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Chapter 23: Synaptic Plasticity (NMDA receptor (a glutamate receptor that…
Chapter 23: Synaptic Plasticity
Synaptic plasticity
Preexisting synapses can get stronger or weaker, new synapses can form, old synapses are pruned away
Important not just for learning and memory, not just during development
for everyday functions of nervous systems (neurons and their connections are ALWAYS changing)
synaptic plasticity in development and in learning and memory use same molecular mechanisms
Synaptic plasticity in visual system development
mature brain is PRECISELY wired to process sensory information into coherent patterns of activity that form basis of our perception, thoughts, and actions
PRECISE wiring is not fully developed at birth
development in visual system occurs in 2 stages
prenatal development
broad pattern of connections emerges as a result of cell recognition events
chemoattractive and chemorepulsive mechanisms get axons in APPROXIMATELY the right place
COARSE retinotopic map, result is not nearly as good as normal retinotopy found in adult
requires second stage of development
postnatal development (activity dependent stage of development)
coarse connections in PRENATAL development is REFINED by ACTIVITY DEPENDENT MECHANISMS
activity dependent stage of development: interactions between organism and its environment
influence of environment on the brain changes with AGE
Processes of both SEGREGATION and CONVERGENCE of axonal projections
Ocular dominance columns
LGN inputs go to layer 4C in V1
Asynchrony promotes SEGREGATION of inputs, Synchrony promotes CONVERGENCE of inputs
inputs from left and right eyes are completely SEGREGATED in layer 4C and generate OCULAR DOMINANCE COLUMNS
layer 4C is MONOCULAR
Deprivation change dimensions of ocular dominance columns in layer 4C
projections from each eye initially spread out ALL OVER layer 4
each projection is trying to form topographical map of retina
over time, some connections retract and ocular dominance columns are formed
In monocular deprivation during critical period: deprived eye inputs to cortex are at a competitive DISADVANTAGE and RETRACT their inputs to an ABNORMAL EXTEND
axon terminals from non-deprived eye continue to OCCUPY cortical space that would normally be given up to the other eye
above and below layer 4C, most cells are BINOCULAR, generally dominated by one eye or the other
formation of ocular dominance columns: 2 important mechanisms
Neural activity: critical factor regulating both competition and cooperation
COOPERATION between fibers from same eye
evidence for COOPERATION
retinal fibers are spontaneously active in utero
neighboring cells in retina tend to be active together, firing in synchronous bursts
neighboring cells would have similar patterns of activity (CORRELATED ACTIVITY) --> LGN--> cortex
activity patterns in 2 eyes that are not correlated with each other (UNCORRELATED ACTIVITY)
COMPETITION for target space between fibers from 2 eyes
evidence for COMPETITION
in monocular deprivation, competition is REDUCED
inputs from open eye form complete topographic map within the single neural space of layer 4C
no competition --> no columns
Competition and cooperation for cortical targets
spontaneous firing of group of fibers and the resulting synchronous excitation of the target
strengthen those synapses whose presynaptic fibers are active together (COOPERATION)
HEBB'S Postulate for learning: coincident activity in PRE and POSTsynaptic elements of a synapse leads to its strengthening (increased efficacy) "THINGS THAT FIRE TOGETHER, WIRE TOGETHER"
strengthening of synapses in developing V1 is mediated by an NMDA-receptor dependent mechanism
weaken those synapses whose presynaptic fibers are inactive/out of synchrony (COMPETITION)
Quantifying ocular dominance
if binocular cell is dominated by left eye, when visual stimulus passes receptive field, cell will fire more in the left eye
Ocular deprivation
monocular deprivation: one eyelid sealed closed
AMBLIOPIA: animals are cortically blind in deprived eye
if monocular deprivation began shortly after birth
"closed-eye" columns will shrink
"open-eye" columns will expand in width
monocular deprivation leaves few neurons responsive to deprived eye
in the striate cortex, cells can only be driven by NON-DEPRIVED eye
deprived eye loses out in some sort of COMPETITION for TARGET SPACE
eye with more visual activity "wins" target space
Effects of monocular deprivation decline with age
Critical periods of development
critical period: a limited period of time when a particular aspect of brain development is SENSITIVE to a change in the external environment
after critical period, you get no effect of monocular deprivation
Binocular deprivation
NORMAL distribution but cells are not quite normal (animal has POOR ACUITY (vision))
critical period for normal development of binocular vision in humans: 2-4 years
Alternating deprivation
Ocular dominance bands are much SHARPER than normal
no binocular vision (no stereopsis)
no 3D depth perception
STRABISMUS (eye misalignment) gives same results as alternating deprivation
will lead to AMBLIOPIA if not corrected
treatment
mild strabismus: patch good eye, strengthens eye muscles for alignment, forces use of eye that is becoming ambliopic
severe strabismus: surgical intervention to realign eyes
child born with STRABISMUS initially has good vision (acuity), but cannot fuse image in the 2 eyes, so they FAVOR ONE EYE
NMDA receptor
a glutamate receptor that is BOTH a ligand and voltage-gated ion channel
ligand: glutamate
Voltage gate: at resting Vm, channel is blocked by Mg++
Mg++ block is removed by depolarization
channel opening is ACTIVITY DEPENDENT
Neighboring retinal ganglion cells tend to fire TOGETHER
summation of synaptic inputs raises Vm enough to the point where Mg++ block in NMDA receptors is removed
Na+ and Ca++ enter postsynaptic cell
increase in Ca++ coming into the cell, activates intracellular 2nd messenger systems leading to the STRENGTHENING OF ACTIVE SYNAPSES
NMDA receptor is a coincidence detector
channel only opens when pre and post synaptic elements are active (Hebb's postulate for learning)
presynaptic cell is active
releasing glutamate
postsynaptic cell is active
depolarized and Mg++ block in NMDA receptor channel is removed
BCM for bidirectional synaptic plasticity (extension of Hebb's theory)
synapses that are active when postsynaptic cell is STRONGLY DEPOLARIZED will undergo LTP
synapses that are active when postsynaptic cell is WEAKLY DEPOLARIZED will undergo LTD
corresponds to Ca++ influx
protein kinases (phosphorylate proteins)
activated by HIGH Ca influx and yield LTP
AMPA receptors are phosphorylated by stimulation that produces LTD
protein phosphates (dephosphorylate proteins)
activated by LOW Ca influx and yield LTD
AMPA receptors are dephosphorylated by stimulation that produces LTD
Role of calcium in plasticity: kinases, AMPA, CREB
Short term plasticity: CaMKII unmasks silent AMPA receptors and ADDS new AMPA receptors
results from covalent modification of PREEXISTING PROTEINS like phosphorylation of channels or receptors
CamKII is the most important kinase for short term LTP
Long term plasticity (and memory)
require activation of GENE TRANSCRIPTION and SYNTHESIS of new proteins, via PKA and/or CamKII and CREB
Plasticity in adult visual system: effects of retinal lesion on cortical topography
visual space represented by a grid mapped onto RETINA
focal retinal lesion with laser
mapping visual cortex revels cortical scotoma (region of cortex receiving inputs from lesioned area is now SILENT)
2 months later remap: neurons that would normally represent portion of visual field associated with lesion is NO LONGER SILENT, but receptive fields have shifted to the EDGES of scotoma
now there is an ENLARGED representation of visual space immediately surrounding the scotoma "filling in"
modifications of cortical maps could reflect changes in effectiveness of previously existing INTRINSIC HORIZONTAL CONNECTIONS