Repeated administration of orexin into the thalamic paraventricular nucleus inhibits the development of morphine-induced analgesia

2021 ◽  
Vol 28 ◽  
Author(s):  
Fatemeh Samani ◽  
Masoumeh Kourosh Arami
Keyword(s):  
Paraventricular Nucleus ◽  
Formalin Test ◽  
Repeated Administration ◽  
Treated Group ◽  
Pain Modulation ◽  
Morphine Injection ◽  
Chronic Morphine ◽  
Analgesic Effects ◽  
Male Wistar Rats ◽  
The Brain

Background: Hypothalamic neuropeptides, orexins, play pivotal roles in nociception and pain modulation. Objective: In this study, we investigated the effect of the administration of orexin into the paraventricular nucleus (PVT) on the development of morphine-induced analgesia in rats. Method. Male Wistar rats weighing 250-300 g received subcutaneous (s.c.) chronic morphine (6, 16, 26, 36, 46, 56 and 66 mg/kg, 2 ml/kg) at an interval of 24 hours for 7 days. Animals were divided into two experimental groups in which the orexin (100 μM, 200 nl) and its vehicle were microinjected into the PVT nucleus for 7 days before each morphine injection. Then, the formalin test was performed for the assessment of pain-related behaviors. Results: The results demonstrated that the rats pretreated by intra-PVT orexin exhibited higher pain-related behaviors than the morphine-treated group. The analgesic effects of morphine were significantly lower in orexin plus morphine-treated rats than the vehicle plus morphine-treated ones. Conclusion: Our findings suggested that the animals receiving the prolonged intra-PVT application of orexin before morphine injection demonstrated a significant increase in the development of nociceptive behaviors in all phases. Therefore, the present study highlighted a new area of the brain involved in the effect of orexin on analgesia induced by morphine.

scholarly journals Placebo analgesia

2018 ◽  
Vol 10 (3) ◽  
pp. 108-115
Author(s):  
G. R. Tabeeva
Keyword(s):  
Pain Therapy ◽  
Brain Structures ◽  
Emotional Reactions ◽  
Pain Modulation ◽  
Placebo Analgesia ◽  
Analgesic Effects ◽  
Pain Syndromes ◽  
Affective Processes ◽  
Different Types ◽  
The Brain

Placebos are drugs, devices, or other treatments that are physically and pharmacologically inert. The placebo effects are therapeutic responses to the context of the treatment process. They are mediated by factors, such as training of a patient, his/her expectations associated with treatment, as well as social conditions, the features of cognitive functioning, etc. and can affect the clinical and physiological responses caused by the health status. The analgesic effects of placebo in different types of pain syndromes reach 25–80%. The formation of placebo analgesia involves the brain structures that belong to the pain matrix and are implicated in the basic processes of perception, in the mechanisms of pain modulation, and in a number of other cognitive and affective processes, as well as in the emotional reactions not caused by pain. A deeper understanding of the mechanisms of action of placebo analgesia can optimize the strategy of current pain therapy.

scholarly journals Spinal protein kinase A and phosphorylated extracellular signal-regulated kinase signaling are involved in the antinociceptive effect of phytohormone abscisic acid in rats

2020 ◽  
Vol 78 (1) ◽  
pp. 21-27
Author(s):  
Mahtab MOLLASHAHI ◽  
Mehdi ABBASNEJAD ◽  
Saeed ESMAEILI-MAHANI
Keyword(s):  
Abscisic Acid ◽  
Antinociceptive Effect ◽  
Treated Group ◽  
Tail Flick ◽  
Animal Cells ◽  
Hot Plate ◽  
Analgesic Effects ◽  
Extracellular Signal ◽  
Dorsal Portion ◽  
Male Wistar Rats

