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Neural plasticity without postsynaptic action potentials: less-active inputs become dominant when kitten visual
1Division of Neurosciences, University of California, San Francisco 94143-0444.
Summary
Postsynaptic activity is crucial for ocular dominance plasticity in the visual cortex. Blocking postsynaptic cell firing during monocular deprivation unexpectedly shifted plasticity towards the deprived eye, demonstrating plasticity without spikes.
Area of Science:
- Neuroscience
- Neuroplasticity
- Visual Cortex Function
Background:
- Conventional models of synaptic plasticity link postsynaptic activity to enhanced presynaptic input efficacy.
- The visual cortex exhibits rapid ocular dominance plasticity during a critical developmental period, responding to visual input changes.
Purpose of the Study:
- To investigate the role of postsynaptic activity in ocular dominance plasticity within the visual cortex.
- To determine if postsynaptic spike activity is essential for inducing and directing plasticity.
Main Methods:
- Monocular deprivation was performed during the critical period in the visual cortex.
- Cortical cell discharges were selectively inhibited using muscimol, an inhibitory neurotransmitter agonist, via intracortical infusion.
- Single-unit recordings were used to assess visual cortex responsiveness after the muscimol blockade.
Main Results:
- Inhibition of postsynaptic cell discharges resulted in a shift of visual cortex responsiveness favoring the deprived (closed) eye.
- This plasticity occurred in favor of the less-active eye, contrary to typical activity-dependent plasticity.
- Regions not affected by muscimol showed the expected plasticity favoring the more-active (open) eye.
Conclusions:
- Postsynaptic neuronal activity is a critical factor in visual cortex plasticity.
- The direction and expression of plasticity are influenced by postsynaptic membrane properties like conductance or polarization.
- Synaptic plasticity can be induced and expressed even in the absence of postsynaptic spiking activity.