Figure 2.

Potential mechanisms underlying the physiological effects of NE and ACh on sensory cortex neurons. The summary presented here is mostly based on findings obtained in the visual and auditory cortex. (A) Alpha1 noradrenergic receptors can control the glutamaergic transmission (thalamo-cortical and cortico-cortical) by effects occurring at the presynaptic level. They can also control the excitability of layer I inhibitory interneurons (Salgado et al., 2011). Beta and alpha2 receptors can both contribute to control the post-synaptic excitability of cortical cells (Manunta and Edeline, 1997, 1999; Salgado et al., 2011). (B) Muscarinic receptors increase the post-synaptic excitability of pyramidal cells (Metherate et al., 1992; Cox et al., 1994) but also of some types of interneurons (Disney and Aoki, 2008) and can decrease the release of GABA by Fast-Spiking interneurons (Kruglikov and Rudy, 2008). Nicotinic receptors can act presynaptically on the thalamo-cortical and can increase the excitability of several types of GABAergic interneurons (Disney et al., 2007; review in Metherate, 2004, 2011).