Abstract Objective: The phytohormone abscisic acid (ABA) as a signaling molecule exists in various types of organisms from early multicellular to animal cells and tissues. It has been demonstrated that ABA has an antinociceptive effect in rodents. The present study was designed to assess the possible role of PKA and phosphorylated ERK (p-ERK) on the antinociceptive effects of intrathecal (i.t.) ABA in male Wistar rats. Methods: The animals were cannulated intrathecally and divided into different experimental groups (n=6‒7): Control (no surgery), vehicle (received ABA vehicle), ABA-treated groups (received ABA in doses of 10 or 20 µg/rat), ABA plus H.89 (PKA inhibitor)-treated group which received the inhibitor 15 min prior to the ABA injection. Tail-flick and hot-plate tests were used as acute nociceptive stimulators to assess ABA analgesic effects. p-ERK was evaluated in the dorsal portion of the spinal cord using immunoblotting. Results: Data showed that a microinjection of ABA (10 and 20 µg/rat, i.t.) significantly increased the nociceptive threshold in tail flick and hot plate tests. The application of PKA inhibitor (H.89, 100 nM/rat) significantly inhibited ABA-induced analgesic effects. Expression of p-ERK was significantly decreased in ABA-injected animals, which were not observed in the ABA+H.89-treated group. Conclusions: Overall, i.t. administration of ABA (10 µg/rat) induced analgesia and p-ERK down-expression likely by involving the PKA-dependent mechanism.

scholarly journals c-Fos expression in the hypothalamic paraventricular nucleus after a single treatment with a typical haloperidol and nine atypical antipsychotics: a pilot study

2018 ◽  
Vol 52 (2) ◽  
pp. 93-100 ◽  
Author(s):  
Alexander Kiss
Keyword(s):  
Pilot Study ◽  
Paraventricular Nucleus ◽  
Acute Effect ◽  
Hypothalamic Paraventricular Nucleus ◽  
Target Area ◽  
Male Wistar Rats ◽  
Fos Expression ◽  
The Brain ◽  
Present Pilot Study ◽  
Different Doses

AbstractObjective. The aim of the present study was to find out whether acute effect of different doses of selected antipsychotics including aripiprazole (ARI), amisulpride (AMI), asenapine (ASE), haloperidol (HAL), clozapine (CLO), risperidone (RIS), quetiapine (QUE), olanzapine (OLA), ziprasidone (ZIP), and paliperidone (PAL) may have a stimulatory impact on the c-Fos expression in the hypothalamic paraventricular nucleus (PVN) neurons.Methods. Adult male Wistar rats weighing 280–300 g were used. They were injected intraperitoneally with vehicle or antipsychotics in the following doses (mg/kg of b.w.): ARI (1, 10, 30), AMI (10, 30), ASE (0.3), HAL (1.0, 2.0), CLO (10, 20), RIS (0.5, 2.0), QUE (10, 20), OLA (5, 10), ZIP (10, 30), and PAL (1.0). Ninety min later, the animals were anesthetized with Zoletil and Xylariem and sacrificed by a transcardial perfusion with 60 ml of saline containing 450 μl of heparin (5000 IU/l) followed by 250 ml of fixative containing 4% paraformaldehyde in 0.1 M phosphate buffer (PB, pH 7.4). The brains were postfixed in a fresh fixative overnight, washed two times in 0.1 M PB, infiltrated with 30% sucrose for 2 days at 4 °C, frozen at −80 °C for 120 min, and cut into 30 μm thick serial coronal sections at −16 °C. c-Fos profiles were visualized by nickel intensified DAB immunohistochemistry and examined under Axio-Imager A1 (Zeiss) light microscope.Results. From ten sorts of antipsychotics tested, only six (ARI-10, CLO-10 and CLO-20, HAL-2, AMI-30, OLA-10, RIS-2 mg/kg b.w.) induced distinct c-Fos expression in the PVN. The antipsychotics predominantly targeted the medial parvocellular subdivision of the PVN.Conclusions. The present pilot study revealed c-Fos expression increase predominantly in the PVN medial parvocellular subdivision neurons by action of only several sorts of antipsychotics tested indicating that this structure of the brain does not represent a common extra-striatal target area for all antipsychotics.

