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Striatal synaptic adaptations in Parkinson's disease
2022, Neurobiology of DiseaseCitation Excerpt :Recent work has resolved this issue and shown that nitric oxide (NO) signaling arising from LTSIs that express nitric oxide synthase (NOS) induces a robust form of postsynaptic LTD in both iSPNs and dSPNs (Rafalovich et al., 2015). NO signaling molecules (e.g., sGC, protein kinase G) have long been known to be abundantly expressed in the striatum (Ariano, 1983; Ding et al., 2004), but their role in striatal physiology has been unclear. Calabresi and colleagues initially reported that pharmacological suppression of NO and cGMP signaling prevented LTD induction by tetanic stimulation of corticostriatal afferents (Calabresi et al., 1999).
Striatal synapses, circuits, and Parkinson's disease
2018, Current Opinion in NeurobiologyNitric Oxide Signaling in the Striatum
2016, Handbook of Behavioral NeuroscienceCitation Excerpt :Electrophysiological studies performed in intact animals and striatal slices have demonstrated that NO potently modulates the activity of MSNs via the activation of sGC and cGMP synthesis (Calabresi et al., 1999a,b; Padovan-Neto et al., 2015; West and Grace, 2004) (Fig. 11.1) (see also chapter: Regulation of Corticostriatal Synaptic Plasticity in Physiological and Pathological Conditions). MSNs contain very high levels of this NO effector enzyme as well as the other components of the sGC-cGMP second messenger system (Ariano, 1983; Ariano and Ufkes, 1983), and sGC activity is reported to be higher in the rat striatum than in any other region of the brain (Hofmann et al., 1977; Matsuoka et al., 1992). Ultrastructural studies show that nNOS immunoreactive processes form synaptic contacts on dendritic spine shafts of MSNs in the rat dorsal striatum and nucleus accumbens (NAc) and indicate that the sGC signaling cascade is postsynaptic to presynaptic sources of NO (Calabresi et al., 1999b; French et al., 2005; Hidaka and Totterdell, 2001; Sancesario et al., 2000).
Interneuronal Nitric Oxide Signaling Mediates Post-synaptic Long-Term Depression of Striatal Glutamatergic Synapses
2015, Cell ReportsCitation Excerpt :NO can have both direct and indirect effects on proteins involved in synaptic transmission (Garthwaite, 2008). Because its striatal expression is robust (Ariano, 1983), our working hypothesis was that the NO donor effects were mediated by soluble GC (sGC) activation. NO stimulates sGC, increasing cytoplasmic cyclic guanosine monophosphate (cGMP) production and the activation of PKG (Figure 1D).
Role of nitric oxide in the regulation of motor function. An overview of behavioral, biochemical and histological studies in animal models
2013, Pharmacological ReportsCitation Excerpt :The striatal MSNs have been shown to receive synaptic inputs from NO producing interneurons [49, 67, 135]. These synaptic inputs, terminate on the shafts of dendritic spines of MSNs known to express the highest levels of sGC in the brain [5, 41]. Apart from sGC, MSNs also express high levels of cGMP, cGMP-dependent protein kinase (PKG) and cyclic nucleotide phosphodiesterases (PDEs) [6, 27, 41, 58].
Cyclic Nucleotide Regulation by Calmodulin
2012, Calmodulin and Signal Transduction