FIGURE 2.
A working model of how catecholamines may gate inputs onto prefrontal cortex (PFC) neurons. Electrophysiological and anatomical data suggest that norepinephrine (NE) acts at α2A-adrenoceptors on dendritic spines to enhance connectivity with inputs from other neurons with shared characteristics, and thus increase the “signal” of that neuron. For example, a neuron spatial tuned for 90° needs to connect with other 90° neurons in order to generate network firing to represent this spatial location in the absence of environmental stimulation. α2A-Adrenoceptors increase this connectivity with other members of the network by inhibiting cAMP production in the dendritic spine, thus closing nearby hyperpolarization-activated cyclic nucleotide-gated (HCN) channels, increasing membrane resistance and strengthening inputs onto the spine.48 In contrast, D1 receptors on separate spines appear to gate out inputs from neurons with dissimilar properties (e.g., 45°), thus decreasing “noise.”77 This appears to be accomplished, at least in part, by increasing the production of cAMP within the spine, opening HCN channels, and shunting inputs onto that spine. This may occur in a dynamic fashion, to narrow or broaden the tuning of the neuron according to task demands.