scholarly journals IMMUNOHISTOCHEMICAL IDENTIFICATION AND DISTRIBUTION OF GLUTAMATERGIC NMDA AND mGlu1 RECEPTORS IN THE PONTINE INTERTRIGEMINAL REGION IN RATS

2019 ◽  
pp. 064
Author(s):  
Milan Stoiljkovic
Keyword(s):  
Polyclonal Antibodies ◽  
Neuronal Cell ◽  
Image Analysis System ◽  
Sprague Dawley ◽  
Cardiorespiratory Control ◽  
Signal Distribution ◽  
Similar Expression Profile ◽  
Neuronal Cell Bodies ◽  
Sprague Dawley Rats ◽  
Analysis System

Local glutamate simulation of intertrigeminal region (ITR) in the lateral pons evoked immediate cardiovascular and respiratory effects proposing its role in central cardiorespiratory control. Since pharmacological studies provided only functional evidence for the existence of glutamate receptors in the ITR and thereby specifying putative neurochemical substrate involved in this control, here we employed immunohistochemistry to examine expression and distribution of NMDA and mGlu1 receptors in this structure. Thirty adult male Sprague-Dawley rats were perfuse-fixed, their brains frozen and cut into sequential series of 20 µm thick sections through the ITR. Immunohistochemistry was performed using polyclonal antibodies against NMDA-NR1, NMDA-NR2A and mGlu1 receptors. Labeled neurons in the ITR were analyzed using light microscope and computerized image analysis system for quantification of relative immunoreactivity as the mean of integrated optical density (IOD), and counting the immunopositive cells. Light microscopic analyses demonstrated NMDA-NR1-immunoreactivity mainly localized in the neuronal cell bodies with sparse distribution on primary dendrites, while NMDA-NR2A-immunoreactivity was basically somatically distributed. The mGlu1-immunoreactivity was moderate and observed both in neuronal bodies and primary dendrites or extracellular matrix suggesting somatodendritic localization. Quantitative analyses of IOD showed very strong expression of NMDA-NR1, weak of NMDA-NR2A and strong-to-moderate expression of mGluR1, with differences in immunostaining signal distribution over rostro-caudal span of the ITR. Counting of immunopositive cells followed similar expression profile. Our data directly confirm the presence of glutamatergic NMDA and mGlu1 receptors in the ITR apparently involved in signaling pathways by which this region modulates cardiorespiratory functions such as blood pressure, heart rate and breathing.

Nucleus Gracilis: An Integrator for Visceral and Somatic Information

1997 ◽  
Vol 78 (1) ◽  
pp. 521-527 ◽  
Author(s):  
Elie D. Al-Chaer ◽  
Karin N. Westlund ◽  
William D. Willis
Keyword(s):  
Kainic Acid ◽  
Visceral Pain ◽  
Neuronal Cell ◽  
Dorsal Column ◽  
Sprague Dawley ◽  
Nucleus Gracilis ◽  
Abdominal Organs ◽  
Neuronal Cell Bodies ◽  
Sprague Dawley Rats ◽  
Before And After

Al-Chaer, Elie D., Karin N. Westlund, and William D. Willis. Nucleus gracilis: an integrator for visceral and somatic information. J. Neurophysiol. 78: 521–527, 1997. The nucleus gracilis (NG) receives an abundance of visceral input from various abdominal organs and is proposed to play an important role in visceral pain processing. The purpose of this study was to investigate the necessity of the NG for colorectal input into the ventral posterolateral (VPL) nucleus of the thalamus. Single-cell recordings were made from nine VPL cells isolated in nine different male Sprague Dawley rats anesthetized with pentobarbital sodium. Responses of the VPL cells to colorectal distension (CRD) and to cutaneous stimuli were obtained before and after lesioning of the NG. Electrolytic ( n = 5) and chemical ( n = 4) lesions of the NG were made in different preparations. The chemical lesions were made by injecting a solution of kainic acid into the NG. Kainic acid presumably kills neuronal cell bodies and spares axons of passage. The results indicate that a lesion of the NG, regardless of its type, reduces dramatically the responses of VPL neurons to innocuous cutaneous stimuli, and, to a lesser extent, the responses to CRD. Attenuation of VPL neuronal responses to CRD as well as to innocuous cutaneous stimuli by the NG lesions emphasizes the role of the dorsal column in visceral nociception and suggests that the NG is an integration center for visceral and cutaneous information flowing into the VPL nucleus.

Quantitative and qualitative immunohistochemical detection of myc and src oncogene proteins in normal, nodule, and neoplastic rat liver.

