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experience−induced plasticity, mEPSC, mouse, NMDA receptors, visual cortex
Abstract:
Prolonged imbalance in sensory experience leads to dramatic
readjustments in cortical representation. Neuromodulatory systems
play a critical role in habilitating experience−induced plasticity and
regulate memory processes in vivo. Here, we show that a brief
period of intense patterned visual stimulation combined with
systemic activation of alpha−1 adrenergic neuromodulator receptors
(a1−ARs) leads to a rapid, reversible, and NMDAR−dependent
depression of AMPAR−mediated transmission from ascending
inputs to layer II/III pyramidal cells in the visual cortex of young
and adult mice. The magnitude of this form of a1−AR long−term
depression (LTD), measured ex vivo with miniature EPSC recordings,
is graded by the number of orientations used during visual
experience. Moreover, behavioral tests of visual function following
the induction of a1−AR LTD reveal that discrimination accuracy of
sinusoidal drifting gratings is selectively reduced at high spatial
frequencies in a reversible, orientation−specific, and NMDARdependent
manner. Thus, a1−ARs enable rapid cortical synaptic
depression which correlates with an orientation−specific decrease
in visual discrimination. These findings contribute to our understanding
of how adrenergic receptors interact with neuronal
networks in response to changes in active sensory experience to
produce adaptive behavior
