The real-time in vivo electrochemical measurement of nitric oxide and carbon monoxide release upon direct epidural electrical stimulation of the rat neocortex

Park, Sarah S.; Hong, MunPyo; Ha, Yejin; Sim, Jeongeun; Jhon, Gil‐Ja; Lee, Young-Mi; Suh, Minah

doi:10.1039/c5an00122f

Cited by 22 publications

(26 citation statements)

References 38 publications

(46 reference statements)

Supporting

Mentioning

Contrasting

Order By: Relevance

“…In addition, the decrease in HO-2 expression, which produces CO, may contribute to the reduced functional hemodynamic responses in the stress group, although the role of CO in stress has not been reported. Recent evidence from an in vivo microsensor study demonstrates that CO has a tight relationship with increased metabolic demands and cerebral blood flow (Park et al, 2015 ). In this study, the endogenous CO release nicely reflects the robust hemodynamic response, which is induced by epidural electrical stimulation in the rat somatosensory cortex.…”

Section: Discussionmentioning

confidence: 99%

Chronic Stress Decreases Cerebrovascular Responses During Rat Hindlimb Electrical Stimulation

et al. 2015

Self Cite

View full text Add to dashboard Cite

Repeated stress is one of the major risk factors for cerebrovascular disease, including stroke, and vascular dementia. However, the functional alterations in the cerebral hemodynamic response induced by chronic stress have not been clarified. Here, we investigated the in vivo cerebral hemodynamic changes and accompanying cellular and molecular changes in chronically stressed rats. After 3 weeks of restraint stress, the elicitation of stress was verified by behavioral despair in the forced swimming test and by physical indicators of stress. The evoked changes in the cerebral blood volume and pial artery responses following hindpaw electrical stimulation were measured using optical intrinsic signal imaging. We observed that, compared to the control group, animals under chronic restraint stress exhibited a decreased hemodynamic response, with a smaller pial arterial dilation in the somatosensory cortex during hindpaw electrical stimulation. The effect of chronic restraint stress on vasomodulator enzymes, including neuronal nitric oxide synthase (nNOS) and heme oxygenase-2 (HO-2), was assessed in the somatosensory cortex. Chronic restraint stress downregulated nNOS and HO-2 compared to the control group. In addition, we examined the subtypes of cells that can explain the environmental changes due to the decreased vasomodulators. The expression of parvalbumin in GABAergic interneurons and glutamate receptor-1 in neurons were decreased, whereas the microglial activation was increased. Our results suggest that the chronic stress-induced alterations in cerebral vascular function and the modulations of the cellular expression in the neuro-vasomodulatory system may be crucial contributing factors in the development of various vascular-induced conditions in the brain.

show abstract

Section: Discussionmentioning

confidence: 99%

Chronic Stress Decreases Cerebrovascular Responses During Rat Hindlimb Electrical Stimulation

et al. 2015

Self Cite

View full text Add to dashboard Cite

show abstract

“…The NO sensors demonstrated negligible responses (<1%) from most of the interfering species including ascorbic acid, serotonin, DOPAC, dopamine, l -gluthathione, hydrogen peroxide, 5-HIAA, homovanillic acid, nitrite and uric acid. Further selectivity studies were undertaken against more recent identified interferents including the electroactive gasotransmitters CO and H 2 S. Concentrations representative of their physiological levels were chosen [23,24]. A comparable selectivity over H 2 S (<1%, 1.6 ± 0.1 pA·µM −1 , n = 4) and a slightly higher contribution from CO (ca.…”

Section: Methodsmentioning

confidence: 99%

Long Term Amperometric Recordings in the Brain Extracellular Fluid of Freely Moving Immunocompromised NOD SCID Mice

