scholarly journals The Occurrence of Pain-Induced Depression Is Different between Rat Models of Inflammatory and Neuropathic Pain

2021 ◽  
Vol 10 (17) ◽  
pp. 4016
Author(s):  
Yung-Chi Hsu ◽  
Kuo-Hsing Ma ◽  
Shu-Lin Guo ◽  
Bo-Feng Lin ◽  
Chien-Sung Tsai ◽  
...  
Keyword(s):  
Neuropathic Pain ◽  
Early Stage ◽  
Preference Test ◽  
Time Frame ◽  
Brain Regions ◽  
Rat Models ◽  
Positron Emission ◽  
Initial Injury ◽  
Sucrose Preference Test ◽  
The Brain

Various pain conditions may be associated with depressed mood. However, the effect of inflammatory or neuropathic pain on depression-like behavior and its associated time frame has not been well established in rat models. This frontward study investigated the differences in pain behavior, depression-like behavior, and serotonin transporter (SERT) distribution in the brain between rats subjected to spared nerve injury (SNI)-induced neuropathic pain or complete Freund’s adjuvant (CFA)-induced inflammatory pain. A dynamic plantar aesthesiometer and an acetone spray test were used to evaluate mechanical and cold allodynia responses, and depression-like behavior was examined using a forced swimming test and sucrose preference test. We also investigated SERT expression by using positron emission tomography. We found that the inflammation-induced pain was less severe than neuropathic pain from days 3 to 28 after induced pain; however, the CFA-injected rats exhibited more noticeable depression-like behavior and had significantly reduced SERT expression in the brain regions (thalamus and striatum) at an early stage (on days 14, 21, and 28 in two groups of CFA-injected rats versus day 28 in SNI rats). We speculated that not only the pain response after initial injury but also the subsequent neuroinflammation may have been the crucial factors influencing depression-like behavior in rats.

scholarly journals Pain Detection and the Privacy of Subjective Experience

2007 ◽  
Vol 33 (2-3) ◽  
pp. 433-456 ◽  
Author(s):  
Adam J. Kolber
Keyword(s):  
Subjective Experience ◽  
Brain Regions ◽  
Physical Pain ◽  
Medical Evidence ◽  
Functional Magnetic Resonance ◽  
Positron Emission ◽  
Pain Symptoms ◽  
The Brain ◽  
Insight Into ◽  
Neuroimaging Techniques

A neurologist with abdominal pain goes to see a gastroenterologist for treatment. The gastroenterologist asks the neurologist where it hurts. The neurologist replies, “In my head, of course.” Indeed, while we can feel pain throughout much of our bodies, pain signals undergo most of their processing in the brain. Using neuroimaging techniques like functional magnetic resonance imaging (“fMRI”) and positron emission tomography (“PET”), researchers have more precisely identified brain regions that enable us to experience physical pain. Certain regions of the brain's cortex, for example, increase in activation when subjects are exposed to painful stimuli. Furthermore, the amount of activation increases with the intensity of the painful stimulus. These findings suggest that we may be able to gain insight into the amount of pain a particular person is experiencing by non-invasively imaging his brain.Such insight could be particularly valuable in the courtroom where we often have no definitive medical evidence to prove or disprove claims about the existence and extent of pain symptoms.

Tumor Classification Based on Regional Heterogeneity Using Pixel Level Feature Descriptors

2021 ◽  
Vol 11 (5) ◽  
pp. 1481-1488
Author(s):  
C. Gunasundari ◽  
K. Selva Bhuvaneswari
Keyword(s):  
Texture Analysis ◽  
Early Stage ◽  
Pituitary Tumors ◽  
Brain Regions ◽  
Regional Heterogeneity ◽  
Gradient Based ◽  
Classification Of Tumors ◽  
Effective Diagnosis ◽  
The Brain

Brain tumor is considered to be widely analyzed disease for effective diagnosis and treatment planning. Several approaches were framed to detect and diagnose tumor at early stage. In this work, texture analysis is carried out to analyze the nature of tumor and categorize it. Around 3064 images were analyzed during this study consisting of meningioma, glioma and pituitary tumors. Intensity and gradient pixel based texture analysis is carried out in this analysis. Results confirm that the tumors can be classified and categorized based on the intensity and gradient pixel information. A total of 2216 feature vector is extracted it is observed that the gradient based information aids for better classification of tumors. Localized binary patterns are found to provide detailed information about the subtle variation in the brain regions due to the presence of abnormality in brain tissues. It is further observed that the normalized feature vectors show better differentiation between tumor categories. The ROC and PRC curves exhibit the high classification ability using the extracted features to differentiate tumor grades.