Chronic immobilization stress induces anxiety-related behaviors and affects brain essential minerals in male rats

2020 ◽  
pp. 1-8
Author(s):  
Zafer Sahin ◽  
Alpaslan Ozkurkculer ◽  
Omer Faruk Kalkan ◽  
Ahmet Ozkaya ◽  
Aynur Koc ◽  
...  
Keyword(s):  
Immobilization Stress ◽  
Central Area ◽  
Essential Elements ◽  
Male Rats ◽  
Control Group ◽  
Male Wistar Rats ◽  
Swimming Test ◽  
The Brain ◽  
Center Area ◽  
Chronic Immobilization Stress

Abstract. Alterations of essential elements in the brain are associated with the pathophysiology of many neuropsychiatric disorders. It is known that chronic/overwhelming stress may cause some anxiety and/or depression. We aimed to investigate the effects of two different chronic immobilization stress protocols on anxiety-related behaviors and brain minerals. Adult male Wistar rats were divided into 3 groups as follows ( n = 10/group): control, immobilization stress-1 (45 minutes daily for 7-day) and immobilization stress-2 (45 minutes twice a day for 7-day). Stress-related behaviors were evaluated by open field test and forced swimming test. In the immobilization stress-1 and immobilization stress-2 groups, percentage of time spent in the central area (6.38 ± 0.41% and 6.28 ± 1.03% respectively, p < 0.05) and rearing frequency (2.75 ± 0.41 and 3.85 ± 0.46, p < 0.01 and p < 0.05, respectively) were lower, latency to center area (49.11 ± 5.87 s and 44.92 ± 8.04 s, p < 0.01 and p < 0.01, respectively), were higher than the control group (8.65 ± 0.49%, 5.37 ± 0.44 and 15.3 ± 3.32 s, respectively). In the immobilization stress-1 group, zinc (12.65 ± 0.1 ppm, p < 0.001), magnesium (170.4 ± 1.7 ppm, p < 0.005) and phosphate (2.76 ± 0.1 ppm, p < 0.05) levels were lower than the control group (13.87 ± 0.16 ppm, 179.31 ± 1.87 ppm and 3.11 ± 0.06 ppm, respectively). In the immobilization stress-2 group, magnesium (171.56 ± 1.87 ppm, p < 0.05), phosphate (2.44 ± 0.07 ppm, p < 0.001) levels were lower, and manganese (373.68 ± 5.76 ppb, p < 0.001) and copper (2.79 ± 0.15 ppm, p < 0.05) levels were higher than the control group (179.31 ± 1.87 ppm, 3.11 ± 0.06 ppm, 327.25 ± 8.35 ppb and 2.45 ± 0.05 ppm, respectively). Our results indicated that 7-day chronic immobilization stress increased anxiety-related behaviors in both stress groups. Zinc, magnesium, phosphate, copper and manganese levels were affected in the brain.

Role of Quercetin in Mitigation of Lindane Induced Toxicity in Terms of Oxidative Responses and Metabolic Status in Mice Brain

2020 ◽  
Vol 16 ◽  
Author(s):  
Anupama Sharma ◽  
Renu Bist ◽  
Hemant Pareek
Keyword(s):  
Citrate Synthase ◽  
Thiobarbituric Acid ◽  
Tca Cycle ◽  
Treated Group ◽  
Protein Carbonyl ◽  
Protein Carbonyl Content ◽  
Mice Brain ◽  
The Brain ◽  
Oxidative Responses

Background:: Current study evaluated the protective potential of quercetin against lindane induced toxicity in mice brain. For investigation, mice were allocated into four groups; First group was control. Second group was administered with oral dose of lindane (25 mg/kg bw) for 4 consecutive days. Third group was exposed to quercetin (40 mg/kg bw) and in fourth group, quercetin was administered 1 hour prior to the exposure of lindane. Objective:: Two major objectives were decided for study. First was to create lesions in the brain by lindane and; second was to evaluate the neuroprotective potential of quercetin. Methods:: To study oxidative responses, level of thiobarbituric acid reactive substances (TBARS), protein carbonyl content (PCC), reduced glutathione (GSH), superoxide dismutase (SOD), Catalase (CAT), and glutathione peroxidase (GPx) were measured in brain homogenates. Three key step regulating enzymes of tricarboxylic acid (TCA) cycle viz citrate synthase (CS), pyruvate dehydrogenase (PDH) and fumarase were also assayed. Results:: Lindane treatment significantly enhanced the levels of TBARS (P<0.001),PCC (P<0.001), GPx (P<0.001), SOD (P<0.05), PDH (P<0.05) and fumarase (P<0.001) in brains of mice compared to control. Meanwhile, it alleviated GSH, CAT and CS (P<0.05) activity. Conclusion:: Pretreatment with quercetin in lindane treated group not only restored, previously altered biochemical parameters after lindane treatment and also significantly improved them too which suggests that quercetin is not only invulnerable rather neuroprotective against lindane intoxication.

