Adenosine Production Is Essential for Closing the Critical Period of Cortical Plasticity

Sensory inputs from the external world are represented as highly organized systems in the adult brain for effective adaptation to the environment. At the cortical level, this organization is referred to as cortical maps. The establishment of cortical maps begins with early life experiences during the critical period, a brief period during development of heightened sensitivity to sensory stimuli. During this time, organization of cortical maps is plastic and highly subject to change through passive sensory experience. As an animal matures, the critical period closes and changes to cortical maps occur less freely. The cellular mechanisms of cortical map plasticity in adults remain unknown, and are thought to underlie perceptual learning and memory. Based on work in brain slices, it has previously been suggested that the mechanism of cortical map plasticity in the primary auditory cortex (AI) occurs at thalamocortical (TC) synapses in the form of synaptic plasticity. As the critical period closes, adults develop an adenosine-dependent presynaptic gate that prevents TC synaptic plasticity from occurring. By removing the adenosine gate, synaptic plasticity is able to be induced at mature TC synapses. In the present study, I examined if adenosine-dependent presynaptic gating at TC synapses underlies AI cortical map plasticity in live animals. Through genetic deletion of adenosine machinery at TC synapses, I found that cortical map plasticity at AI in adult mice could be induced through passive tone exposure, which was only thought to work during the auditory critical period