29 POSITRON EMISSION TOMOGRAPHY IMAGING OF BRAIN METABOLISM AND DOPAMINERGIC NEURON DESTRUCTION IN PARKINSON'S DISEASE MODEL PIG

2017 ◽  
Vol 29 (1) ◽  
pp. 122
Author(s):  
H. J. Oh ◽  
J. Moon ◽  
G. A. Kim ◽  
S. Lee ◽  
S. H. Paek ◽  
...  
Keyword(s):  
Positron Emission Tomography ◽  
Dopaminergic Neuron ◽  
Brain Metabolism ◽  
Brain Research ◽  
Brain Regions ◽  
Emission Tomography ◽  
Positron Emission ◽  
Significant Difference ◽  
And Control ◽  
The Brain

Due to similarities between human and porcine, pigs have been proposed as an excellent experimental animal for human medical research. Especially in paediatric brain research, piglets share similarities with human infants in the extent of peak brain growth at the time of birth and the growth pattern of brain. Thus, these findings have supported the wider use of pigs rather than rodents in neuroscience research. Previously, we reported the production of porcine model of Parkinson's disease (PD) by nuclear transfer using donor cell that had been stably infected with lentivirus containing the human α-synuclein gene. The purpose of this study was to determine the alternation of brain metabolism and dopaminergic neuron destruction using noninvasive method in a 2-yr-old PD model and a control pig. The positron emission tomography (PET) scan was done using Biograph TruePoint40 with a TrueV (Siemens, Munich, Germany). The [18F]N-(3-fluoropropyl)-2β-carbomethoxy-3β-(4-iodophenyl) nortropane (FP-CIT) was administrated via the ear vein. Static images of the brain for 15 min were acquired from 2 h after injection. The 18F-fluorodeoxy-D-glucose PET (18F-FDG PET) images of the brain were obtained for 15 min at 45 min post-injection. Computed tomography (CT) scan and magnetic resonance imaging (MRI) were performed at the same location of the brain. In both MRI and CT images, there was no difference in brain regions between PD model and control pigs. However, administration of [18F]FP-CIT was markedly decreased in the bilateral putamen of the PD model pig compared with the control pigs. Moreover, [18F]FP-CIT administration was asymmetrical in the PD model pig but it was symmetrical in control pigs. Regional brain metabolism was also assessed and there was no significant difference in cortical metabolism of PD model and control pigs. We demonstrated that PET imaging could provide a foundation for translational Parkinson neuroimaging in transgenic pigs. In the present study, a 2-yr-old PD model pig showed dopaminergic neuron destruction in brain regions. Therefore, PD model pig expressing human α-synuclein gene would be an efficient model for human PD patients. This study was supported by Korea IPET (#311011–05–5-SB010), Research Institute for Veterinary Science, TS Corporation and the BK21 plus program.

scholarly journals Medial Orbitofrontal Cortex Is Associated with Fatigue Sensation

2010 ◽  
Vol 2010 ◽  
pp. 1-5 ◽  
Author(s):  
Seiki Tajima ◽  
Shigeyuki Yamamoto ◽  
Masaaki Tanaka ◽  
Yosky Kataoka ◽  
Masao Iwase ◽  
...  
Keyword(s):  
Positron Emission Tomography ◽  
Orbitofrontal Cortex ◽  
Brain Region ◽  
Statistical Parametric Mapping ◽  
Brain Regions ◽  
Mapping Method ◽  
Emission Tomography ◽  
Neural Basis ◽  
Positron Emission ◽  
The Brain

Fatigue is an indispensable bioalarm to avoid exhaustive state caused by overwork or stresses. It is necessary to elucidate the neural mechanism of fatigue sensation for managing fatigue properly. We performedH2O  15positron emission tomography scans to indicate neural activations while subjects were performing 35-min fatigue-inducing task trials twice. During the positron emission tomography experiment, subjects performed advanced trail-making tests, touching the target circles in sequence located on the display of a touch-panel screen. In order to identify the brain regions associated with fatigue sensation, correlation analysis was performed using statistical parametric mapping method. The brain region exhibiting a positive correlation in activity with subjective sensation of fatigue, measured immediately after each positron emission tomography scan, was located in medial orbitofrontal cortex (Brodmann's area 10/11). Hence, the medial orbitofrontal cortex is a brain region associated with mental fatigue sensation. Our findings provide a new perspective on the neural basis of fatigue.

