Murine social stress results in long lasting voiding dysfunction

Butler, Stephan; Luz, Sandra; McFadden, Kile; Fesi, Joanna; Long, Christopher J.; Spruce, Lynn A.; Seeholzer, Steven H.; Canning, Douglas A.; Valentino, Rita J.; Zderic, Stephen A.

doi:10.1016/j.physbeh.2017.09.020

Cited by 13 publications

(18 citation statements)

References 35 publications

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“…The concept that CRH release may function to inhibit the bladder from ''unnecessary'' contractions or otherwise act as a ''brake'' upon Bar in triggering voiding is supported by studies using mouse models of social stress, which report retentive phenotypes in the setting of elevated CRH neuropeptide levels [45][46][47]. Furthermore, intrathecal administration of CRH in rats reduces the magnitude of bladder contractions following microinjection of glutamate into Bar, whereas the CRH receptor antagonist (D-PheCRHt2) has the opposite effect [32], providing further support for this hypothesis.…”

Section: Discussionmentioning

confidence: 99%

Non-Crh Glutamatergic Neurons in Barrington’s Nucleus Control Micturition via Glutamatergic Afferents from the Midbrain and Hypothalamus

et al. 2019

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with data analysis, Lian Guo for help with cystometry, Arjan Gijsberts (IIT, Genova IT) for custom MATLAB scripts and codes, Michael Lazerus and Patrick Fuller (BIDMC, Boston USA) for generating the AAV-DIO-DTA construct and vector, and Pavlos Gorelik (HMS-instrumentation core facility, Boston USA) for help with generating behavior cages. We especially acknowledge Patrick Fuller for his advice and constructive criticism of early versions of this manuscript, Brad Lowell and Clif Saper, and members of the laboratories for general support, helpful discussions, and comments on the manuscript.

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Section: Discussionmentioning

confidence: 99%

Non-Crh Glutamatergic Neurons in Barrington’s Nucleus Control Micturition via Glutamatergic Afferents from the Midbrain and Hypothalamus

et al. 2019

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“…In support of this hypothesis, c-Fos positivity was increased in this area after numerous stressor exposure. Moreover, some stressors, such as water avoidance stress, may increase the urinary frequency [171] and social stress-induced long-lasting voiding dysfunction [172], further connecting B to stress. In relation, upregulation of the CRH in B accompanied the social stress-induced urinary retention and a CRHR1 antagonist prevented this abnormal urodynamics [173].…”

Section: Assumed Function Of Each Crh-containing Brainstem Nuclei In Stressmentioning

confidence: 99%

Stress Adaptation and the Brainstem with Focus on Corticotropin-Releasing Hormone

Chaves

Fazekas

Horváth

et al. 2021

IJMS

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Stress adaptation is of utmost importance for the maintenance of homeostasis and, therefore, of life itself. The prevalence of stress-related disorders is increasing, emphasizing the importance of exploratory research on stress adaptation. Two major regulatory pathways exist: the hypothalamic–pituitary–adrenocortical axis and the sympathetic adrenomedullary axis. They act in unison, ensured by the enormous bidirectional connection between their centers, the paraventricular nucleus of the hypothalamus (PVN), and the brainstem monoaminergic cell groups, respectively. PVN and especially their corticotropin-releasing hormone (CRH) producing neurons are considered to be the centrum of stress regulation. However, the brainstem seems to be equally important. Therefore, we aimed to summarize the present knowledge on the role of classical neurotransmitters of the brainstem (GABA, glutamate as well as serotonin, noradrenaline, adrenaline, and dopamine) in stress adaptation. Neuropeptides, including CRH, might be co-localized in the brainstem nuclei. Here we focused on CRH as its role in stress regulation is well-known and widely accepted and other CRH neurons scattered along the brain may also complement the function of the PVN. Although CRH-positive cells are present on some parts of the brainstem, sometimes even in comparable amounts as in the PVN, not much is known about their contribution to stress adaptation. Based on the role of the Barrington’s nucleus in micturition and the inferior olivary complex in the regulation of fine motoric—as the main CRH-containing brainstem areas—we might assume that these areas regulate stress-induced urination and locomotion, respectively. Further studies are necessary for the field.

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“…The use of fluoxetine has been shown to mitigate the spatial avoidance behaviors in murine models of social defeat. However, the effect of fluoxetine did not restore a normal voiding phenotype 5 . The reasons may be attributed to that selective serotonin reuptake inhibitor (SSRI) take longer time to take effect.…”

Section: Introductionmentioning

confidence: 99%

“…2,3 The stress-related bladder dysfunction even persisted 1 month after removal of stressors. As antidepressant could ameliorate stress-related sequelae, 4,5 we hypothesize that antidepressant could also help improve the stress-related lower urinary tract dysfunction. The use of fluoxetine has been shown to mitigate the spatial avoidance behaviors in murine models of social defeat.…”

Section: Introductionmentioning

confidence: 99%

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Does ketamine ameliorate the social stress‐related bladder dysfunction in mice?

Yang

Chang

2020

Neurourology and Urodynamics

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Aims The aim of this study is to investigate whether ketamine could relieve the social stress (SS)‐related bladder dysfunction in mice. Materials and Methods The FVB mice were randomly assigned to either undergo SS exposure for 60 minutes per day on seven consecutive days for 4 weeks (SS1) or control without SS (SS0). The SS0 were then allocated to single or no injection of ketamine (SS0K1 and SS0K0). In the group of SS1, the SS1 mice were allocated to receive single injection of saline (SS1K0), single dose (SS1K1) or five daily dose of (SS1K5) ketamine injection (25 mg/kg/day/ip) since day 22. In vivo cystometry and tissue bath wire myography were performed on day 29. Serum and urine level of brain‐derived neurotrophic factor (BDNF) were measured with enzyme‐linked immunosorbent assay. Results In mice without social stress exposure, ketamine administration did not significantly affect voiding frequency (P > .05). SS1K0, SS1K1, and SS1K5 had significantly lower voiding frequency than that of control (SS1K0) (each n = 15, P < .05). Ketamine administration reversed the trend of decreased voiding frequency in SS1 mice. Stressed mice had significant higher serum level of BDNF that reduced by short‐term ketamine. Stressed mice had detrusor overactivity and impaired detrusor contractility which were not reversed by short‐term ketamine. Conclusions Social stress leads to elevated serum BDNF, infrequent voiding, detrusor overactivity, and impaired contractility. Short‐term administration of ketamine may improve SS‐related infrequent voiding and elevated serum BDNF level. However, ketamine did not improve SS‐related bladder dysfunction on urodynamic and myography studies.

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Murine social stress results in long lasting voiding dysfunction

Cited by 13 publications

References 35 publications

Non-Crh Glutamatergic Neurons in Barrington’s Nucleus Control Micturition via Glutamatergic Afferents from the Midbrain and Hypothalamus

Non-Crh Glutamatergic Neurons in Barrington’s Nucleus Control Micturition via Glutamatergic Afferents from the Midbrain and Hypothalamus

Stress Adaptation and the Brainstem with Focus on Corticotropin-Releasing Hormone

Does ketamine ameliorate the social stress‐related bladder dysfunction in mice?

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