Molecular mechanism for loss of visual cortical responsiveness following brief monocular deprivation.
A dramatic form of experience-dependent synaptic plasticity is revealed in visual cortex when one eye is temporarily deprived of vision during early postnatal life. Monocular deprivation (MD) alters synaptic transmission such that cortical neurons cease to respond to stimulation of the deprived eye, but how this occurs is poorly understood. Here we show in rat visual cortex that brief MD sets in motion the same molecular and functional changes as the experimental model of homosynaptic long-term depression (LTD), and that prior synaptic depression by MD occludes subsequent induction of LTD. The mechanisms of LTD, about which there is now a detailed understanding, therefore contribute to visual cortical plasticity.
Heynen
Arnold J
AJ
Howard Hughes Medical Institute, The Picower Center for Learning and Memory, and Department of Brain and Cognitive Sciences, Massachusetts Institute of Technology, Cambridge, Massachusetts 02139, USA.
Yoon
Bong-June
BJ
Liu
Cheng-Hang
CH
Chung
Hee J
HJ
Huganir
Richard L
RL
Bear
Mark F
MF
D000818:Animals; D002462:Cell Membrane / Q000378:metabolism; D005074:Evoked Potentials, Visual; D007839:Functional Laterality; D036881:Long-Term Synaptic Depression; D009474:Neurons / Q000378:metabolism; D010766:Phosphorylation; D051381:Rats; D020318:Rats, Long-Evans; D018091:Receptors, AMPA / Q000378:metabolism; D012683:Sensory Deprivation / Q000502:physiology*; D013569:Synapses / Q000502:physiology; D013997:Time Factors; D015349:Vision, Monocular / Q000502:physiology*; D014785:Vision, Ocular; D014793:Visual Cortex / Q000378:metabolism / Q000502:physiology*
D018091:Receptors, AMPA