scholarly journals Oxidative Stress and Cognitive Alterations Induced by Cancer Chemotherapy Drugs: A Scoping Review

Antioxidants ◽  
2021 ◽  
Vol 10 (7) ◽  
pp. 1116
Author(s):  
Omar Cauli
Keyword(s):  
Oxidative Stress ◽  
Cancer Patients ◽  
Repeated Administration ◽  
Caffeic Acid Phenethyl Ester ◽  
Scientific Basis ◽  
Clinical Settings ◽  
Chemotherapy Drugs ◽  
Scientific Attention ◽  
The Brain ◽  
Cognitive Alterations

Cognitive impairment is one of the most deleterious effects of chemotherapy treatment in cancer patients, and this problem sometimes remains even after chemotherapy ends. Common classes of chemotherapy-based regimens such as anthracyclines, taxanes, and platinum derivatives can induce both oxidative stress in the blood and in the brain, and these effects can be reproduced in neuronal and glia cell cultures. In rodent models, both the acute and repeated administration of doxorubicin or adriamycin (anthracyclines) or cisplatin impairs cognitive functions, as shown by their diminished performance in different learning and memory behavioural tasks. Administration of compounds with strong antioxidant effects such as N-acetylcysteine, gamma-glutamyl cysteine ethyl ester, polydatin, caffeic acid phenethyl ester, and 2-mercaptoethane sulfonate sodium (MESNA) counteract both oxidative stress and cognitive alterations induced by chemotherapeutic drugs. These antioxidant molecules provide the scientific basis to design clinical trials in patients with the aim of reducing the oxidative stress and cognitive alterations, among other probable central nervous system changes, elicited by chemotherapy in cancer patients. In particular, N-acetylcysteine and MESNA are currently used in clinical settings and are therefore attracting scientific attention.

Norepinephrine regulates arginine vasopressin secretion in hypothalamic paraventricular nucleus relating with pain modulation

Neuropeptides ◽  
2009 ◽  
Vol 43 (4) ◽  
pp. 259-265 ◽  
Author(s):  
Jun Yang ◽  
Hui-Feng Yuan ◽  
Wen-Yan Liu ◽  
Xiao-Xia Zhang ◽  
Jian-Peng Feng ◽  
...  
Keyword(s):  
Paraventricular Nucleus ◽  
Arginine Vasopressin ◽  
Pain Modulation ◽  
Hypothalamic Paraventricular Nucleus ◽  
Vasopressin Secretion

scholarly journals Inhibition of Leukocyte Entry into the Brain by the Selectin Blocker Fucoidin Decreases Interleukin-1 (IL-1) Levels but Increases IL-8 Levels in Cerebrospinal Fluid during Experimental Pneumococcal Meningitis in Rabbits

2000 ◽  
Vol 68 (6) ◽  
pp. 3153-3157 ◽  
Author(s):  
Christian Østergaard ◽  
Runa Vavia Yieng-Kow ◽  
Thomas Benfield ◽  
Niels Frimodt-Møller ◽  
Frank Espersen ◽  
...  
Keyword(s):  
Cerebrospinal Fluid ◽  
Pneumococcal Meningitis ◽  
Interleukin 1 ◽  
Treated Group ◽  
Control Group ◽  
Necrosis Factor Alpha ◽  
Tnf Α ◽  
Significant Difference ◽  
The Brain ◽  
Experimental Pneumococcal Meningitis