1988 ◽  
Vol 36 (2) ◽  
pp. 179-184 ◽  
Author(s):  
R E Richmond ◽  
M A Pereira ◽  
J H Carter ◽  
H W Carter ◽  
R E Long
Keyword(s):  
Quantitative Method ◽  
Staining Pattern ◽  
Normal Liver ◽  
Image Analysis System ◽  
Immunohistochemical Detection ◽  
Sprague Dawley ◽  
Treatment Groups ◽  
Sprague Dawley Rats ◽  
Qualitative Technique ◽  
Analysis System

This study examined the possibility of using an immunohistochemical technique to detect the expression of myc and src oncogene proteins (ops) in livers of male Sprague-Dawley rats after treatment with the carcinogen diethylnitrosamine (with or without phenobarbital promotion) or untreated. We found that the majority of nodules and tumors from these livers stained for myc and src ops, indicating that myc and src expression did occur in these structures. These results were expected, since myc and src expression has been previously observed by others using different techniques. However, in our study, myc and src op staining was also noted in normal liver areas from rats in any of the four treatment groups (DENA, DENA + PB, PB alone, or untreated). The staining pattern of normal liver was different for each oncogene probe but was consistent within the four groups. In most cases, oncogene expression of normal liver occurred at sites of abnormal (but non-neoplastic) hepatocytes. The method reported here used both a qualitative technique of op expression analysis and a quantitative method using a Zeiss computer-driven image analysis system.

scholarly journals Immunolocalization of inhibin in the mammary gland of rats treated with hCG.

1993 ◽  
Vol 41 (1) ◽  
pp. 29-34 ◽  
Author(s):  
M V Alvarado ◽  
J Russo ◽  
I H Russo
Keyword(s):  
Mammary Gland ◽  
Polyclonal Antibodies ◽  
Critical Role ◽  
Virgin Female ◽  
Sprague Dawley ◽  
Alveolar Cells ◽  
Glycoprotein Hormone ◽  
Ductal Cells ◽  
Sprague Dawley Rats ◽  
Pre Treatment

Human chorionic gonadotropin (hCG) induces profuse lobular development in the mammary gland of young virgin rats. To clarify whether the effect of hCG is locally mediated by inhibin, a non-steroidal glycoprotein, we detected its localization immunocytochemically in the mammary gland with polyclonal antibodies against the alpha- and beta-chains. Virgin female Sprague-Dawley rats were sacrificed after treatment with a daily IP injection of 100 IU hCG for 5, 10, 15, or 21 days of treatment or 20 days after the last injection. Whereas the mammary gland of control animals did not contain immunoreactive inhibin, hCG treatment induced the expression of inhibin in the cytoplasm of alveolar cells but not in ductal cells. The reaction became evident by Day 10 of treatment and reached its maximal intensity by Day 15. Thereafter, the reaction became evident in the stroma, which exhibited maximal positivity by Day 20. Once hCG treatment was terminated, the mammary gland regressed to its pre-treatment condition, appearing similar both in morphology and inhibin content to that of control animals. The expression of this glycoprotein hormone in the mammary gland after hCG administration at the time of maximal lobulolveolar development, and its diffusion towards the stroma during regression, suggest a critical role of inhibin as a modulator of mammary growth and differentiation.

scholarly journals Propolis increases neuronal count in hippocampal area CA1 and prefrontal cortex in stressed rats

2017 ◽  
Vol 36 (3) ◽  
pp. 214
Author(s):  
Kuswati Nugroho ◽  
Ety Sari Handayani ◽  
Zainuri Sabta Nugraha
Keyword(s):  
Prefrontal Cortex ◽  
Cell Count ◽  
Neuroprotective Effect ◽  
Neuronal Cell ◽  
Sprague Dawley ◽  
Stress Group ◽  
Induced Stress ◽  
Area Ca1 ◽  
Sprague Dawley Rats ◽  
Hippocampal Area

Background <br />Stress induces neuronal cell damage in the hippocampus and prefrontal cortex. Propolis has a neuroprotective effect that can inhibit apoptosis and decrease neuronal cell count. This study aimed to determine the effect of propolis on neuronal cell count in hippocampal area CA1 and prefrontal cortex in Sprague Dawley rats with induced stress.<br /><br />Methods<br />A study of laboratory experimental design was conducted involving 24 male Sprague-Dawley Rattus norvegicus. The animals were randomly divided into 4 groups, i.e. controls (K), and stress groups P1, P2 and P3. Controls did not receive treatment, stress group (P1) received stress treatment, groups P2 and P3 received stress and propolis at 100 and 200 mg/kgBW, respectively. Stress and propolis were given for 14 days, followed by termination. The number of neurons in the hippocampal area CA1 and prefrontal cortex were counted. One way ANOVA was used to analyze the data.<br /><br />Results <br />The neuronal count in the hippocampal area CA1 and prefrontal cortex in the stress group (P1) was lower than in groups K, P2 and P3. There were significant differences in the neuronal count of the hippocampal area CA1 between P1 and P3 and P1 and K (p=0.019) and also in the neuronal count of the prefrontal cortex between P1 and P2, P3 and K (p=0.002).<br /><br />Conclusions <br />This study strongly suggest that propolis inhibits the decrease in neuronal count in in the hippocampal area CA1 and prefrontal cortex of Sprague Dawley rats with induced stress. The present study suggests a potential neuroprotective effect of propolis in the prevention of neurodegenerative disorders.

