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.

Pelvic visceral input into the nucleus gracilis is largely mediated by the postsynaptic dorsal column pathway

1996 ◽  
Vol 76 (4) ◽  
pp. 2675-2690 ◽  
Author(s):  
E. D. Al-Chaer ◽  
N. B. Lawand ◽  
K. N. Westlund ◽  
W. D. Willis
Keyword(s):  
Intravenous Injection ◽  
Visceral Pain ◽  
Background Activity ◽  
Dorsal Column ◽  
Mustard Oil ◽  
Medial Lemniscus ◽  
Afferent Pathways ◽  
Nucleus Gracilis ◽  
Before And After ◽  
Postsynaptic Dorsal Column

1. The purpose of this study was to investigate a proposed role for the postsynaptic dorsal column (PSDC) pathway in mediating visceral nociceptive input into the dorsal column (DC) nuclei. 2. In one group of animals, the hypogastric nerves were sectioned, thereby restricting colorectal input into the cord to pelvic afferent pathways known to coverage on lower lumbar and sacral segments. Extracellular recording were made from 41 nucleus gracilis (NG) cells that responded to colorectal distension (CRD). Results reported are from 15 NG cells that were tested before and after the administration of morphine into the sacral cord by microdialysis. 3. The responses of 11 NG cells to CRD were dramatically reduced by morphine infused into the sacral cord through a microdialysis fiber. This reduction was reversed by an intravenous injection of naloxone. Microdialysis administration of 6-cyano-7-nitro-quinoxaline-2,3-dione (CNQX) or a lesion of the DC also abolished the responses of the NG cells to CRD. 4. Four NG cells that responded to CRD showed an increase in their background activity approximately 25 min after an injection of mustard oil (MO). This increase in activity was counteracted by morphine or by a lesion of the DC. 5. In a second group of animals, recordings were made from 28 PSDC cells in the L0-S1 segments of the cord. These units were antidromically activated by stimulation of the upper cervical fasciculus gracilis. The projections of five PSDC neurons into the NG were traced with the use of antidromic mapping. Results are reported for the responses of 12 PSDC cells to CRD and to cutaneous stimuli before and after morphine administration into the sacral cord by microdialysis. 6. Morphine given spinally reduced the responses of 12 PSDC cells to CRD. This reduction was reversed by an intravenous injection of naloxone. CNQX administered spinally also abolished the responses to CRD of the PSDC cells tested. 7. Four other PSDC cells were studied before and after an injection of MO into the colon. Their background activity started to increase within 25 min after the injection. Morphine suppressed this increase in background activity and this effect of morphine was reversed by naloxone. 8. The responses of NG cells to cutaneous stimuli were not significantly affected by morphine in the dose used. On the other hand, morphine significantly reduced the responses of PSDC cells to noxious cutaneous stimuli although this effect was not as dramatic as that on responses to visceral stimuli. 9. From the results of the studies described in this and the companion paper, we conclude that there is an important pelvic visceral nociceptive pathway involving PSDC neurons that synapse in the NG. The NG in turn activates neurons in the ventral posterolateral (VPL) nucleus of the thalamus. We presume that activation of VPL neurons by noxious visceral stimulation contributes to visceral pain sensation and thus that pelvic visceral pain depends largely on activity in the DC-medial lemniscus system.

scholarly journals Microglia: a newly discovered role in visceral hypersensitivity?

2006 ◽  
Vol 2 (4) ◽  
pp. 271-277 ◽  
Author(s):  
Carl Y. Saab ◽  
Jing Wang ◽  
Chunping Gu ◽  
Kirsten N. Garner ◽  
Elie D. Al-Chaer
Keyword(s):  
Visceral Pain ◽  
Thermal Hyperalgesia ◽  
Radiant Heat ◽  
Pain Modulation ◽  
Visceral Hypersensitivity ◽  
Visceral Sensitivity ◽  
Sprague Dawley ◽  
Sprague Dawley Rats ◽  
Before And After

AbstractGiven the growing body of evidence for a role of glia in pain modulation, it is plausible that the exaggerated visceral pain in chronic conditions might be regulated by glial activation. In this study, we have investigated a possible role for microglia in rats with chronic visceral hypersensitivity and previously documented altered neuronal function. Experiments were performed on adult male Sprague-Dawley rats pre-treated with neonatal colon irritation (CI) and on control rats. Effects of fractalkine (FKN, a chemokine involved in neuron-to-microglia signaling) and of minocycline (an inhibitor of microglia) on visceral sensitivity were examined. Visceral sensitivity was assessed by recording the electromyographic (EMG) responses to graded colorectal distension (CRD) in mildly sedated rats. Responses to CRD were recorded before and after injection of FKN, minocycline or vehicle. Somatic thermal hyperalgesia was measured by latency of paw withdrawal to radiant heat. The pattern and intensity of microglial distribution at L6–S2 in the spinal cord was also compared in rats with CI and controls by fluorescence microscopy using OX-42. Results show that: (1) FKN significantly facilitated EMG responses to noxious CRD by >52% in control rats. FKN also induced thermal hyperalgesia in control rats, consistent with previous reports; (2) minocycline significantly inhibited EMG responses to noxious CRD by >70% in rats with CI compared to controls 60 min after injection. The anti-nociceptive effect of minocycline lasted for 180 min in rats with CI, reaching peak values 60 min after injection. Our results show that FKN enhances visceral and somatic nociception, whereas minocycline inhibits visceral hypersensitivity in chronically sensitized rats, which indicates a role for microglia in visceral hypersensitivity.

