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3 results

  • Chapter 2 - Interoceptive Afferent Neurons and Autonomic Regulation with Special Emphasis on the Viscera

  • from Part I - The Autonomic Nervous System: Functional Anatomy and Interoceptive Afferents
  • Wilfrid Jänig, Christian-Albrechts Universität zu Kiel, Germany
  • Book:
    The Integrative Action of the Autonomic Nervous System
    Published online:
    16 July 2022
    Print publication:
    04 August 2022, pp 34-70

  • Summary

    Visceral organs are innervated by vagal and spinal visceral afferent neurons. Of the axons in the vagal nerves, 85% are afferent and have their cell bodies in the nodose or jugular ganglion. Vagal afferents are involved in autonomic reflexes and regulation, and in visceral sensations but not pain. They project viscerotopically to the nucleus tractus solitarii. Spinal visceral afferent neurons have their cell bodies in the dorsal root ganglia. They are involved in organ reflexes, organ regulation (pelvic organs), extraspinal "peripheral" reflexes, protective "axon reflex"-mediated effector reactions, non-painful visceral sensations and visceral pain. Thoracolumbar spinal visceral afferent neurons are polymodal and activated by mechanical and chemical stimuli. Sacral visceral afferent neurons are involved in specific organ regulation, and sacro-lumbar reflexes. Spinal visceral afferents project to lamina I, lamina V and deeper laminae of the spinal gray matter. All spinal neurons receiving synaptic input from spinal visceral afferents are convergent viscero-somatic neurons. In primates, lamina I neurons project topographically to the posterior part of the ventromedial nucleus of the thalamus. This nucleus projects topographically to the dorsal posterior insula, which is the primary interoceptive cortex and represents sensations related to the states of the body tissues.

  • EPA-1109 - Nmda Receptor Antagonists as Analgesics in a Rat Model of Visceral Pain

  • D. Srebro, S. Vuckovic, K. Savic Vujovic, B. Medic, R. Stojanovic, A. Vujovic, M. Prostran
  • Journal:
    European Psychiatry / Volume 29 / Issue S1 / 2014
    Published online by Cambridge University Press:
    15 April 2020, p. 1
    • Article
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  • Introduction:

    N-methyl-D-aspartate (NMDA) receptors are ligand-gated receptor complexes that have been associated with learning and memory, pain transmission, depression, schizophrenia and neurodegenerative disorders. In these processes deficiency of magnesium has a significant role. Magnesium and MK-801, noncompetitive NMDA receptor antagonists, have been demonstrated analgesic efficacy against neuropathic pain, but there are no data about the effects of these compounds on visceral pain.

    Objective:

    Comparison of the analgesic activity of NMDA antagonists against visceral inflammatory pain.

    Aim:

    This study aimed at evaluating the effect of magnesium sulphate (MS) and MK-801 in writhing test in rats.

    Methods:

    In writhing test, a model of visceral inflammatory pain, injection of diluted acetic acid into the peritoneal cavity of male Wistar rats induced pain. MS and MK-801 were given subcutaneously 15 min before the intraperitoneal injection of 0.7% acetic acid.

    Results:

    MS at doses of 5 and 15 mg/kg did not affect the number of writhing in rats, but doses of 30 and 45 mg/kg significantly potentiated writhing 2.9 and 2.4 times, respectively. MK-801 (0.005 and 0.01 mg/kg) produced dose-dependent antinociception manifested as reduction in the number of writhing and the maximum antinociceptive activity was 61.3%.

    Conclusions:

    MK-801 in the writhing test produced antinociception likely due to the inhibition of NMDA receptors. Effect of magnesium was different from MK-801. MS did not inhibit and even aggravated pain evoked by chemical stimuli in visceral pain test. The present results suggest that the MS may not be useful systemic analgesic in the therapy of visceral inflammatory pain.

  • Microglia: a newly discovered role in visceral hypersensitivity?

  • Carl Y. Saab, Jing Wang, Chunping Gu, Kirsten N. Garner, Elie D. Al-Chaer
  • Journal:
    Neuron Glia Biology / Volume 2 / Issue 4 / November 2006
    Published online by Cambridge University Press:
    13 April 2007, pp. 271-277
    Print publication:
    November 2006

  • Given 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.