scholarly journals Angiotensin II-mediated posttranslational modification of nNOS in the PVN of rats with CHF: role for PIN

2013 ◽  
Vol 305 (6) ◽  
pp. H843-H855 ◽  
Author(s):  
Neeru M. Sharma ◽  
Tamra L. Llewellyn ◽  
Hong Zheng ◽  
Kaushik P. Patel
Keyword(s):  
Nitric Oxide ◽  
Angiotensin Ii ◽  
Molecular Mechanism ◽  
Neuronal Cell ◽  
Coronary Artery Ligation ◽  
Ang Ii ◽  
Sprague Dawley ◽  
Artery Ligation ◽  
Sprague Dawley Rats ◽  
Catalytically Active

An increased sympathetic drive is an adverse characteristic in chronic heart failure (CHF). The protein expression of neuronal nitric oxide synthase (nNOS)- and hence nitric oxide (NO)-mediated sympathoinhibition is reduced in the paraventricular nucleus (PVN) of rats with CHF. However, the molecular mechanism(s) of nNOS downregulation remain(s) unclear. The aim of the study was to reveal the underlying molecular mechanism for the downregulation of nNOS in the PVN of CHF rats. Sprague-Dawley rats with CHF (6–8 wk after coronary artery ligation) demonstrated decreased nNOS dimer/monomer ratio (42%), with a concomitant increase in the expression of PIN (a protein inhibitor of nNOS known to dissociate nNOS dimers into monomers) by 47% in the PVN. Similarly, PIN expression is increased in a neuronal cell line (NG108) treated with angiotensin II (ANG II). Furthermore, there is an increased accumulation of high-molecular-weight nNOS-ubiquitin (nNOS-Ub) conjugates in the PVN of CHF rats (29%). ANG II treatment in NG108 cells in the presence of a proteasome inhibitor, lactacystin, also leads to a 69% increase in accumulation of nNOS-Ub conjugates immunoprecipitated by an antiubiquitin antibody. There is an ANG II-driven, PIN-mediated decrease in the dimeric catalytically active nNOS in the PVN, due to ubiquitin-dependent proteolytic degradation in CHF. Our results show a novel intermediary mechanism that leads to decreased levels of active nNOS in the PVN, involved in subsequent reduction in sympathoinhibition during CHF, offering a new target for the treatment of CHF and other cardiovascular diseases.

scholarly journals Mechanism of acute endosulfan intoxication-induced neurotoxicity in Sprague-Dawley rats / Mehanizam akutne neurotoksičnosti u Sprague-Dawley štakora izazvane trovanjem endosulfanom

2016 ◽  
Vol 67 (1) ◽  
pp. 9-17 ◽  
Author(s):  
Tae-chang Jang ◽  
Jung-hee Jang ◽  
Kyung-won Lee
Keyword(s):  
Cell Death ◽  
Molecular Mechanism ◽  
Inflammatory Responses ◽  
Neuronal Cell Death ◽  
Neuronal Cell ◽  
Heme Oxygenase 1 ◽  
Sprague Dawley ◽  
Oxidative Damages ◽  
Sprague Dawley Rats ◽  
Factor Α

Abstract The purpose of this study was to investigate the molecular mechanism underlying oxidative and inflammatory neuronal cell death induced by endosulfan, a pesticide belonging to the chemical family of organochlorines. The cortical and hippocampal tissues derived from Sprague-Dawley (SD) rats treated with endosulfan exhibited increased intracellular accumulation of reactive oxygen species and oxidative damages to cellular macromolecules such as depletion of glutathione, lipid peroxidation, and protein carbonylation. Conversely, the expression of antioxidant enzymes including γ-glutamylcysteine ligase (GCL), superoxide dismutase (SOD), and heme oxygenase-1 (HO-1) was markedly reduced in the brain tissues exposed to endosulfan. Moreover, during endosulfan-induced neuronal cell death, mRNA expression of pro-inflammatory cytokines such as tumour necrosis factor-α (TNF-α) and interleukin-1β (IL-1β) was elevated, which seemed to be mediated by the activation of nuclear factor-kappa B (NF-κB) by phosphorylation of p65 subunit. These results suggest a new molecular mechanism underlying the endosulfan-induced acute neurotoxicity via induction of oxidative stress and pro-inflammatory responses.

scholarly journals Absence of pituitary prolactin epitopes in immunoreactive prolactin of rat brain.