scholarly journals A Single Subanesthetic Dose of Ketamine Relieves Depression-like Behaviors Induced by Neuropathic Pain in Rats

2011 ◽  
Vol 115 (4) ◽  
pp. 812-821 ◽  
Author(s):  
Jing Wang ◽  
Yossef Goffer ◽  
Duo Xu ◽  
David S. Tukey ◽  
D. B. Shamir ◽  
...  
Keyword(s):  
Neuropathic Pain ◽  
Nerve Injury ◽  
Forced Swim Test ◽  
Preference Test ◽  
Sucrose Preference ◽  
Spared Nerve Injury ◽  
Chronic Neuropathic Pain ◽  
Swim Test ◽  
Forced Swim ◽  
Sucrose Preference Test

Background Chronic pain is associated with depression. In rodents, pain is often assessed by sensory hypersensitivity, which does not sufficiently measure affective responses. Low-dose ketamine has been used to treat both pain and depression, but it is not clear whether ketamine can relieve depression associated with chronic pain and whether this antidepressant effect depends on its antinociceptive properties. Methods The authors examined whether the spared nerve injury model of neuropathic pain induces depressive behavior in rats, using sucrose preference test and forced swim test, and tested whether a subanesthetic dose of ketamine treats spared nerve injury-induced depression. Results Spared nerve injury-treated rats, compared with control rats, showed decreased sucrose preference (0.719 ± 0.068 (mean ± SEM) vs. 0.946 ± 0.010) and enhanced immobility in the forced swim test (107.3 ± 14.6s vs. 56.2 ± 12.5s). Further, sham-operated rats demonstrated depressive behaviors in the acute postoperative period (0.790 ± 0.062 on postoperative day 2). A single subanesthetic dose of ketamine (10 mg/kg) did not alter spared nerve injury-induced hypersensitivity; however, it treated spared nerve injury-associated depression-like behaviors (0.896 ± 0.020 for ketamine vs. 0.663 ± 0.080 for control rats 1 day after administration; 0.858 ± 0.017 for ketamine vs. 0.683 ± 0.077 for control rats 5 days after administration). Conclusions Chronic neuropathic pain leads to depression-like behaviors. The postoperative period also confers vulnerability to depression, possibly due to acute pain. Sucrose preference test and forced swim test may be used to compliment sensory tests for assessment of pain in animal studies. Low-dose ketamine can treat depression-like behaviors induced by chronic neuropathic pain.

scholarly journals Possible role for brain prostanoid pathways in the development of angiotensin II-salt hypertension in rats

2016 ◽  
Vol 311 (2) ◽  
pp. R232-R242 ◽  
Author(s):  
Ninitha Asirvatham-Jeyaraj ◽  
Gregory D. Fink
Keyword(s):  
Time Frame ◽  
Brain Regions ◽  
Lamina Terminalis ◽  
Ang Ii ◽  
Neurogenic Hypertension ◽  
Salt Hypertension ◽  
Pressor Activity ◽  
Organum Vasculosum ◽  
The Brain ◽  
Infusion Period

Prostanoids generated by the cyclooxygenase (COX) pathway appear to contribute to the neurogenic hypertension (HTN) in rats. The first goal of this study was to establish the time frame during which prostanoids participate in ANG II-salt HTN. We induced HTN using ANG II (150 ng·kg−1·min−1 sc) infusion for 14 days in rats on a high-salt (2% NaCl) diet. When ketoprofen pretreatment was combined with treatment during the first 7 days of ANG II infusion, development of HTN and increased neurogenic pressor activity (indexed by the depressor response to ganglion blockade) were significantly attenuated for the entire ANG II infusion period. This suggests that prostanoid generation caused by administration of ANG II and salt leads to an increase in neurogenic pressor activity and blood pressure (BP) via a mechanism that persists without the need for continuing prostanoid input. The second goal of this study was to determine whether prostanoid products specifically in the brain contribute to HTN development. Expression of prostanoid pathway genes was measured in brain regions known to affect neurogenic BP regulation. ANG II-treated rats exhibited changes in gene expression of phospholipase A2 (upregulated in organum vasculosum of the lamina terminalis, paraventricular nucleus, nucleus of the solitary tract, and middle cerebral artery) and lipocalin-type prostaglandin D synthase (upregulated in the organum vasculosum of the lamina terminalis). On the basis of our results, we propose that activation of the brain prostanoid synthesis pathway both upstream and downstream from COX at early stages plays an important role in the development of the neurogenic component of ANG II-salt HTN.

