Dynamic changes in the relationship of microglia to cardiovascular neurons in response to increases and decreases in blood pressure

Kapoor, Komal; Bhandare, Amol M.; Nedoboy, Polina E.; Mohammed, Suja; Farnham, Melissa M.J.; Pilowsky, Paul M.

doi:10.1016/j.neuroscience.2016.04.044

Cited by 20 publications

(20 citation statements)

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“…Evidently, a recent study has shown a strong relationship between up‐regulated microglia and neurons involved in the control of cardiovascular function (Kapoor et al . ). Accordingly, the data from Takesue et al .…”

Section: Discussionmentioning

confidence: 97%

“…Although no significant increase was seen in microglia count, the morphology of the CD11b-positive cells and field are suggestive of the onset of inflammatory response and DAMP signaling events. Evidently, a recent study has shown a strong relationship between up-regulated microglia and neurons involved in the control of cardiovascular function (Kapoor et al 2016). Accordingly, the data from Takesue et al (2016a,b) showed that both Ang II infusion model and SHR showed an increase in microglia activation in the PVN, and was associated with an elevated blood pressure; probably through sympathoexcitation.…”

Section: Microglia and Astrocytic Activation In The Pvn Of Shrmentioning

confidence: 99%

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Age‐dependent alterations to paraventricular nucleus insulin‐like growth factor 1 receptor as a possible link between sympathoexcitation and inflammation

Ogundele

Lee

Francis

2016

Journal of Neurochemistry

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Modifications to neural circuits of the paraventricular hypothalamic nucleus (PVN) have been implicated in sympathoexcitation and systemic cardiovascular dysfunction. However, to date, the role of insulin-like growth factor 1 receptor (IGF-1R) expression on PVN pathophysiology is unknown. Using confocal immunofluorescence quantification and electrophysiological recordings from acute PVN slices, we investigated the mechanism through which age-dependent IGF-1R depletion contributes to the progression of inflammation and sympathoexcitation in the PVN of spontaneously hypertensive rats (SHR). Four and twenty weeks old SHR and Wistar Kyoto (WKY) rats were used for this study. Our data showed that Angiotensin I/II and pro-inflammatory high mobility box group protein 1 (HMGB1) exhibited increased expression in the PVN of SHR versus WKY at 4 weeks (p<0.01), and were even more highly expressed with age in SHR (p<0.001). This correlated with a significant decrease in IGF-1R expression, with age, in the PVN of SHR when compared with WKY (p<0.001) and were accompanied by related changes in astrocytes and microglia. In subsequent analyses, we found an age-dependent change in the expression of proteins associated with IGF-1R signaling pathways involved in inflammatory responses and synaptic function in the PVN. MAPK/ErK was more highly expressed in the PVN of SHR by the 4th week (p<0.001; vs WKY), while expression of neuronal nitric oxide synthase (nNOS; p<0.001) and calcium-calmodulin dependent kinase II alpha (CamKIIα; p<0.001) were significantly decreased by the 4th and 20th week respectively. Age-dependent changes in MAPK/ErK expression in the PVN correlated with an increase in the expression of vesicular glutamate transporter (VGLUT2) (p<0.001 vs WKY), while decreased levels of CamKIIα was associated with a decreased expression of tyrosine hydroxylase (p<0.001) by the 20th week. In addition, reduced labeling for GABA in the PVN of SHR (p<0.001) correlated with a decrease in nNOS labeling (p<0.001) when compared with the WKY by the 20th week. Electrophysiological recordings from neurons in acute slice preparations of the PVN of 4 weeks old SHR revealed spontaneous post-synaptic currents of higher frequency when compared with neurons from WKY PNV slices of the same age (p<0.001; n=14 cells). This also correlated with an increase in post-synaptic densities (PSD-95) in the PVN of SHR when compared with the WKY (p<0.001). Overall, we found an age-dependent reduction of IGF-1R, and related altered expression of associated downstream signaling molecules that may represent a link between the concurrent progression of synaptic dysfunction and inflammation in the PVN of SHR.

