Role of Glutamate Receptors in the Development and Maintenance of Bladder Overactivity After Cerebral Infarction in the Rat

Yokoyama, Osamu; Mizuno, Hiroaki; Komatsu, Kazuto; Akino, Hironobu; Tanase, Kazuya; Namiki, Mikio

doi:10.1097/01.ju.0000104861.73314.fe

Cited by 15 publications

(15 citation statements)

References 17 publications

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“…An initiation phase that occurs at the time of infarction seems to function like long-term potentiation to induce a persistent facilitation of micturition (the second phase). The initial phase is not affected by pretreatment with an AMPA glutamatergic antagonist (NBQX) but can be blocked by administration of an NMDA antagonist (MK-801) (687), suggesting that plasticity at glutamatergic synapses can trigger this form of neurogenic bladder dysfunction (724). Rats with middle cerebral artery occlusion also exhibit an upregulation of D2-like dopamine receptor-mediated excitatory mechanism that contributes to DO (690) and a disruption of GABAergic inhibitory mechanism in the brain that enhances the micturition reflex (304).…”

Section: Disease-induced Changes In Micturitionmentioning

confidence: 99%

Neural Control of the Lower Urinary Tract

Groat

Griffiths

Yoshimura

2014

Comprehensive Physiology

348

527

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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: Disease-induced Changes In Micturitionmentioning

confidence: 99%

Neural Control of the Lower Urinary Tract

Groat

Griffiths

Yoshimura

2014

Comprehensive Physiology

348

527

View full text Add to dashboard Cite

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“…This model of bladder hyperactivity has been utilized to study pathophysiology and therapeutic approaches. When dizocilpine or MK‐801, NMDA glutamate receptor antagonist, was given to rats at the time of the MCA occlusion, bladder hyperactivity was prevented, suggesting a role for glutamatergic stimulation in the initial stage of the development of bladder dysfunction 102, 103. There is evidence of involvement of COX‐2 and nitric oxide in bladder hyperactivity following MCA occlusion 103, 104…”

Section: Disease Modelsmentioning

confidence: 99%

Rodent models for urodynamic investigation

Andersson

Soler

Füllhase

2011

Neurourology and Urodynamics

173

219

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Rodents, most commonly rats, mice, and guinea pigs are widely used to investigate urinary storage and voiding functions, both in normal animals and in models of disease. An often used methodology is cystometry. Micturitions in rodents and humans differ significantly and this must be considered when cystometry is used to interpret voiding in rodent models. Cystometry in humans requires active participation of the investigated patient (subject), and this can for obvious reasons not be achieved in the animals. Cystometric parameters in rodents are often poorly defined and do not correspond to those used in humans. This means that it is important that the terminology used for description of what is measured should be defined, and that the specific terminology used in human cystometry should be avoided. Available disease models in rodents have limited translational value, but despite many limitations, rodent cystometry may give important information on bladder physiology and pharmacology. The present review discusses the principles of urodynamics in rodents, techniques, and terminology, as well as some commonly used disease models, and their translational value.

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“…Recently Yokoyama et al reported that NBQX (1,2,3,4,-tetrahydro-6-nitro-2,3-dioxo-benzo(f) quinoxaline-7-sulfonamide disodium) suppressed bladder overactivity only when it was injected before performing MCA occlusion. 18 …”

Section: Rat Model Of Overactive Bladder and Drug Effectsmentioning

confidence: 97%