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.

scholarly journals Chronic intermittent hypoxia alters ventilatory and metabolic responses to acute hypoxia in rats

2016 ◽  
Vol 120 (10) ◽  
pp. 1186-1195 ◽  
Author(s):  
Barbara J. Morgan ◽  
Russell Adrian ◽  
Zun-yi Wang ◽  
Melissa L. Bates ◽  
John M. Dopp
Keyword(s):  
Intermittent Hypoxia ◽  
Acute Hypoxia ◽  
Sprague Dawley ◽  
Glomus Cell ◽  
Stimulus Response ◽  
Sprague Dawley Rats ◽  
Ventilatory Equivalent ◽  
Before And After ◽  
Conscious Animals ◽  
Carotid Body Glomus Cells

We determined the effects of chronic exposure to intermittent hypoxia (CIH) on chemoreflex control of ventilation in conscious animals. Adult male Sprague-Dawley rats were exposed to CIH [nadir oxygen saturation (SpO2), 75%; 15 events/h; 10 h/day] or normoxia (NORM) for 21 days. We assessed the following responses to acute, graded hypoxia before and after exposures: ventilation (V̇e, via barometric plethysmography), V̇o2 and V̇co2 (analysis of expired air), heart rate (HR), and SpO2 (pulse oximetry via neck collar). We quantified hypoxia-induced chemoreceptor sensitivity by calculating the stimulus-response relationship between SpO2 and the ventilatory equivalent for V̇co2 (linear regression). An additional aim was to determine whether CIH causes proliferation of carotid body glomus cells (using bromodeoxyuridine). CIH exposure increased the slope of the V̇e/V̇co2/SpO2 relationship and caused hyperventilation in normoxia. Bromodeoxyuridine staining was comparable in CIH and NORM. Thus our CIH paradigm augmented hypoxic chemosensitivity without causing glomus cell proliferation.

CHANGES IN SERUM LEVELS OF FOLLICLE STIMULATING HORMONE AND LUTEINIZING HORMONE SHORTLY BEFORE AND AFTER PARTURITION IN RATS

1974 ◽  
Vol 75 (3) ◽  
pp. 491-496 ◽  
Author(s):  
Junichi Mori ◽  
Hiroshi Nagasawa ◽  
Reiko Yanai ◽  
Junji Masaki
Keyword(s):  
Luteinizing Hormone ◽  
Follicle Stimulating Hormone ◽  
Serum Levels ◽  
Sprague Dawley ◽  
Appreciable Change ◽  
Serum Lh ◽  
Sprague Dawley Rats ◽  
Before And After ◽  
Average Serum ◽  
Stimulating Hormone

ABSTRACT The sequence of changes in the serum levels of follicle stimulating hormone (FSH) and luteinizing hormone (LH) from 2 days before to 24 h after parturition of primiparous Sprague-Dawley rats was investigated by radioimmunoassay. No appreciable change in average serum FSH levels was observed during 2 days before and 1 h after parturition. After this the levels increased gradually to show a peak at 7 h after parturition and then declined gradually until 24 h after parturition. However, the level at 24 h after parturition was still twice as high as that at parturition (0 h). The average serum LH levels which were low between 2 days before and 1 h after parturition, showed a peak at 7 h and decreased toward 13 h after parturition. The same levels as at parturition were maintained between 13 and 24 h after parturition. The time of surge of either FSH or LH was closely related to the time after parturition. There were some differences between FSH and LH in the patterns of sequence of changes in the serum levels near parturition.

scholarly journals Toxicity associated with ingestion of a polyacrylic acid hydrogel dog pad

2018 ◽  
Vol 30 (5) ◽  
pp. 708-714 ◽  
Author(s):  
David C. Dorman ◽  
Melanie L. Foster ◽  
Brooke Olesnevich ◽  
Brad Bolon ◽  
Aude Castel ◽  
...  
Keyword(s):  
Motor Activity ◽  
Polyacrylic Acid ◽  
Muscle Tone ◽  
Clinical Signs ◽  
High Dose ◽  
Sprague Dawley ◽  
Sprague Dawley Rats ◽  
Before And After ◽  
Acute Neurotoxicity ◽  
Disposable Diapers

