Developmental plasticity

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Fig:

When all whiskers are intact the receptive fields stay their relevant space,

however when for example all but 1 whisker are removed (D1) the receptive field

grows to try to compensate to the loss in sensory input, however the resolution

would decrease massively. See fig for other situations.

a |

Somatic inhibition by fast-spiking parvalbumin-positive (PV+) cells

(green) expressing the potassium channel Kv3.1 is mediated by the GABAA

(γ-aminobutyric acid type A) α1-subunit, whereas axonal inhibition is mediated

by the GABAA α2-subunit. Somatic inhibition is ideally situated for

suppression, or 'editing' of unwanted spikes, preventing them from

back-propagating through the cell body into the dendritic tree (red arrow).

This is an 'instructive' model, as individual action potentials can produce

long-term potentiation (LTP) or depression (LTD) based on precise spike-timing

dependent windows at individual synapses of coincident pre- and postsynaptic

activity123, 124. Notably, failure to regulate excess spiking at

the axon initial segment can still be differentiated by fast-spiking inhibition

at the cell body. b | Gap junctional coupling endows networks of

parvalbumin-positive (PV+) interneurons with the ability to detect

synchronous input128, 129, 130. Even a slight jitter in input timing (for

example, between eyes) dampens network activity through reciprocal

GABA-mediated contacts (enriched with GABAA-receptor α1-subunits131). Only synchronous open-eye input will produce

maximal, activity-dependent release or uptake of 'permissive' factors for

neurite growth (for example, tissue-type plasminogen activator78, 86 and brain-derived neurotrophic factor).

Competition is determined extracellularly.

components of cortical plasticity

mechanisms

barrel cortex plasticity

molecular mechanisms of visual plasticity/ circuit plasticit