Brain Plasticity Flashcards
What is brain plasticity?
The ability of the brain to modify its structure and function, including strategies employed by neurons to facilitate the strengthening and weakening of synaptic connections.
Activity-dependent synaptic rearrangment
Rearrangement of synapses as a consequence of neuron activity and synaptic transmission before and after birth (critical period & hardwiring.) “Use it or lose it.”
Activity-dependent synaptic rearrangement at the NMJ
During development. At first, motor neuron axons innervates multiple muscle fibers. After rearrangement, one motor neuron axon innervates one muscle fiber. (Synaptic elimination.)
Occurs when the host synaptic muscle cell is activated at the same time as the neuron (fire together, wire together.)
How do axons go to the LGN?
Axons from contralateral side first, then ipsilateral. These axons from the two eyes segregate into “eye-specific domains.”
Synaptic segregation in the LGN
Formation (?) of “eye-specific domains” during development.
A segregation of retinal inputs to the LGN.
How does this segregation occur in utero?
Ganglion cells fire in retinal waves, because there is no light in utero.
Connections retained when the ganglion cell terminal is active at the same time as LGN neuron.
Hebb synapses
can be modified by synaptic segregation.
Winner takes all. Neurons that fire together fire together. Those out of sync lose their link.
Neurons that fire together wire together
Synapse strengthened when presynaptic axon is active at the same time that the postsynaptic neuron is strongly activated
Plasticity in the segregation of LGN inputs to V1
Activity and experience dependent synaptic rearrangement in the ocular dominance columns of young monkeys
Ocular dominance shift in monkeys
Ocular dominance columns in V1 shift (stripes change) due one eye having more visual input and thus becoming dominant.
Closed eye columns decrease in width (loses influence).
Activity and experience dependent
Ocular dominance shift in monkeys experiment
Carried out by Weisel and Hubel. Eyelid of one of a monkey’s eyes was sealed closed after birth (monocular deprivation).
Can the monkey’s ocular dominance columns shift back?
It depends. There is a critical period (about 6 weeks for monkeys) of plasticity. If the patch is removed during these 6 weeks, they shift back.
If patch is removed after, the change becomes hardwired.
Critical period and examples.
A period of time in which parts of the brain are subject to change… Changes the developmental fate of nervous tissue.
Plasticity constricts with age.
Konrad Lorenz and Imprinting (can’t be reverse) on geese.
Romanian orphans.
Modulatory influences on plasticity
Cat with monocular dominance (patch) shows an ocular dominance shift in the layers of the LGN.
Shift not seen (even with patch) if cholinergic and norepinephrine input to V1 is cut.
Why is the ocular dominance shift not seen in a monocular dominant cat if certain pathways are cut?
Cholinergic and norepinephrine input to V1 are arousal pathways that makes animal alert to visual world.
Does not show shift? Visual input AND awareness of that visual input are critical.
Mechanisms of Cortical Synaptic Plasticity: excitatory synaptic transmission in the immature visual system. What processes are occurring here and what are the major players?
Long term synaptic potentiation (LTP) and long term synaptic depression (LTD). AMPA and NMDA (ionotropic) receptors play a big role.
Traits of the NMDA receptor
Ligand gated: blocked by Mg2+. Requires depolarization to remove (hebbian).
Voltage gated-ion channel.
Ca2+ permeable.
AMPA has to be activated first.
LTP
Increase in synaptic strength long term
Increased activity of a synapse and EPSP that leads to LTP can be accounted for by
Insertion of AMPA receptors into the membrane.
Increase in AMPA activity.
Increase in glutamate release in the presynaptic neuron.
Synapse with AMPA and NMDA receptors not undergoing strengthening by LTP
AP-> NT -> glu R (purely AMPA) -> excitatory post synaptic potential (EPSP) is not that strong
Synapse undergoing strengthening by LTP
Many rapid AP -> depolarizes MORE -> lots of glu -> sufficient depolarization activates NMDA->
NMDA->influx of Ca2+ -> more AMPA-> more depolarization
influx of Ca2+ -> calmodulin -> CaMK11 phosphorylates AMPA -> increase in AMPA activity, increase in AMPA receptors in membrane from stores
->EPSP increases in size consistently -> increase in synaptic strength
LTD
When neurons fire out of sync, they lose their link.
Mechanism opposite of LTP causes retration of AMPA receptors by endocytosis.
Is LTD equally important to LTP?
Yes. Weakening of synapses is ESSENTIAL.
Weakening of an inhibitory synapse/pathway -> increase excitation.
What drives synaptic elimination at the NMJ?
The loss of ACh receptors in post-synaptic neuron due to insufficient receptor activation in an otherwise active muscle.
