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Abstract

Neuromodulatory systems are thought to gate cortical neuronal excitability – a generalized state consisting of high frequency (20 to 200 Hz) local field potential (LFP) oscillations. Stimulating neuromodulatory centers evokes a non-specific response across all components of the excited cortical state (beta and gamma band LFP oscillations). The non-specificity of neuromodulation is at odds with the fact that neuromodulators regulate distinct cognitive functions that are affiliated with different cortical LFP oscillations. For example, various dopamine and norepinephrine-dependent cognitive functions (e.g., working memory, spatial navigation, and top-down attention) are each accompanied by power increases within different LFP frequency bands. How can neuromodulators contribute to cognitive processes associated with different LFP frequency bands if they non-specifically modulate cortical LFP? Here, rather than perturbing neuromodulatory systems with stimulation, we recorded spontaneous unit activity from two primary sources of cortical neuromodulators (the noradrenergic locus coeruleus, LC, and dopaminergic ventral tegmental area, VTA) and correlated it with LFP power fluctuations in the prefrontal, visual, and somatosensory cortex of urethane-anesthetized rats. We found that neuromodulatory population spike rate rhythmically fluctuates at 1 – 2 Hz (delta band) in both LC and VTA. But, in the LC, an additional 5 – 7 Hz (theta band) fluctuation of spike rate occurred. While neuromodulatory delta oscillations non-specifically regulated the power of all cortical LFP oscillations over 20 Hz, theta spike rate oscillations were exclusively associated with cortical high gamma band (60 – 200 Hz) activity. As LC population spiking rhythmically rose and fell, two types of LC single units (characterized by narrow or wide action potentials) fired in phasic opposition, potentially providing differential cortical state regulation. Our results demonstrate that the noradrenergic system is a unique neuromodulatory center that can affect specific cortical activity patterns, rather than merely gate a generalized state of cortical excitability.