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. Author manuscript; available in PMC: 2021 May 28.
Published in final edited form as: Eur J Neurosci. 2021 Apr 26;53(8):2421–2442. doi: 10.1111/ejn.15135

Figure 2. Nicotinic-mediated striatal GABAergic circuits.

Figure 2.

So far, two distinct GABAergic striatal microcircuits involving β2-subunit containing nicotinic receptor (β2*-nAChR) have been described. Left. Optogenetic activation of striatal cholinergic interneurons (CINs) evoke a disynaptic composite IPSC in SPNs. This inhibition can be subdivided into a fast and a slow component. While the slow component is mediated by CINs activation of neurogliaform interneurons (NGF), the source of the fast IPSC is still under investigation. Right. Single CIN activation or optogenetic stimulation of populations of CINs induces polysynaptic recurrent inhibition among CINs which can participate in synchronizing CINs activity. Part of this inhibition involves nicotinic receptors activation on THINs, which are reciprocally connected with CINs. The contribution of other subtypes of striatal GABAergic interneurons or extrinsic GABAergic afferents is yet to discover.