NORADRENERGIC SUPPRESSION OF SYNAPTIC TRANSMISSION MAY INFLUENCE CORTICAL SIGNAL-TO-NOISE RATIO

Norepinephrine has been proposed to influence signal-to-noise ratio wi thin cortical structures, but the exact cellular mechanisms underlying this influence have not been described in detail. Here we present dat a on a cellular effect of norepinephrine that could contribute to the influence on signal-to-noise ratio. In brain slice preparations of the rat piriform (olfactory) cortex, perfusion of norepinephrine causes a dose-dependent suppression of excitatory synaptic potentials in the l ayer containing synapses among pyramidal cells in the cortex (layer Ib ), while having a weaker effect on synaptic potentials in the afferent fiber layer (layer Ia). Effects of norepinephrine were similar in dos e-response characteristics and laminar selectivity to the effects of t he cholinergic agonist carbachol, and combined perfusion of both agoni sts caused effects similar to an equivalent concentration of a single agonist. In a computational model of the piriform cortex, we have anal yzed the effect of noradrenergic suppression of synaptic transmission on signal-to-noise ratio. The selective suppression of excitatory intr insic connectivity decreases the background activity of modeled neuron s relative to the activity of neurons receiving direct afferent input. This can be interpreted as an increase in signal-to-noise ratio, but the term noise does not accurately characterize activity dependent on the intrinsic spread of excitation, which would more accurately be des cribed as interpretation or retrieval. Increases in levels of norepine phrine mediated by locus coeruleus activity appear to enhance the infl uence of extrinsic input on cortical representations, allowing a pulse of norepinephrine in an arousing context to mediate formation of memo ries with a strong influence of environmental variables.