1991 ◽  
Vol 39 (2) ◽  
pp. 221-224 ◽  
Author(s):  
R E Harlan ◽  
J G Scammell
Keyword(s):  
Rat Brain ◽  
Polyclonal Antibodies ◽  
Neuronal Cell ◽  
Polyclonal Antiserum ◽  
Neuronal Cell Bodies ◽  
Rat Pituitary ◽  
Neuronal Processes ◽  
Pituitary Glands ◽  
Pituitary Prolactin ◽  
The Brain

Immunoreactive prolactin (ir-PRL) in rat brain has been consistently documented. However, the identity of this ir-PRL is controversial. Ir-PRL is defined by its ability to bind to PRL antibodies. All previous studies of brain ir-PRL have used polyclonal antibodies, at least one of which apparently crossreacts with a portion of the proopiomelanocortin molecule. To begin to define the epitopes comprising ir-PRL in the brain, we utilized two monoclonal antibodies (MAb) that recognize pituitary PRL in a variety of species, including rat. Immunocytochemistry was performed on rat brains and pituitary glands using two monoclonal and one polyclonal PRL antibody. Although both MAb immunostained lactotrophs of the rat pituitary gland, neither antibody immunostained cell bodies or neuronal processes in the brain. However, the polyclonal antiserum immunostained lactotrophs and a system of neuronal cell bodies and processes in the brain. Thus, epitopes found in pituitary PRL from several species are not found in ir-PRL in rat brain.

Ultrastructural Investigation of Spontaneous Pituitary Adenomas in Aging Sprague-Dawley Rats

1982 ◽  
Vol 40 ◽  
pp. 216-217
Author(s):  
D. J. McComb ◽  
J. Beri ◽  
F. Zak ◽  
K. Kovacs
Keyword(s):  
Microscopic Study ◽  
Pituitary Adenomas ◽  
Wistar Rats ◽  
Microscopic Level ◽  
Sprague Dawley ◽  
Prolactin Cells ◽  
Light Microscopic Level ◽  
Ultrastructural Investigation ◽  
Sprague Dawley Rats ◽  
Long Evans

Investigation of the spontaneous pituitary adenomas in rat have been limited mainly to light microscopic study. Furth et al. (1973) described them as chromophobic, secreting prolactin. Kovacs et al. (1977) in an ul trastructural investigation of adenomas of old female Long-Evans rats, found that they were composed of prolactin cells. Berkvens et al. (1980) using immunocytochemistry at the light microscopic level, demonstrated that some spontaneous tumors of old Wistar rats could contain GH, TSH or ACTH as well as PRL.

Early Development of Drug-Induced Hepatic Necrosis

1971 ◽  
Vol 29 ◽  
pp. 576-577
Author(s):  
F. G. Zaki ◽  
E. Detzi ◽  
C. H. Keysser
Keyword(s):  
Early Development ◽  
Hepatic Necrosis ◽  
Screening Tests ◽  
Dense Matrix ◽  
Sprague Dawley ◽  
Electron Microscopic ◽  
Drug Induced ◽  
Hepatocellular Damage ◽  
Sprague Dawley Rats ◽  
Microscopic Studies

This study represents the first in a series of investigations carried out to elucidate the mechanism(s) of early hepatocellular damage induced by drugs and other related compounds. During screening tests of CNS-active compounds in rats, it has been found that daily oral administration of one of these compounds at a dose level of 40 mg. per kg. of body weight induced diffuse massive hepatic necrosis within 7 weeks in Charles River Sprague Dawley rats of both sexes. Partial hepatectomy enhanced the development of this peculiar type of necrosis (3 weeks instead of 7) while treatment with phenobarbital prior to the administration of the drug delayed the appearance of necrosis but did not reduce its severity.Electron microscopic studies revealed that early development of this liver injury (2 days after the administration of the drug) appeared in the form of small dark osmiophilic vesicles located around the bile canaliculi of all hepatocytes (Fig. 1). These structures differed from the regular microbodies or the pericanalicular multivesicular bodies. They first appeared regularly rounded with electron dense matrix bound with a single membrane. After one week on the drug, these vesicles appeared vacuolated and resembled autophagosomes which soon developed whorls of concentric lamellae or cisterns characteristic of lysosomes (Fig. 2). These lysosomes were found, later on, scattered all over the hepatocytes.

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