Superabsorbent sodium polyacrylate polymeric hydrogels that retain large amounts of liquids are used in disposable diapers, sanitary napkins, and other applications. These polymers are generally considered “nontoxic” with acute oral median lethal doses (LD50) >5 g/kg. Despite this favorable toxicity profile, we identified a novel toxic syndrome in dogs and rats following the ingestion of a commercial dog pad composed primarily of a polyacrylic acid hydrogel. Inappropriate mentation, cerebellar ataxia, vomiting, and intention tremors were observed within 24 h after the ingestion of up to 15.7 g/kg of the hydrogel by an adult, castrated male Australian Shepherd mix. These observations prompted an experimental study in rats to further characterize the toxicity of the hydrogel. Adult, female Sprague Dawley rats ( n = 9) were assessed before and after hydrogel ingestion (2.6–19.2 g/kg over 4 h) using a functional observation battery and spontaneous motor activity. Clinical signs consistent with neurotoxicity emerged in rats as early as 2 h after the end of hydrogel exposure, including decreased activity in an open field, hunched posture, gait changes, reduced reaction to handling, decreased muscle tone, and abnormal surface righting. Hydrogel-exposed rats also had reduced motor activity when compared with pre-exposure baseline data. Rats that ingested the hydrogel did not develop nervous system lesions. These findings support the conclusion that some pet pad hydrogel products can induce acute neurotoxicity in animals under high-dose exposure conditions.

Carvacrol attenuates amikacin-induced nephrotoxicity in the rat

2021 ◽  
Author(s):  
Atta Mohammad Dost ◽  
Mehmet Gunata ◽  
Onural Ozhan ◽  
Azibe Yildiz ◽  
Nigar Vardi ◽  
...  
Keyword(s):  
Inflammatory Cell ◽  
Kidney Tissue ◽  
Control Group ◽  
Histopathological Changes ◽  
Sprague Dawley ◽  
Tissue Samples ◽  
Sprague Dawley Rats ◽  
Before And After ◽  
Per Oral

Abstract Amikacin (AK) is frequently used in the treatment of gram-negative and some gram-positive infections. However, its use is limited due to nephrotoxicity due to the increase in reactive oxygen radicals. The aim of this study was to investigate the role of carvacrol (CAR) against AK-induced nephrotoxicity in rats. Thirty-two Sprague Dawley rats were randomly divided into four groups as control (Vehicle), AK (400 mg/kg), CAR + AK (80 mg/kg CAR + 400 mg/kg AK), and AK + CAR (400 mg/kg AK + 80 mg/kg CAR) groups. AK and CAR were administered via intramuscular and per-oral for 7 days, respectively. Blood and kidney tissue samples were taken at the end of the experiment. Renal function and histopathological changes were compared, and the relevant parameters of oxidative stress and inflammation were detected. Histopathological findings (necrotic changes and dilatation and inflammatory cell infiltration) significantly increased in the AK group compared to the control group. Also, the rats in the AK group lost weight significantly. It was found that CAR treatment before and after AK significantly improved nephrotoxicity histopathologically (p < 0.05). However, this improvement was not detected biochemically. These results show that CAR treatment before and after AK improves nephrotoxicity in the histopathological level.

Loss of hypoxic pulmonary vasoconstriction in chronic pneumonia is not mediated by nitric oxide

1993 ◽  
Vol 265 (5) ◽  
pp. H1523-H1528 ◽  
Author(s):  
D. G. McCormack ◽  
N. A. Paterson
Keyword(s):  
Nitric Oxide ◽  
Pressor Response ◽  
Hypoxic Pulmonary Vasoconstriction ◽  
Sprague Dawley ◽  
Absolute Increase ◽  
Pulmonary Vasoconstriction ◽  
Sprague Dawley Rats ◽  
Before And After ◽  
Inflammatory Processes ◽  
The Difference

In pulmonary inflammatory processes such as pneumonia there is diminished hypoxic pulmonary vasoconstriction (HPV). We investigated whether the attenuated HPV in pneumonia is a due to excess nitric oxide (NO) release. Sprague-Dawley rats were anesthetized, and a slurry (0.06 ml) of infected agar beads (containing 6 x 10(5) Pseudomonas aeruginosa organisms) or control (sterile) beads was then injected into a distal bronchus through a tracheotomy. After the establishment of a chronic P. aeruginosa pneumonia (7-10 days later) animals were instrumented for hemodynamic monitoring, and the response to exposure to hypoxic gas (fraction of inspired O2 = 0.08) was recorded before and after the administration of NG-monomethyl-L-arginine (L-NMMA; 50 mg/kg), an inhibitor of NO synthesis. The hypoxic pressor response, as assessed by the absolute increase in pulmonary arterial pressure (PAP) and total pulmonary resistance (TPR), was reduced in infected animals compared with control animals. The change in PAP and TPR was 8.5 +/- 0.7 and 0.053 +/- 0.007, respectively, in control animals compared with 5.9 +/- 0.5 and 0.041 +/- 0.011 in infected animals. After L-NMMA the increase in PAP and TPR during hypoxia was greater in both control and infected animals. However, treatment with L-NMMA did not affect the difference between control and infected animals. We conclude that excess release of NO does not account for the attenuated hypoxic pressor response in pneumonia.

