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- J. M. Young, M. B. Calford,
and K. Obermayer. Homeostatic gain changes and ocular dominance diversity
can account for the differential expansion of the left- and right-eye
receptive fields of cortical neurons after monocular retinal lesions.
.
In Proceedings of the 7th Meeting of the German Neuroscience Society /
31th Gõttingen Neurobiology Conference 2007, 2007.
Cortical neurons initially respond to the loss of subcortically
mediated feedforward input by expanding their receptive fields, apparently
due to an increase in the efficacy of the input arriving via intrinsic
horizontal connections. This appears to be a strategy aimed at recovering
from a deficiency in synaptic drive whereby subthreshold input connections
are rendered suprathreshold and can thus engage in activity-dependent Hebbian
competition. It is plausible that this sub- to supra-threshold transformation
is achieved by some kind of response gain modulation, where the efficacy of
all synapses are scaled such that excitatory neurons become more responsive
and/or local inhibitory neurons become less responsive to input (effectively
producing disinhibition). However, studies have repeatedly observed that
binocular neurons in primary visual cortex, after being partially
deafferented by a monocular retinal lesion, appear to show receptive field
expansion via their lesioned eye receptive fields only. Such a bias appears
to be inconsistent with the hypothesis that a global increase in response
gain underlies this receptive field expansion. Here we examined experimental
results from monocular lesion experiments and compared them to the behaviour
of a network model. The feedforward and horizontal connectivity of each
modeled neuron population had a specific ocular bias, and the distribution of
ocular dominance within the population was based on in vivo data. We found
that if the modeled neurons underwent gain changes proportional to their
input loss the distribution of the ratios of lesioned eye to non-lesioned eye
receptive field expansion matched the distributions observed in vivo. Our
results support the hypothesis that single neurons or neuronal circuits
respond to a substantial reduction of excitatory input by undergoing an
increase in gain which indiscriminately amplifies responses to all excitatory
inputs.
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