Title:
Activity-dependent formation and reorganization of visual neural circuits

Yoshio Hata
Professor
Div. Integrative Bioscience, Tottori Univ. Graduate School of Medical Sciences

Abstract:
The refinement of neural circuit during brain development is regulated by experience-driven neural activity. In the mammalian visual cortex, monocular visual deprivation in the early postnatal life causes a loss of cortical responses to a deprived eye (ocular dominance plasticity). Anatomically, the input axons from the lateral geniculate nucleus carrying information from the deprived eye show a significant retraction and ultimately lose their cortical territory. A competitive interaction between inputs serving both eyes for a limiting resources such as synaptic space has been supposed to underlie the effects of monocular deprivation, because the loss of cortical response is much weaker when both eyes are deprived of vision. In addition, the input axons do not retract following binocular deprivation.
Previous works using cats have demonstrated a role of the activity of cortical cells in the ocular dominance plasticity. For example, monocular deprivation does not induce ocular dominance plasticity when the activity of cortical cells and their inputs from the lateral geniculate nucleus are both blocked by a Na-channel blocker, tetrodotoxin. Moreover, the activity of cortical cells themselves was shown to control the direction of ocular dominance plasticity. When monocular deprivation is combined with a pharmacological inhibition of the visual cortex by administering a GABAA agonist, muscimol, leaving the activity of input axons intact, cortical neurons lose their responses to an open eye, and active axons serving an open eye selectively retract. In contrast to the ocular dominance plasticity in normal cortex, the input axons serving an open eye significantly retract in the inhibited cortex regardless of whether the other eye is closed, thus presynaptic activity in the absence of postsynaptic cortical activity can solely lead to the retraction of input axons. These results suggest that a homosynaptic mechanism, rather than a heterosynaptic competition between inputs, may operate to prune the axons which fail to activate their target neurons, and play an important role in the experience-driven reorganization of visual neural circuits.