Reid

Finnerty

2017

Sensors

View full text Add to dashboard Cite

Abstract:We describe the in vivo characterization of microamperometric sensors for the real-time monitoring of nitric oxide (NO) and oxygen (O 2 ) in the striatum of immunocompromised NOD SCID mice. The latter strain has been utilized routinely in the establishment of humanized models of disease e.g., Parkinson's disease. NOD SCID mice were implanted with highly sensitive and selective NO and O 2 sensors that have been previously characterized both in vitro and in freely moving rats. Animals were systemically administered compounds that perturbed the amperometric current and confirmed sensor performance. Furthermore, the stability of the amperometric current was investigated and 24 h recordings examined. Saline injections caused transient changes in both currents that were not significant from baseline. L-NAME caused significant decreases in NO (p < 0.05) and O 2 (p < 0.001) currents compared to saline. L-Arginine produced a significant increase (p < 0.001) in NO current, and chloral hydrate and Diamox (acetazolamide) caused significant increases in O 2 signal (p < 0.01) compared against saline. The stability of both currents were confirmed over an eight-day period and analysis of 24-h recordings identified diurnal variations in both signals. These findings confirm the efficacy of the amperometric sensors to perform continuous and reliable recordings in immunocompromised mice.

show abstract

“…These fixed and modifiable risk factors give rise to the injury mediators amyloid b, inflammation, reactive oxygen and nitrogen species (RONS), and suppression of endothelial nitric oxide synthase (eNOS) which, in turn, damage macro-and microvascular components of the cerebral circulation. The resultant impairment of cerebral blood supply causes neurodegeneration which culminates in neurocognitive impairment peptides [25][26][27] associated with altered tissue PO 2 . 28 However, atherosclerotic disease in the cerebral supply arteries limits the vascular reserve that is required for autoregulation of cerebral blood flow and exposes the otherwise healthy, active brain to the potential damage of sustained hypoxia and ischemia.…”

Section: Cerebrovascular Function and Admentioning

confidence: 99%

Intermittent hypoxia training protects cerebrovascular function in Alzheimer's disease

Манухина

Downey

Shi

et al. 2016

Exp Biol Med (Maywood)

View full text Add to dashboard Cite

Alzheimer's disease (AD) is a leading cause of death and disability among older adults. Modifiable vascular risk factors for AD (VRF) include obesity, hypertension, type 2 diabetes mellitus, sleep apnea, and metabolic syndrome. Here, interactions between cerebrovascular function and development of AD are reviewed, as are interventions to improve cerebral blood flow and reduce VRF. Atherosclerosis and small vessel cerebral disease impair metabolic regulation of cerebral blood flow and, along with microvascular rarefaction and altered trans-capillary exchange, create conditions favoring AD development. Although currently there are no definitive therapies for treatment or prevention of AD, reduction of VRFs lowers the risk for cognitive decline. There is increasing evidence that brief repeated exposures to moderate hypoxia, i.e. intermittent hypoxic training (IHT), improve cerebral vascular function and reduce VRFs including systemic hypertension, cardiac arrhythmias, and mental stress. In experimental AD, IHT nearly prevented endothelial dysfunction of both cerebral and extra-cerebral blood vessels, rarefaction of the brain vascular network, and the loss of neurons in the brain cortex. Associated with these vasoprotective effects, IHT improved memory and lessened AD pathology. IHT increases endothelial production of nitric oxide (NO), thereby increasing regional cerebral blood flow and augmenting the vaso-and neuroprotective effects of endothelial NO. On the other hand, in AD excessive production of NO in microglia, astrocytes, and cortical neurons generates neurotoxic peroxynitrite. IHT enhances storage of excessive NO in the form of S-nitrosothiols and dinitrosyl iron complexes. Oxidative stress plays a pivotal role in the pathogenesis of AD, and IHT reduces oxidative stress in a number of experimental pathologies. Beneficial effects of IHT in experimental neuropathologies other than AD, including dyscirculatory encephalopathy, ischemic stroke injury, audiogenic epilepsy, spinal cord injury, and alcohol withdrawal stress have also been reported. Further research on the potential benefits of IHT in AD and other brain pathologies is warranted.

show abstract

The real-time in vivo electrochemical measurement of nitric oxide and carbon monoxide release upon direct epidural electrical stimulation of the rat neocortex

Cited by 22 publications

References 38 publications

Chronic Stress Decreases Cerebrovascular Responses During Rat Hindlimb Electrical Stimulation

Chronic Stress Decreases Cerebrovascular Responses During Rat Hindlimb Electrical Stimulation

Long Term Amperometric Recordings in the Brain Extracellular Fluid of Freely Moving Immunocompromised NOD SCID Mice

Intermittent hypoxia training protects cerebrovascular function in Alzheimer's disease

Contact Info

Product

Resources

About