Dorsal raphe nucleus

Dorsal raphe nucleus
Brain: Dorsal raphe nucleus
Drn.png
Outline of the nucleus raphe dorsalis: DRif interfascicular subnucleus, DRv ventral subnucleus, DRvl ventrolateral subnucleus, DRd dorsal subnucleus, mlf medial longitudinal fasciculus, Aq cerebral aqueduct, IVn trochlear nucleus.
Latin nucleus raphe posterior, nucleus raphe dorsalis
NeuroNames hier-503
NeuroLex ID birnlex_982

The dorsal raphe nucleus is located on the midline of the brainstem and is part of the raphe nucleus, consisting of the rostral and caudal subdivisions.

  • The rostral aspect of the dorsal raphe is further divided into interfascicular, ventral, ventrolateral and dorsal subnuclei.
  • The projections of the dorsal raphe have been found to vary topographically, and thus the subnuclei differ in their projections.[1]

An increased number of cells in the lateral aspects of the dorsal raphe is characteristic of humans and other primates.

Contents

Serotonin

The dorsal raphe is the largest serotonergic nucleus and provides a substantial proportion of the serotonin innervation to the forebrain.

Serotonergic neurons are found throughout the dorsal raphe nucleus and tend to be larger than other cells. A substantial population of cells synthesizing substance P are found in the rostral aspects, many of these co-express serotonin and substance P. There is also a population of catecholamine synthesizing neurons in the rostral dorsal raphe, and these cells appear to be relatively large.[2]

The dorsal raphe nucleus is rich in pre-synaptic serotonin 5-HT1A autoreceptors, and it's believed that the action of the selective serotonin reuptake inhibitors (SSRIs) in this region is responsible for the latency of their antidepressant effect.[3]

Projections

Ten percent of the axons from the nucleus raphe dorsalis of the rat have been shown to project to the amygdala,[4] while only medium cells seem to project to the caudate and putamen and olfactory bulb.,[5]

[6]

Role in naloxone-induced morphine withdrawal

The nucleus raphe dorsalis has also been implicated in naloxone-induced morphine withdrawal. It is known that endogenous opioid receptors exist on the nucleus raphe dorsalis, and that it is a focal point as an ascending and descending regulator. Pourshanazari et al. showed in their 2000 paper that electrical stimulation of the nucleus raphe dorsalis can partially alleviate morphine withdrawal symptoms via electrical stimulation of the raphe nucleus in question.[7]

These are fascinating results; however no control was provided for the spread of electrical charge to other parts of the brain stem. It is quite possible that the charge spread to the nucleus raphe magnus and induced analgesia upon the rats. Knowing that the spread of charge across such a short area is very plausible, as is an alternate connection to the raphe magnus, these results could be called into question.

Role in narcolepsy

Wu M.F. et al. studied the raphe dorsalis as it pertained to narcolepsy, this is logical, as the raphe nuclei have been known to play a role in the sleep/wake cycle. Cataplexy is the symptom of narcolepsy when full awareness of the environment is maintained, but all muscle tone is lost. This has thought to be a dissociation of what normally happens during REM sleep, when all muscle tone is lost except for the eyes. The raphe dorsalis have been known to project to the lateral hypothalamus, along with the locus coeruleus and the tuberomammillary nucleus. The neurotransmitters of these three aforementioned nuclei, which project to the lateral hypothalamus, are serotonin, norepinephrine and histamine respectively. These neurotransmitters are fully active during waking hours, partially active during non-REM sleep, and have almost ceased during REM sleep. In cats with pontine lesions, their normal atonia is not present, the raphe dorsalis is fully active, as opposed to the cessation of action under normal conditions. A muscle relaxant, known as Mephenesin, reduces to activity of the dorsal nucleus, as well as microinjections of carbachol (which induces atonia while awake).[8]

See also

References

  1. ^ O'Hearn E, Molliver ME (December 1984). "Organization of raphe-cortical projections in rat: a quantitative retrograde study". Brain Res. Bull. 13 (6): 709–26. doi:10.1016/0361-9230(84)90232-6. PMID 6099744. 
  2. ^ Baker KG, Halliday GM, Hornung JP, Geffen LB, Cotton RG, Törk I (1991). "Distribution, morphology and number of monoamine-synthesizing and substance P-containing neurons in the human dorsal raphe nucleus". Neuroscience 42 (3): 757–75. doi:10.1016/0306-4522(91)90043-N. PMID 1720227. http://linkinghub.elsevier.com/retrieve/pii/0306-4522(91)90043-N. 
  3. ^ Briley M, Moret C (October 1993). "Neurobiological mechanisms involved in antidepressant therapies". Clin Neuropharmacol 16 (5): 387–400. doi:10.1097/00002826-199310000-00002. PMID 8221701. 
  4. ^ Ma QP, Yin GF, Ai MK, Han JS (December 1991). "Serotonergic projections from the nucleus raphe dorsalis to the amygdala in the rat". Neurosci. Lett. 134 (1): 21–4. doi:10.1016/0304-3940(91)90499-J. PMID 1815148. http://linkinghub.elsevier.com/retrieve/pii/0304-3940(91)90499-J. 
  5. ^ Steinbusch HW, Nieuwenhuys R, Verhofstad AA, Van der Kooy D (1981). "The nucleus raphe dorsalis of the rat and its projection upon the caudatoputamen. A combined cytoarchitectonic, immunohistochemical and retrograde transport study". J. Physiol. (Paris) 77 (2-3): 157–74. PMID 6169825. 
  6. ^ Petzold GC, Hagiwara A, Murthy VN (June 2009). "Serotonergic modulation of odor input to the mammalian olfactory bulb". Nat. Neurosci. 12 (6): 784–91. doi:10.1038/nn.2335. PMID 19430472. 
  7. ^ Pourshanazari, A.A. ; Alaei ; Rafati (2000). "Effects of Electrical Stimulation of Nucleus Raphe Dorsalis on initiation of morphine self administration in rats". Medical Journal of Islamic Academy of Sciences 13 (2): 63–7. 
  8. ^ Wu MF, John J, Boehmer LN, Yau D, Nguyen GB, Siegel JM (January 2004). "Activity of dorsal raphe cells across the sleep-waking cycle and during cataplexy in narcoleptic dogs". J. Physiol. (Lond.) 554 (Pt 1): 202–15. doi:10.1113/jphysiol.2003.052134. PMC 1664742. PMID 14678502. http://www.jphysiol.org/cgi/content/full/554/1/202. 

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