In fact, distinct classes of GABAergic interneurons inhibit particular compartments of principal neurons; “basket” cells, that target the somatic and perisomatic compartment, “chandelier” cells that selectively inhibit the axon initial segment, or “Martinotti” cells that preferentially target the apical dendritic tuft are just a few classic examples of this

compartmentalization of inhibition. Morphological differences are however not the only properties that contribute to the diversity of cortical inhibitory neurons. Interneurons can be also subdivided based on intrinsic electrophysiological Obeticholic Acid supplier properties, synaptic characteristics, and protein expression patterns. Probably because of the many dimensions that can be used to describe an interneuron, no consensus yet exists with regard to their categorization. Strikingly, in contrast to the large amount of information that exists on the properties of the various types of cortical inhibitory neurons, knowledge of the specific role that each one plays in orchestrating cortical activity is still extremely limited. Thus, in

this review, unless explicitly mentioned, we remain agnostic as to the specific interneuron subtypes phosphatase inhibitor library mediating inhibition. The specific contribution of different subtypes of interneurons to cortical inhibition is still largely unknown, and is likely to strongly depend on the activity pattern of the network. An important open question is

whether specific subtypes of interneurons have unique functional roles in cortical processing. Through the recruitment of interneurons via feedforward and/or feedback excitatory projections, inhibition generated in cortical networks is somehow proportional to local and/or through incoming excitation. This proportionality has been observed in several sensory cortical regions where changes in the intensity or other features of a sensory stimulus lead to concomitant changes in the strength of both cortical excitation and inhibition (Figure 2A; Anderson et al., 2000, Poo and Isaacson, 2009, Wehr and Zador, 2003, Wilent and Contreras, 2004 and Zhang et al., 2003). In addition, during spontaneous cortical activity, increases in excitation are invariably accompanied by increases in inhibition (Figure 2B; Atallah and Scanziani, 2009, Haider et al., 2006 and Okun and Lampl, 2008). Furthermore, acute experimental manipulations selectively decreasing either inhibition or excitation shift cortical activity to a hyperexcitable (epileptiform) or silent (comatose) state (Dudek and Sutula, 2007). Thus, not only does excitation and inhibition increase and decrease together during physiological cortical activity (van Vreeswijk and Sompolinsky, 1996), but interference of this relationship appears to be highly disruptive.