Brain Plasticity

Question 1

What is brain plasticity?

Answer 1

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.

Question 2

Activity-dependent synaptic rearrangment

Answer 2

Rearrangement of synapses as a consequence of neuron activity and synaptic transmission before and after birth (critical period & hardwiring.) “Use it or lose it.”

Question 3

Activity-dependent synaptic rearrangement at the NMJ

Answer 3

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.)

Question 4

How do axons go to the LGN?

Answer 4

Axons from contralateral side first, then ipsilateral. These axons from the two eyes segregate into “eye-specific domains.”

Question 5

Synaptic segregation in the LGN

Answer 5

Formation (?) of “eye-specific domains” during development.

A segregation of retinal inputs to the LGN.

Question 6

How does this segregation occur in utero?

Answer 6

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.

Question 7

Hebb synapses

Answer 7

can be modified by synaptic segregation.

Winner takes all. Neurons that fire together fire together. Those out of sync lose their link.

Question 8

Neurons that fire together wire together

Answer 8

Synapse strengthened when presynaptic axon is active at the same time that the postsynaptic neuron is strongly activated

Question 9

Plasticity in the segregation of LGN inputs to V1

Answer 9

Activity and experience dependent synaptic rearrangement in the ocular dominance columns of young monkeys

Question 10

Ocular dominance shift in monkeys

Answer 10

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

Question 11

Ocular dominance shift in monkeys experiment

Answer 11

Carried out by Weisel and Hubel. Eyelid of one of a monkey’s eyes was sealed closed after birth (monocular deprivation).

Question 12

Can the monkey’s ocular dominance columns shift back?

Answer 12

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.

Question 13

Critical period and examples.

Answer 13

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.

Question 14

Modulatory influences on plasticity

Answer 14

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.

Question 15

Why is the ocular dominance shift not seen in a monocular dominant cat if certain pathways are cut?

Answer 15

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.

Question 16

Mechanisms of Cortical Synaptic Plasticity: excitatory synaptic transmission in the immature visual system. What processes are occurring here and what are the major players?

Answer 16

Long term synaptic potentiation (LTP) and long term synaptic depression (LTD). AMPA and NMDA (ionotropic) receptors play a big role.

Question 17

Traits of the NMDA receptor

Answer 17

Ligand gated: blocked by Mg2+. Requires depolarization to remove (hebbian).
Voltage gated-ion channel.
Ca2+ permeable.
AMPA has to be activated first.

Question 18

LTP

Answer 18

Increase in synaptic strength long term

Question 19

Increased activity of a synapse and EPSP that leads to LTP can be accounted for by

Answer 19

Insertion of AMPA receptors into the membrane.
Increase in AMPA activity.
Increase in glutamate release in the presynaptic neuron.

Question 20

Synapse with AMPA and NMDA receptors not undergoing strengthening by LTP

Answer 20

AP-> NT -> glu R (purely AMPA) -> excitatory post synaptic potential (EPSP) is not that strong

Question 21

Synapse undergoing strengthening by LTP

Answer 21

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

Question 22

LTD

Answer 22

When neurons fire out of sync, they lose their link.

Mechanism opposite of LTP causes retration of AMPA receptors by endocytosis.

Question 23

Is LTD equally important to LTP?

Answer 23

Yes. Weakening of synapses is ESSENTIAL.

Weakening of an inhibitory synapse/pathway -> increase excitation.

Question 24

What drives synaptic elimination at the NMJ?

Answer 24

The loss of ACh receptors in post-synaptic neuron due to insufficient receptor activation in an otherwise active muscle.

Question 25

Synaptic stabilization

Answer 25

Stabilizes (strengthens?) the circuit. Occurs through activity dependent survival.

Question 26

Synaptic segregation

Answer 26

Axons arrive at LGN, have specific places where they synapse and innervate

Question 27

Synaptic rearrangement

Answer 27

Innervation pattern changes

Question 28

What drives LTP on a molecular level?

Answer 28

The recruitment and insertion of AMPA receptors

Question 29

What drives LTD on a molecular level?

Answer 29

The retraction and decrease (through endocytosis) of AMPA receptors