scholarly journals Mutant huntingtin reduces vesicular zinc level by inhibiting the binding of Sp1 to ZnT3 promoter

2020 ◽  
Author(s):  
Li Niu ◽  
Shiming Yang ◽  
Weixi Wang ◽  
Cui-fang Ye ◽  
He Li
Keyword(s):  
Molecular Mechanisms ◽  
Early Stage ◽  
Brain Regions ◽  
Zinc Level ◽  
Significant Loss ◽  
Zinc Homeostasis ◽  
Synaptic Dysfunction ◽  
Mutant Huntingtin ◽  
Bhk Cells ◽  
The Brain

Abstract Background Synaptic dysfunction caused by mutant huntingtin greatly contributes to Huntington’s disease (HD) pathogenesis. HD patients show cognitive impairment as well as uncontrolled movements. Vesicular zinc is closely linked to modulating synaptic transmission and maintaining cognitive ability. However, whether does mutant huntingtin affect zinc homeostasis in the brain or not? This will be of great significance for further revealing the pathogenesis of HD. Methods N171-HD82Q transgenic mice and cultured BHK cells expressing N-terminal mutant huntingtin fragment containing 160 glutamines (160Q BHK cells) were used to investigate the effect of mutant huntingtin on zinc homeostasis and its molecular mechanisms. Results Herein, we have demonstrated that the density of synaptic vesicular zinc decreases in the cortex, striatum and hippocampus of N171-82Q mice. Given that vesicular zinc concentration depends on the abundance of zinc transporter 3 (ZnT3) on the membrane of synaptic vesicles, ZnT3 expression is detected in the brain of N171-82Q mice and 160Q BHK cells. Mutant huntingtin leads to a dramatical decrease in ZnT3 mRNA and protein levels in the three brain regions of these mice aged from 14 to 20 weeks. Significantly, Sp1 activates ZnT3 transcription via its binding to the GC boxes in ZnT3 promoter. Nevertheless, mutant huntingtin inhibits the binding of Sp1 to the promoter of ZnT3 gene and down-regulates ZnT3 expression. Furthermore, the overexpression of Sp1 ameliorates inhibition of ZnT3 gene transcription by mutant huntingtin. Conclusions Collectively, this first study to reveal a significant loss of synaptic vesicular zinc and ZnT3 expression caused by mutant huntingtin in the early stage of HD. Our findings have revealed the molecular mechanism underlying this change. Mutant huntingtin inhibits the binding of Sp1 to ZnT3 gene promoter to reduce ZnT3 expression. The imbalance of vesicular zinc homeostasis may be closely associated with synaptic dysfunction and cognitive deficits in HD. This work sheds novel mechanistic insights into the pathogenesis of HD and promises a potential therapeutic strategy for HD.

scholarly journals Regional Cerebral l-[14C-Methyl]Methionine Incorporation into Proteins: Evidence for Methionine Recycling in the Rat Brain

1992 ◽  
Vol 12 (4) ◽  
pp. 603-612 ◽  
Author(s):  
Anna M. Planas ◽  
Christian Prenant ◽  
Bernard M. Mazoyer ◽  
Dominique Comar ◽  
Luigi Di Giamberardino
Keyword(s):  
Rat Brain ◽  
Specific Activity ◽  
Plasma Source ◽  
Brain Regions ◽  
Emission Tomography ◽  
Protein Breakdown ◽  
Isotopic Equilibrium ◽  
Positron Emission ◽  
Time Periods ◽  
The Brain

The specific activity (SA) of free methionine was measured in plasma and in different regions of the rat brain at 15, 30, or 60 min after intravenous infusion of l-[14C- methyl]methionine. Within these time periods, an apparent steady state of labeled free methionine in plasma and in brain was reached. However, the brain-to-plasma free methionine SA ratio was found to be ∼0.5, showing that an isotopic equilibrium between brain and plasma was not attained. This suggests the presence of an endogenous source of brain free methionine (likely originating from protein breakdown), in addition to the plasma source. The contribution of this endogenous source to the content of free methionine varies significantly among the different brain regions. Our results indicate that the regional rates of protein synthesis measured with l-[11C- methyl]methionine using positron emission tomography would be underestimated, since the local fraction of brain methionine derived from protein degradation would not be considered.

scholarly journals The Brain at High Altitude: Hypometabolism as a Defense against Chronic Hypoxia?

