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. 2008 Oct 1;28(40):10062–10074. doi: 10.1523/JNEUROSCI.0259-08.2008

Figure 1.

Figure 1.

Summary diagram of the interactions represented in the model. Arrowheads denote excitatory pathways, circles denote inhibitory pathways, and hemidisks denote synapses at which learning occurs. Thin lines at bottom left show the anatomical connections proposed by Brown et al. (1999). These control the phasic dopaminergic responses via one fixed and two adaptive pathways: an excitatory pathway via hypothalamus and the PPTN that relays primary reward information to dopaminergic cells; a pathway from CS representations via ventral striatum, ventral pallidum, and PPTN that can learn to excite DA cells at the onset of a reward-predicting CS; and an adaptive striosomal MSPN pathway by which a CS can inhibit dopaminergic neurons after a learned time delay. Thick lines show the pathways proposed in the current model. Striatal GABAergic interneurons [both nitric-oxide synthesizing interneuron (NOS-INs) and FS-INs], TANs, and matricial SP-D1-MSPNs (M) receive inputs from the CS representation, the latter via synaptic weights that adapt in the same way as at synapses onto ventral striatal cells (WiS). Both TANs and GABAergic NOS-INs are recipients of thalamic centromedian–parafascicular nuclei (CM–Pf) projections. NOS-INs inhibit TANs, whereas ACh released by TANs excites matricial SP-D1-MSPNs and GABAergic interneurons (both NOS-INs and FS-INs). The latter effect is mediated by nicotinic ACh receptors (nAChRs). ACh also inhibits GABAergic transmission between FS-INs and matricial SP-D1-MSPNs presynaptically, via muscarinic ACh receptors (mAChRs). Matricial SP-D1-MSPNs, in turn, send projections to both SNr cells (SR) and SNc dopaminergic cells, whose dendrites reach into SNr. SP-D1-MSPN terminals in the SN corelease GABA and SP, which act simultaneously on distal dendrites of dopaminergic neurons. GABA also acts presynaptically, via GABAB receptors, to oppose SP and GABA release. Dashed arrows indicate sites where axon terminals of DA cells release DA, which acts as a reinforcement signal at corticostriatal synapses onto ventral striatal, matricial, and striosome MSPNs. DA also modulates ACh release from TANs.