Fundamentals Of Neuroscience Sensory Plasticity

Front 1

Describe Topographic Maps for sensory systems.

Back 1

Topographic maps are orderly representations of sensory surfaces that exist throughout the nervous system.

Front 2

What are two ways a topographic map can be organized in the Cortex?

Back 2

Columns: Cells in a verticle cluster share the same tuning for a given receptive field attribute, ie ocular dominance and orientation selectivity.

Layers: Thalamocortical, intracortical connections.

Front 3

Adult cortical maps and receptive fields are dynamic. How can they change?

Back 3

Cortical maps and receptive fields can change because of sensory experience, neuronal activity, and refinement of neural circuits.

Front 4

What are two ways Neuronal Activity occurs in the cortex?

Back 4

Spontaneous activity: activity independent of sensory input or motor output, ie. retinal waves.

Experience driven: the use of cortical pathways drives spike trains with varying frequency and precise timing.

Front 5

What are evidences of cortical plasticity?

Back 5

Large scale maps and columns and single receptive fields resulting from precise thalamocortical and intracortical connections. Possibly caused by neuronal activity refining neural circuits.

Cortical maps are dynamic. Sensory experience drives change.

Front 6

Connections seem to be perfect in the cortex. How could this be accomplished?

Back 6

One dendrite could branch to many axons, eventually being pared down to only one as neural activity pairs efficient transmissions. Alternatively, many dendrites could target one axon, but only the most robust dendrite will withstand the culling process due to transmission efficiency.

Front 7

Describe how activity dependant developmental plasticity could work.

Back 7

Neural activity takes place subsequent to chemical growth signaling of neurons. The neural signaling would lead to more precise connections, by culling off non-robust connections.

Front 8

How can neural activity modify connections?

Back 8

Neural activity can signal transduction pathways that target structural components of dendrites, adhesion molecules and transcription factors.

Front 9

Describe Hebbian Plasticity.

Back 9

When an axon of cell A is near enough to excite cell B, and repeatedly or persistently takes part in firing it, some growth process or metabolic change takes place in one or both cells, such that A's efficiency, as one of the cells firing B, is increased.

Front 10

Describe Homeostatic Plasticity.

Back 10

A neurons capacity to regulate its own excitability or synaptic strength to maintain firing rate within a preferred range to prevent neural circuits from becoming hyper- or hypo-active

Front 11

What are the two proposed methods of synaptic plasticity?

Back 11

Hebbian and Homeostatic Plasticity.

Front 12

Who showed spike timing dependency?

Back 12

Zhang.

Front 13

Describe the results of spike timing dependency.

Back 13

Pre long before post - no increased excitatory post synaptic potential (EPSP)

Pre before Post co-incident - increased EPSP amplitude

Post before Pre - decreased EPSP amplitude.

Front 14

To show homeostatic plasticity, researchers blocked or induced firing of a neural circuit. What results were the results?

Back 14

When excitatory transmission was blocked, they found that after taking away the block, the excitatory synapses were strenghtened.

After over exciting the circuit, they found that inhibitory interneuron synapses were strengthened.

Front 15

The Critical Period neuronal development refers to a time during development which a behavior is especially susceptible to specific environmental influences to develop normally. What does a failure to expose a specific stimuli lead to?

Back 15

Most likely leads to a permanent deficit in functionality and cortical connectivity rearrangement.

Front 16

When is the critical period for language?

Back 16

3 to 7 years of age.

Front 17

Hubel and Wiesel showed what two phenomena with regard to synaptic plasticity?

Back 17

Ocular dominance plasticity and Critical Period for synaptic plasticity.

Front 18

Hubel and Wiesel found that monocular deprivation lead to what effects in early postnatal animals?

Back 18

Irreversible effects on neuronal connectivity in the visual cortex or V1

Front 19

In Hubel and Wiesels division of Ocular Dominance. Where were groups 1 and 7?

Back 19

1 and 7 were monocular, and as such in Layer 4C of the visual cortex.

Front 20

In Hubel and Wiesels division of Ocular Dominance. Where were groups 2 thru 6?

Back 20

Distributed between Layers 2/3, 5, and 6 in the visual cortex.

Front 21

The results to Hubel and Wiesel experiments in cortical plasticity indicated what effects for Monocular Deprived, Binocular Deprived, and Decorrelated animals?

Back 21

Monocular Deprived - most cells in the visual cortex were monocular.
Binocular Deprived - looked normal.
Decorrelated - monocular for group 1 and 7.

Front 22

What was the main finding of the Hubel and Wiesel experiments in synaptic plasticity?

Back 22

Abnormality in connectivity not caused by disuse, but rather from Hebbian competition. Neuronal activity from good eye will facilitate plasticity and strengthen its connectivity with cortical neurons.

Front 23

Hubel and Wiesel showed that the Critical Period for monocular deprivation was within the first few weeks of life. How was this shown?

Back 23

They gave kittens temporary monocular deprivation and compared that to an adult cats deprivation. The result was that the kitten had deficits whereas the adult did not.

Front 24

How is the critical period thought to be controlled with neurotransmitters?

Back 24

Increases in GABA causes earlier onset of the critical period. Inversely, decreases in GABA cause later onset.