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Noninvasive neuromodulation in Parkinson's disease: Neuroplasticity implication and therapeutic perspectives
2022, Handbook of Clinical NeurologyCitation Excerpt :However, there is growing evidence that the effects of cortical stimulation may spread widely across the cortico-basal ganglia-thalamo-cortical network. Animal studies have shown that dopamine release within the basal ganglia circuits can be enhanced by activating direct glutamatergic cortico-striatal projections (Nieoullon et al., 1978; Whitton, 1997). Accordingly, it has been proven that “facilitatory” high-frequency rTMS, when applied over the frontal cortex, can induce ipsilateral endogenous dopamine release in the striatum both in healthy humans (Strafella et al., 2001, 2003) and in patients with PD (Strafella et al., 2005).
The role of dopamine in huntington's disease
2014, Progress in Brain ResearchCitation Excerpt :As MSNs from the striosomes project to the substantia nigra pars compacta, it may be that early degeneration of these inhibitory neurons produces hyperactivity of the DA pathway, contributing to chorea and other early clinical manifestations of HD. Stimulation of corticostriatal neurons has been shown to activate DA release in the striatum (Nieoullon et al., 1978). In addition, DA neurons that modulate glutamate release in the corticostriatal pathway are subject to afferent glutamate regulation, which is suggested by the presence of glutamate receptors on DA neurons (Meltzer et al., 1997).
The role of the dopamine D2 receptor in descending control of pain induced by motor cortex stimulation in the neuropathic rat
2012, Brain Research BulletinCitation Excerpt :The striatum is involved in processing and sensorimotor gating of nociceptive information (e.g., Belforte and Pazo, 2005; Chudler and Dong, 1995; Lineberry and Vierck, 1975; Neugebauer, 2006). The earlier findings that stimulation of the M1 cortex caused striatal release of dopamine in various species (Kanno et al., 2004; Nieoullon et al., 1978; Strafella et al., 2003), dopaminergic denervation of the striatum augmented nociceptive response (Chudler and Lu, 2008; Saadé et al., 1997; Takeda et al., 2005), and striatal administration of D2R agonists suppressed pain-related responses (Ansah et al., 2007; Lin et al., 1981; Magnusson and Fisher, 2000; Saunier-Rebori and Pazo, 2006) suggest that dopamine acting on striatal D2Rs may play a significant role in striatal control of pain-related responses. In line with this, a number of experimental and clinical studies in humans suggest that striatal D2Rs contribute to regulation of pain (Hagelberg et al., 2004).
A 25 year adventure in the field of tachykinins
2004, PeptidesThe regulation of NMDA-evoked dopamine release by nitric oxide in the frontal cortex and raphe nuclei of the freely moving rat
2001, Brain ResearchCitation Excerpt :In vivo work in both rats and cats has also provided evidence for the involvement of glutamatergic corticostriatal neurones in the presynaptic regulation of DA release [12,26,34,37]. Other brain regions, the hippocampus and substantia nigra for example, containing high densities of glutamate receptor binding have also shown glutamate playing an important role in the regulation of DA release [3,34,47,49]. In the present study, we have investigated the regulation of NMDA-evoked DA release by NO in the raphe nuclei (RN) and frontal cortex (FC) of the freely moving rat using the selective nNOS inhibitor 7-nitroindazole (7NI) [32], the NO donor S-nitroso-N-acetylpenicillamine (SNAP) and the technique of in vivo microdialysis.