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- W93934992 abstract "Nitric oxide (NO) is an important, yet understudied, gaseous regulator of neuronal activity in corticostriatal circuits. Numerous findings indicate that striatal NO signaling plays a key role in the regulation of shortand long-term synaptic plasticity [1, 2], protein kinase and protein phosphatase activities [3, 4], and gene expression [5]. Thus, disruption of striatal NO signaling cascades results in profound changes in behavioral, electrophysiological, and molecular responses to pharmacological manipulations of dopamine (DA) and glutamate transmission [6–8]. Most studies indicate that NO signaling facilitates neuronal activity via the activation of guanylyl cyclase (GC) (see [9] for review). It has been proposed that neuroadaptations in the NO–GC signaling cascade induced by DA depletion have an important role in the pathophysiology of Parkinson’s disease (PD). We will review this evidence and describe our recent work using various in vivo electrophysiological and neuroanatomical techniques aimed at determining how unilateral partial DA lesions alter NO–GC signaling in striatal circuits. Our studies are beginning to unravel the complex neuroadaptations in NO–GC signaling cascades that emerge following modest depletion of striatal DA that potentially mimics the early stages of PD. These neuroadaptations are likely involved in the enduring changes in glutamatergic transmission and motor behaviors observed in parkinsonian animal models and patients with PD." @default.
- W93934992 created "2016-06-24" @default.
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- W93934992 date "2008-12-31" @default.
- W93934992 modified "2023-10-16" @default.
- W93934992 title "Striatal Nitric Oxide–cGMP Signaling in an Animal Model of Parkinson’s Disease" @default.
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- W93934992 doi "https://doi.org/10.1007/978-1-60327-252-0_11" @default.
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