Endogenous nitric oxide modulates behavioural effects elicited by substance P in rat
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Cited by (14)
Nitric Oxide Signaling in the Striatum
2016, Handbook of Behavioral NeuroscienceCitation Excerpt :Disruption of nNOS function also potentiates catalepsy induced via D2-like receptor antagonist administration (Cavas and Navarro, 2002; Del Bel and Guimaraes, 2000). Additionally, locomotion stimulated by substance P (Mancuso et al., 1994), NMDA receptor antagonists (Deutsch et al., 1996), and D1/5 and D2-like receptor agonists (Starr and Starr, 1995) is decreased following systemic administration of NOS inhibitors. The psychomimetic drug phencyclidine has also been reported to modulate locomotor activity in a manner that is sensitive to both NO donors and nNOS inhibitors, although these studies have produced contradictory results (Bujas-Bobanovic et al., 2000; Johansson et al., 1999, 1997; Klamer et al., 2005; Noda et al., 1995, 1996).
Brain kinin B1 receptor is upregulated by the oxidative stress and its activation leads to stereotypic nociceptive behavior in insulin-resistant rats
2015, PeptidesCitation Excerpt :While glutamate is recognized as a classical neurotransmitter involved in various cerebral functions, including NMDA-induced grooming behavior [42], SP is known to initiate stereotypic nocifensive behavior [8,15,29,39] and to contribute to the defence reaction in response to stress [8–10]. In the brain, endogenous NO plays a role in the effect of SP on motor behavior [36]. This is keeping with the presence of all components of the kallikrein–kinin system in normal brain and the upregulation of B1R in pathologic brain [4,11,33,37].
Molsidomine, a nitric oxide donor, modulates rotational behavior and monoamine metabolism in 6-OHDA lesioned rats treated chronically with L-DOPA
2013, Neurochemistry InternationalCitation Excerpt :A growing body of evidence derived from animal models reveals a compelling role of nitric oxide (NO), a unique gaseous neurotransmitter and neuromodulator with a broad spectrum of activities in the mammalian brain (Guix et al., 2005), in the regulation of motor function. Behavioral studies have demonstrated that acute administration of selective or non-selective neuronal nitric oxide synthase (nNOS) inhibitors to rodents, reduced spontaneous locomotor activity (Stewart et al., 1994; Dzoljic et al., 1997; Sandi et al., 1995) and hyperlocomotion induced by cocaine (Pudiak and Bozarth, 1993; Przegaliński and Filip, 1997), morphine (Calignano et al., 1993), substance P (Mancuso et al., 1994) and amphetamine or methamphetamine (Przegaliński and Filip, 1997; Ohno and Watanabe, 1995; Abekawa et al., 1994). Locomotor activity enhanced by selective dopamine D1 and D2 receptor agonists (Starr and Starr, 1995; Przegaliński and Filip, 1997) and the NMDA receptor antagonist MK-801 (Deutsch et al., 1996) was also decreased by these inhibitors.
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 :A growing body of evidence from animals studies indicates that NO is a key modulator of neuronal activity in the dorsal striatum and a critical factor for the regulation of motor function and synaptic plasticity [37, 158]. Behavioral studies carried out on rodents demonstrated that non-selective and selective nNOS inhibitors reduced spontaneous locomotor activity [43, 137, 143] and hyperlocomotion induced by cocaine [122, 123], morphine [19], substance P [100] as well as by amphetamine or metamphetamine [1, 113, 122]. Also locomotor activity stimulated by selective dopamine D1 and D2 receptor agonists [122, 141] and the N-methyl-D-aspartic acid (NMDA) receptor antagonist MK-801 [39] was decreased by these inhibitors.
Nitric Oxide Signaling in the Striatum
2010, Handbook of Behavioral NeuroscienceCitation Excerpt :Disruption of NOS function also potentiates catalepsy induced via D2-like receptor antagonist administration (Del Bel and Guimaraes, 2000; Cavas and Navarro, 2002). Additionally, locomotion stimulated by substance P (Mancuso et al., 1994), NMDA receptor antagonists (Deutsch et al., 1996), and D1/5 and D2-like receptor agonists (Starr and Starr, 1995) is decreased following systemic administration of NOS inhibitors. Elevations in striatal levels of cAMP and cGMP observed in PDE1B knock-out mice are associated with greater locomotor hyperactivity induced via administration of DA agonists (Reed et al., 2002).