Nucleus raphe magnus

(Redirected from Magnus raphe nucleus)

The nucleus raphe magnus (NRM) is one of the seven raphe nuclei. It is situated in the pons in the brainstem,[1]: 306  just rostral to the nucleus raphe obscurus.[citation needed]

Nucleus raphe magnus
Section of the medulla oblongata at about the middle of the olive. (Raphe nuclei not labeled, but 'raphe' labeled at left.)
Details
Identifiers
Latinnucleus raphes magnus
MeSHD065846
NeuroNames739
NeuroLex IDbirnlex_1363
TA98A14.1.04.321
TA26038
FMA72584
Anatomical terms of neuroanatomy

The NRM receives afferent stimuli from the enkephalinergic neurons of the periaqueductal gray; the serotonergic neurons of the NRM then bilaterally project efferents to the enkephalinergic and dynorphin-containing interneurons of the substantia gelatinosa of the posterior grey column of the spinal cord. This neural path thus mediates pain perception through pre-synaptic inhibition of first-order afferent (sensory) neurons.[1]: 225 

Anatomy

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Afferents

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It receives afferents from the spinal cord and cerebellum.[citation needed]

It receives descending afferents from the periaqueductal grey matter (PAG), the paraventricular hypothalamic nucleus, central nucleus of the amygdala, lateral hypothalamic area, parvocellular reticular nucleus and the prelimbic, infralimbic, medial and lateral precentral cortices.[2][non-primary source needed] It is one of the afferent targets of the ascending reticular activating system.[1]: 311 

Efferents

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It projects efferents to the posterior grey column (to modulate pain).[3]

Neurophysiology and function

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The nucleus raphe magnus seems to participate in the endogenous analgesia system. Mounting evidence suggests that the nucleus raphe magnus plays an important role in homeostatic regulation. Its afferents from the spinal cord and cerebellum suggest it may be a part of the motor system.[4][non-primary source needed][5][non-primary source needed]

Pain modulation

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The main function of the nucleus raphe magnus is pain mediation. The nucleus raphe magnus releases serotonin when stimulated. It sends projections to the enkephalin-releasing interneurons of the posterior grey column to directly inhibit pain.[3]

The periaqueductal gray (PAG), an area of the brain involved in mediating analgesia, sends efferent stimuli to the nucleus raphe magnus when stimulated by opioids (endogenous or otherwise); electrical stimulation of the PAG as well as administration of opioid agonists to the PAG or nucleus raphe magnus produces analgesia; the antinociceptic effects of electrical stimulation of the PAG can be blocked by administering naloxone (an opiate antagonist) to the nucleus raphe magnus. Similarly, afferent fibres from the spinothalamic tract synapse at the periaqueductal grey matter which in turn projects to the nucleus raphe magnus, which when stimulated directly inhibits pain fibers in the posterior grey column, alleviating pain. All of this seems to indicate that the nucleus raphe magnus is part of the endogenous opiate system, and acts to inhibit pain in the spinal cord.[citation needed]

References

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  1. ^ a b c Patestas, Maria A.; Gartner, Leslie P. (2016). A Textbook of Neuroanatomy (2nd ed.). Hoboken, New Jersey: Wiley-Blackwell. ISBN 978-1-118-67746-9.
  2. ^ Hermann, Dirk M. et al. Afferent projections to the rat nuclei raphe magnus, raphe pallidus and reticularis gigantocellularis pars demonstrated by iontophoretic application of choleratoxin (subunit b). Journal of Chemical Neuroanatomy Volume 13, Issue 1, June 1997, Pages 1-21
  3. ^ a b Haines, Duane E., and M. D. Ard. Fundamental Neuroscience for Basic and Clinical Applications. Philadelphia, PA: Elsevier/Saunders, 2013.
  4. ^ Hellman, Kevin et al. Activity of murine magnus raphe cells predicts tachypnea and on-going nociceptive responsiveness. Journal of Neurophysiology Volume 98, Issue 6, December 2007, Pages 3121-33.
  5. ^ Hellman, Kevin et al., Opioid microinjection into raphe magnus modulates cardiorespiratory function in mice and rats. American Journal of Physiology Regulator Integratory Comp Physiology. Volume 297, Issue 5, November 2009, Pages R1400-8.