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Abstract:
Norepinephrine (NE) is widely distributed throughout the brain. It modulates intrinsic currents, as well as
amplitude and frequency of synaptic transmission affecting the ‘signal−to−noise ratio' of sensory responses.
In the visual cortex, a1− and b−adrenergic receptors (AR) gate opposing effects on long−term plasticity of
excitatory transmission. Whether and how NE recruits these plastic mechanisms is not clear. Here, we show
that NE modulates glutamatergic inputs with different efficacies for a1− and b−AR. As a consequence, the
priming of synapses with different NE concentrations produces dose−dependent competing effects that
determine the temporal window of spike−timing dependent plasticity (STDP). While a low NE
concentration leads to long−term depression (LTD) over broad positive and negative delays, a high NE
concentration results in bidirectional STDP restricted to very narrow intervals. These results indicate that
the local availability of NE, released during emotional arousal, determines the compound modulatory effect
and the output of STDP
