The dopamine D1 receptor agonist SKF 38393 suppresses detrusor hyperreflexia in the monkey with parkinsonism induced by 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)

Yoshimura, Naoki; Mizuta, Eiji; Kuno, Sadako; Sasa, Masashi; Yoshida, Osamu

doi:10.1016/0028-3908(93)90151-r

Cited by 117 publications

(89 citation statements)

References 19 publications

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“…Similarly, a rat model of PD induced by a unilateral 6-hydroxydopamine lesion of the nigrostriatal pathway also induces DO (715). In these PD animals, DO was suppressed by stimulation of D1-like receptors with SKF 38393 or pergolide (704,706,715), indicating that bladder overactivity in PD is primarily induced by disruption of D1-like dopamine receptor-mediated inhibition of the micturition reflex (Fig. 24).…”

Section: Agingmentioning

confidence: 83%

“…Figure 24 shows the potential dopaminergic and adenosinergic mechanisms inducing bladder dysfunction in PD, including a loss of D1-like receptor-mediated inhibition and upregulation of adenosine A 2A receptor-mediated facilitation of the micturition reflex that is controlled by the spinobulbospinal pathway. In monkeys, disruption of nigrostriatal dopaminergic pathways induced by the neurotoxin MPTP produces Parkinson-like motor symptoms accompanied by DO (11,704,706). Similarly, a rat model of PD induced by a unilateral 6-hydroxydopamine lesion of the nigrostriatal pathway also induces DO (715).…”

Section: Agingmentioning

confidence: 99%

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Neural Control of the Lower Urinary Tract

1997

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This article summarizes anatomical, neurophysiological, pharmacological, and brain imaging studies in humans and animals that have provided insights into the neural circuitry and neurotransmitter mechanisms controlling the lower urinary tract. The functions of the lower urinary tract to store and periodically eliminate urine are regulated by a complex neural control system in the brain, spinal cord, and peripheral autonomic ganglia that coordinates the activity of smooth and striated muscles of the bladder and urethral outlet. The neural control of micturition is organized as a hierarchical system in which spinal storage mechanisms are in turn regulated by circuitry in the rostral brain stem that initiates reflex voiding. Input from the forebrain triggers voluntary voiding by modulating the brain stem circuitry. Many neural circuits controlling the lower urinary tract exhibit switch-like patterns of activity that turn on and off in an all-or-none manner. The major component of the micturition switching circuit is a spinobulbospinal parasympathetic reflex pathway that has essential connections in the periaqueductal gray and pontine micturition center. A computer model of this circuit that mimics the switching functions of the bladder and urethra at the onset of micturition is described. Micturition occurs involuntarily in infants and young children until the age of 3 to 5 years, after which it is regulated voluntarily. Diseases or injuries of the nervous system in adults can cause the re-emergence of involuntary micturition, leading to urinary incontinence. Neuroplasticity underlying these developmental and pathological changes in voiding function is discussed.

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Section: Agingmentioning

confidence: 83%

Section: Agingmentioning

confidence: 99%

Neural Control of the Lower Urinary Tract

1997

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“…It has been suggested that the detrusor hyperreflexia may probably be due to a failure of activation of the dopamine D 1 receptors by the degenerated dopaminergic neurons originating in the SNpc (5,6).…”

Section: Discussionmentioning

confidence: 99%

Neuronal Excitation in the Ventral Tegmental Area Modulates the Micturition Reflex Mediated via the Dopamine D1 and D2 Receptors in Rats

et al. 2003

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Abstract. Involvement of the dopamine D 1 and D 2 receptors in the ventral tegmental area (VTA) in the micturition reflex was investigated using female Sprague Dawley rats under urethane anesthesia. Cystometrograms during continuous infusion of warmed saline into the bladder were recorded. When intervals of bladder contraction became constant, the excitatory amino acid DL-homocysteic acid (DLH) was microinjected into the VTA and changes in the cystometric parameters were observed. The selective D 1 antagonist SCH23390 (0.3 mg / kg) or D 2 antagonist eticlopride (0.1 mg / kg) was subcutaneously injected (s.c.) 15 min prior to the DLH treatment. A low dose of DLH (3 m g) facilitated the micturition reflex, whereas a high dose of DLH (30 mg) inhibited the micturition reflex. However, a middle dose of DLH (10 mg) did not show any effect. The facilitated micturition reflex induced by a low dose of DLH was inhibited by the selective dopamine D 2 antagonist eticlopride, but unaltered by SCH23390, a selective dopamine D 1 antagonist. In contrast, the inhibitory effect induced by a high dose of DLH on the micturition reflex was suppressed by SCH23390 but not eticlopride. These results suggested that the facilitated micturition reflex might be mediated via the dopamine D 2 receptors, while the inhibitory effects on the micturition reflex was mediated via the dopamine D 1 receptors.

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“…Patients with PD often have neurogenic detrusor over activity and voiding dysfunction (Berger et al, 1987), possibly as a consequence of nigrostriatal dopamine depletion and failure to activate inhibitory D1-like receptors (Yoshimura et al, 1993). Micturition, however, can be activated via D2-like receptors involving brainstem and spinal cord circuits.…”

Section: Dopaminementioning

confidence: 99%

“…In PD animal models depletion of dopaminergic neurones induces overactive bladder, (Yoshimura et al, 1993(Yoshimura et al, , 1998(Yoshimura et al, , 2003 and D1 receptor agonists produce inhibition of the micturition reflex in a dose-dependent manner while D2 receptor stimulation facilitates micturition. In PD degeneration of dopaminergic neurons in the substantia nigra leads to detrusor hyperactivity, through an inability to activate the D1-mediated tonic inhibition.…”

Section: The Pathophysiology Of Voiding Dysfunction In Parkinson's DImentioning

confidence: 99%

Botulinum A Toxin Intravesical Injections in the Treatment of Refractory Overactive Bladder in Patients with Parkinson's Disease

Giannantoni¹,

Proietti²,

Conte³

et al. 2011

Towards New Therapies for Parkinson's Disease

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The dopamine D1 receptor agonist SKF 38393 suppresses detrusor hyperreflexia in the monkey with parkinsonism induced by 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)

Cited by 117 publications

References 19 publications

Neural Control of the Lower Urinary Tract

Neural Control of the Lower Urinary Tract

Neuronal Excitation in the Ventral Tegmental Area Modulates the Micturition Reflex Mediated via the Dopamine D1 and D2 Receptors in Rats

Botulinum A Toxin Intravesical Injections in the Treatment of Refractory Overactive Bladder in Patients with Parkinson's Disease

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