ABSTRACT The polysaccharide fucoidin is a selectin blocker that inhibits leukocyte recruitment into the cerebrospinal fluid (CSF) during experimental pneumococcal meningitis. In the present study, the effect of fucoidin treatment on the release of the proinflammatory cytokines tumor necrosis factor alpha (TNF-α), interleukin-1 (IL-1), and IL-8 into the CSF was investigated. Rabbits (n = 7) were treated intravenously with 10 mg of fucoidin/kg of body weight every second hour starting 4 h after intracisternal inoculation of ∼106 CFU of Streptococcus pneumoniae type 3 (untreated control group, n = 7). CSF samples were obtained every second hour during a 16-h study period. Treatment with fucoidin caused a consistent and significant decrease in CSF IL-1 levels (in picograms per milliliter) between 12 and 16 h (0 versus 170, 0 versus 526, and 60 versus 1,467, respectively;P < 0.02). A less consistent decrease in CSF TNF-α levels was observed in the fucoidin-treated group, but with no significant difference between the two groups (P > 0.05). In contrast, there was no attenuation in CSF IL-8 levels. Indeed, there was a significant increase in CSF IL-8 levels (in picograms per milliliter) in the fucoidin-treated group at 10 and 12 h (921 versus 574 and 1,397 versus 569, respectively;P < 0.09). In conclusion, our results suggest that blood-derived leukocytes mainly are responsible for the release of IL-1 and to some degree TNF-α into the CSF during pneumococcal meningitis, whereas IL-8 may be produced by local cells within the brain.

scholarly journals Sevoflurane Exacerbates Cognitive Impairment Induced by Aβ1–40 in Rats through Initiating Neurotoxicity, Neuroinflammation, and Neuronal Apoptosis in Rat Hippocampus

2018 ◽  
Vol 2018 ◽  
pp. 1-10 ◽  
Author(s):  
Yue Tian ◽  
Ke-yan Chen ◽  
Li-dan Liu ◽  
Yun-xia Dong ◽  
Ping Zhao ◽  
...  
Keyword(s):  
Cognitive Impairment ◽  
Calcium Binding ◽  
Neuronal Apoptosis ◽  
Treated Group ◽  
Rat Hippocampus ◽  
Inos Mrna ◽  
Caspase 9 ◽  
Glycation End Products ◽  
Oxide Synthase ◽  
The Brain

Objective. This study was aimed at investigating whether sevoflurane inhalation induced cognitive impairment in rats with a possible mechanism involved in the event. Methods. Thirty-two rats were randomly divided into four groups of normal saline (NS) + O2, NS + sevoflurane (sevo), amyloid-β peptide (Aβ) + O2, and Aβ + sevo. The rats in the four groups received bilateral intrahippocampus injections of NS or Aβ. The treated hippocampus was harvested after inhaling 30% O2 or 2.5% sevoflurane. Evaluation of cognitive function was performed by Morris water maze (MWZ) and an Aβ1–42 level was determined by ELISA. Protein and mRNA expressions were executed by immunohistochemical (IHC) staining, Western blotting, and qRT-PCR. Results. Compared with the NS-treated group, sevoflurane only caused cognitive impairment and increased the level of Aβ1–42 of the brain in the Aβ-treated group. Sevoflurane inhalation but not O2 significantly increased glial fibrillary acidic protein (GFAP) and ionized calcium-binding adaptor molecule (IBA)1 expression in Aβ-treated hippocampus of rats. Expression levels for Bcl-xL, caspase-9, receptor for advanced glycation end products (RAGE) and brain-derived neurotrophic factor (BDNF) were significantly different in quantification of band intensity between the rats that inhaled O2 and sevoflurane in Aβ-treated groups (all P<0.05). Interleukin- (IL-) 1β, nuclear factor-κB (NF-κB), and inducible nitric oxide synthase (iNOS) mRNA expression increased after the rats inhaled sevoflurane in the Aβ-treated group (both P<0.01). There were no significant differences in the change of GFAP, IBA1, Bcl-xL, caspase-9, RAGE, BDNF, IL-1β, NF-κB, and iNOS in the NS + O2 and NS + sevo group (all P>0.05). Conclusion. Sevoflurane exacerbates cognitive impairment induced by Aβ1–40 in rats through initiating neurotoxicity, neuroinflammation, and neuronal apoptosis in rat hippocampus.

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