Differential sympathetic nerve responses to nitric oxide synthase inhibition in anesthetized rats

1995 ◽  
Vol 269 (4) ◽  
pp. R807-R813 ◽  
Author(s):  
T. Hirai ◽  
T. I. Musch ◽  
D. A. Morgan ◽  
K. C. Kregel ◽  
D. E. Claassen ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Sympathetic Nerve ◽  
Sprague Dawley ◽  
Arterial Blood ◽  
Sprague Dawley Rats ◽  
Before And After ◽  
Important Means ◽  
Nos Inhibitor ◽  
Oxide Synthase ◽  
Tonic Excitation

Recent studies have suggested that the interaction between the sympathetic nervous system and nitric oxide (NO) or nitrosyl factors may be an important means by which arterial blood pressure is regulated. We investigated whether NO synthase (NOS) inhibition modulates basal sympathetic nerve discharge (SND) in baroreceptor-innervated and -denervated, chloralose-anesthetized Sprague-Dawley rats. We recorded mean arterial pressure (MAP), renal SND, and lumbar SND before and after administration of the NOS inhibitor, NG-nitro-L-arginine methyl ester (L-NAME, 20 mg/kg iv). Two minutes after L-NAME administration in baroreceptor-innervated rats, MAP increased (+23 +/- 3 mmHg), whereas renal (-45 +/- 6%, n = 7) and lumbar (-35 +/- 2%, n = 6) SND significantly decreased from control levels. These changes persisted for up to 20 min after L-NAME administration. In baroreceptor-denervated rats, L-NAME increased MAP (+40 +/- 6 mmHg) and decreased lumbar SND (n = 7) (-37 +/- 10% from control at 20 min post-L-NAME). In contrast, renal SND progressively increased (+33 +/- 8% at 20 min post-L-NAME) from control after L-NAME administration in baroreceptor-denervated rats (n = 7). These results demonstrate that NOS inhibition can produce nonuniform changes in SND in baroreceptor-denervated rats and suggest that endogenous nitrosyl factors provide tonic excitation to lumbar SND, whereas they provide a tonic restraint to renal SND.

Ventilatory effects of kainic acid injection of the ventrolateral solitary nucleus

1982 ◽  
Vol 52 (1) ◽  
pp. 131-140 ◽  
Author(s):  
A. J. Berger ◽  
K. A. Cooney
Keyword(s):  
Kainic Acid ◽  
Minute Ventilation ◽  
Neuronal Cell ◽  
Neuronal Loss ◽  
Long Term Effects ◽  
Awake State ◽  
Ventilatory Responses ◽  
Neuronal Cell Bodies ◽  
Ventilatory Effects ◽  
Kainic Acid Injection

We studied in cats the long-term effects upon resting ventilation and the ventilatory responses to CO2 breathing of destruction of neuronal cell bodies within the ventrolateral nucleus of the tractus solitarius (vl-NTS) by kainic acid (KA) injection (KAI). Animals were studied in the awake state and under pentobarbital anesthesia both before and 8 wk after stereotaxic bilateral microinjection of the vl-NTS with mock cerebrospinal fluid (CSF) (controls, n = 2) or with KA in mock CSF (KAI, n = 5). KA reduced the number of cell bodies within the vl-NTS by 75%. Under anesthesia minute ventilation (VI) was reduced by 49% after KAI, due primarily to a 54% reduction in breathing frequency (f). Four of five anesthetized KAI animals exhibited a significantly reduced (P less than 0.01) ventilatory sensitivity to inspired CO2 under anesthesia. In the awake state some KAI animals had significant changes (P less than 0.01) in ventilation; VI reduced (2 of 5), tidal volume reduced (1 of 5), f reduced (3 of 5), and inspiratory and expiratory times increased (2 of 5). Decreases in the awake ventilatory CO2 sensitivity were not significant within individual KAI animals but were significant (P less than 0.05) when considered as a group. Thus following 75% neuronal loss within the vl-NTS, rhythmic ventilation was sustained during both anesthesia and wakefulness, although f was reduced in the former state. The vl-NTS may function to set most but not all of the ventilatory sensitivity to CO2 during anesthesia and to a lesser extent during wakefulness.

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