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Section: Discussionmentioning

confidence: 97%

Section: Microglia and Astrocytic Activation In The Pvn Of Shrmentioning

confidence: 99%

Age‐dependent alterations to paraventricular nucleus insulin‐like growth factor 1 receptor as a possible link between sympathoexcitation and inflammation

Ogundele

Lee

Francis

2016

Journal of Neurochemistry

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“…However, microglial morphological analysis revealed no change in their phenotype at least in the vicinity of the RVLM neurons. In this paradigm, as shown recently, physiological stimulus alert microglia (ramified) (Vinet et al, 2012), and change their spatial distribution and extent of end point processes contacting synapses without significant morphological changes (Kapoor et al, 2016c), which might be facilitating the pro-inflammatory effects during chronic epilepsy. Microglial activation into a deleterious phenotype in…”

Section: Discussionmentioning

confidence: 81%

“…Immunohistochemical analysis was done, as described previously Kapoor et al, 2016c), in n = 3 rats from both post-SE and control groups treated with IT PBS. Brainstems were sectioned coronally (40 µm thick) with a vibrating microtome (Leica, VT1200S).…”

Section: Sectioning and Immunohistochemistrymentioning

confidence: 99%

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Inhibition of microglial activation with minocycline at the intrathecal level attenuates sympathoexcitatory and proarrhythmogenic changes in rats with chronic temporal lobe epilepsy

et al. 2017

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(2017) Inhibition of microglial activation with minocycline at the intrathecal level attenuates sympathoexcitatory and proarrhythmogenic changes in rats with chronic temporal lobe epilepsy. Neuroscience, 350 . pp. 23-38 Permanent WRAP URL: http://wrap.warwick.ac.uk/87504 Copyright and reuse:The Warwick Research Archive Portal (WRAP) makes this work by researchers of the University of Warwick available open access under the following conditions. Copyright © and all moral rights to the version of the paper presented here belong to the individual author(s) and/or other copyright owners. To the extent reasonable and practicable the material made available in WRAP has been checked for eligibility before being made available.Copies of full items can be used for personal research or study, educational, or not-for-profit purposes without prior permission or charge. Provided that the authors, title and full bibliographic details are credited, a hyperlink and/or URL is given for the original metadata page and the content is not changed in any way. A note on versions:The version presented here may differ from the published version or, version of record, if you wish to cite this item you are advised to consult the publisher's version. Please see the 'permanent WRAP URL' above for details on accessing the published version and note that access may require a subscription. This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain. Abstract:The incidence of sudden unexpected death in epilepsy ( SE and control rats. We did not notice changes in microglial morphology or changes in a number of M2 phenotype in epileptic nor control rats in the vicinity of RVLM neurons. Our findings establish that microglial activation, and not PACAP, at the IML accounts for higher SNA and proarrhythmogenic changes during chronic epilepsy in rats. This is the first experimental evidence to support a neurotoxic effect of microglia during chronic epilepsy, in contrast to their neuroprotective action during acute seizures.

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The Role of Emotions, Stress, and Mental State in Inflammatory Processes Perturbing Brain-Heart Dialogue

Cipresso¹,

Álvarez²,

Riva³

et al. 2020

Brain and Heart Dynamics

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Dynamic changes in the relationship of microglia to cardiovascular neurons in response to increases and decreases in blood pressure

Cited by 20 publications

References 50 publications

Age‐dependent alterations to paraventricular nucleus insulin‐like growth factor 1 receptor as a possible link between sympathoexcitation and inflammation

Age‐dependent alterations to paraventricular nucleus insulin‐like growth factor 1 receptor as a possible link between sympathoexcitation and inflammation

Inhibition of microglial activation with minocycline at the intrathecal level attenuates sympathoexcitatory and proarrhythmogenic changes in rats with chronic temporal lobe epilepsy

The Role of Emotions, Stress, and Mental State in Inflammatory Processes Perturbing Brain-Heart Dialogue

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