1994 ◽  
Vol 14 (4) ◽  
pp. 671-679 ◽  
Author(s):  
P. W. Hochachka ◽  
C. M. Clark ◽  
W. D. Brown ◽  
C. Stanley ◽  
C. K. Stone ◽  
...  
Keyword(s):  
High Altitude ◽  
Chronic Hypoxia ◽  
Large Fraction ◽  
Brain Regions ◽  
Proton Nuclear Magnetic Resonance ◽  
Resonance Spectroscopy ◽  
Metabolic Rates ◽  
Positron Emission Tomographic ◽  
Positron Emission ◽  
The Brain

The brain of hypoxia-tolerant vertebrates is known to survive extreme limitations of oxygen in part because of very low rates of energy production and utilization. To assess if similar adaptations may be involved in humans during hypoxia adaptation over generational time, volunteer Quechua natives, indigenous to the high Andes between about 3,700 and 4,900 m altitude, served as subjects in positron emission tomographic measurements of brain regional glucose metabolic rates. Two metabolic states were analyzed: (a) the presumed normal (high altitude-adapted) state monitored as soon as possible after leaving the Andes and (b) the deacclimated state monitored after 3 weeks at low altitudes. Proton nuclear magnetic resonance spectroscopy studies of the Quechua brain found normal spectra, with no indication of any unusual lactate accumulation; in contrast, in hypoxia-tolerant species, a relatively large fraction of the glucose taken up by the brain is released as lactate. Positron emission tomographic measurements of [18F]2-deoxy-2-fluoro-d-glucose (FDG) uptake rates, quantified in 26 regions of the brain, indicated systematically lower region-by-region glucose metabolic rates in Quechuas than in lowlanders. The metabolic reductions were least pronounced in primitive brain structures (e.g., cerebellum) and most pronounced in regions classically associated with higher cortical functions (e.g., frontal cortex). These differences between Quechuas with lifetime exposure to hypobaric hypoxia and lowlanders, which seem to be expressed to some degree in most brain regions examined, may be the result of a defense adaptation against chronic hypoxia.

scholarly journals Initial Cerebral HM-PAO Distribution Compared to LCBF: Use of a Model Which Considers Cerebral HM-PAO Trapping Kinetics

1988 ◽  
Vol 8 (1_suppl) ◽  
pp. S31-S37 ◽  
Author(s):  
James L. Lear
Keyword(s):  
Arterial Input Function ◽  
Input Function ◽  
Brain Regions ◽  
Male Rats ◽  
Type Model ◽  
Emission Computed Tomography ◽  
Intravenous Injections ◽  
Positron Emission ◽  
Uptake Pattern ◽  
The Brain

The cerebral uptake of [99mTc]– d,l-hexamethylpropyleneamine oxime complex (HM-PAO) was compared to LCBF determined simultaneously with [14C]iodoantipyrine (IAP) using double radionuclide quantitative digital autoradiography. Awake male rats were given intravenous injections of a mixture of 50 μCi IAP and 15 mCi of HM-PAO and killed 20 s after tracer activity had first reached the brain. Two separate autoradiograms were produced from each 20 μm brain section. The autoradiograms were digitized, corrected for cross-contamination, and then converted into images of individual tracer concentration. The diffusible tracer model was used to convert the IAP concentration images into LCBF images. Regional HM-PAO concentration was found not to be linearly related to LCBF as determined with the IAP, and therefore a simple microsphere type model was inadequate in relating HM-PAO uptake to LCBF. A better HM-PAO uptake–LCBF correlation was obtained when the HM-PAO arterial input function was corrected for very rapidly produced, non-cerebrally extracted, metabolites and a kinetic model was used that considered the rate of intracerebral metabolism of HM-PAO to a retained metabolite. Even using this model, however, some differences between HM-PAO uptake and LCBF occurred in certain brain regions. Because these differences were small and the HM-PAO uptake pattern has been shown to be constant for many minutes, HM-PAO can probably be used to estimate LCBF in patients with single positron emission computed tomography (SPECT) imaging.

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