constant presynaptic stimulation)
glutamate
more than one input to depolarise the cell strongly
how can you determine how strong a synapse is and what can that lead to facilitate more easily?
The number of times the voltage potential of a postsynaptic neuron changes determines the strength of its synapses, i.e., the more it changes its voltage potential, the greater the synaptic strength due to high-frequency presynaptic stimulation.
this will lead to more ion channels opening more easily, allowing greater ion influx
what are ocular dominance columns?
They are stripes of neurons in the visual cortex and LGN that respond preferentially to input from one eye or the other.
what will allow for NMDA receptors to unblock the Mg and for the influx of cations?
what happens to synapse in convers to this?
requires glutamate binding and strong depolarization of the postsynaptic membrane, requiring more than one input from more than one synapse to achieve this. This will allow for ca influx and hence trigger all sorts of strengthening mechanisms to make this synapse stronger and more effective.
On the other hand, if glutamate is released but does not have much effect on its own or not have enough inputs to deoplarise, those synapse will become weakened
what is required to have form vision
both eyes not restricted from the visual world
what allows for functional OD column development
axons from both eyes are strongly driven by the visual world and are openly receiving form vision
what happens when both eyes receive openly form vision and what happens if they dont in terms of OD collumn development
normal form vision in both eyes, OD columns will form as normal with equal access or use of OD cotical machinery
but if one eye is compromised, then that eye will not have access to OD cortical machinery and the other eye will take over its territory
what is amblyopia
another word for lazy eye
reduced vision in one eye caused by abnormal visual development early in life
itsa condition which is also refered to as lazy eye. it occurs when an eye receives reduced visual input and doesnt receive openly form vision during the critical period for which the development and proper function of ocular dominance collumns is key. it can therefore cause the brain to favour the other eye and increase its terriroty to compensate for the affected eye. there are different types of amplyopia for example, stabismus- misalignment of the eye also known as cross eyed. another example is cataract where there is physical obstruction to an eye.
Can OD column shift be reversed and what treatments can be used?
The most common treatment involves patching the good eye and forcing the child to actively work with the bad eye. This requires different amounts of hours for different stages of early life in terms of compromisation. But with the danger of compromising vision in the good eye
and further reducing stereoscopic vision (the ability to view the world in 3D requiring form vision in both eyes)
this can be revered effectively within the critical period/ before the end of the critical period
what is development plasticity confined to
a critical period up until 7-8 years of age
what is monocular deprivation?
when one eye is compromised in terms of receiving form vision
can monocular deprivation with unilateral cataracts be revered?
with surgery it can but confined to within the critical period.
what is cataract
cloudy blockage in the eye restricting form vision
what are the different conditions in which individuals may develop amblyopia?
cataract, ptosis (upper eyelid drooping covering the pupil), anisometropia (when the two eyes have a different refractive power (glasses prescription), so there is unequal focus between the two eyes without glasses), strabismus (the misalignment of the eyes; one moves inwards and the other outwards—cross eyes)
What is the difference between monocular deprivation amblyopia and non-monocular deprivation amblyopia?
What are the reasons for ocular dominance columns looking normal even after non-MD amblyopia?
MDA: occurs during the critical period and causes shifts in ocular dominance columns where one eye will take over the other eye’s territory to compensate for the poor eye.
Non-MDA: This occurs when both eyes receive poor visual input during the critical period, often due to uncorrected or poorly corrected refractive errors (like nearsightedness, farsightedness-which could be due to wrong perscribe refractive powers for their glasses or lens that doesnt match the actual refratcive power of the individual threfore can lead to blurriness, or when they dont wear their corrected refractive powers/ lens as frequntly as they should to allow for clear visible inputs from visual stimuli) in both eyes. Because the visual system does not receive clear images from either eye, the development of visual acuity can be impaired in both eyes.
it doesn’t have much effect on the ocular dominance shift in columns as both eyes are open and receiving vision and the axons are driven by the visual world during the critical period, so the bad eye must of occurred later in life
The plasticity of the brain with new connections forming becomes poorer as we get older.
