These tools will no longer be maintained as of December 31, 2024. Archived website can be found here. PubMed4Hh GitHub repository can be found here. Contact NLM Customer Service if you have questions.


Pubmed for Handhelds

PUBMED FOR HANDHELDS

Search MEDLINE/PubMed

  • Title: Motor neurons in Onuf's nucleus and its rat homologues express the p75 nerve growth factor receptor: sexual dimorphism and regulation by axotomy.
    Author: Koliatsos VE, Price DL, Clatterbuck RE.
    Journal: J Comp Neurol; 1994 Jul 22; 345(4):510-27. PubMed ID: 7962698.
    Abstract:
    The present study establishes that populations of neurons in the lumbosacral cord, which innervate pelvic striated muscles, express p75NGFR throughout their life spans. These neuronal groups comprise the Onuf's nucleus in humans and its principal rat homologues, dorsolateral (DL) and dorsomedial (DM) nuclei, as well as the cremasteric (CRE) nucleus. The p75NGFR in these neurons is localized in the rough endoplasmic reticulum, Golgi complex, and lysosomes. Almost all neurons that project to striated perineal muscles in the male rat express p75NGFR; very low levels of p75NGFR are detected in neurons that innervate perineal sphincters of the female. In the female rat, p75NGFR expression is masculinized with perinatal androgen treatment. In addition, the expression of p75NGFR in DM and DL neurons in the adult is up-regulated by injury (i.e., pudendal axotomy) but is not influenced by gonadectomy. The results of this study establish that neurons of Onuf's nucleus and its rat homologues differ from general somatic motor neurons in that they express p75NGFR from early postnatal life (i.e., when all motor neurons express p75NGFR) into the adult (when the former, but not the latter, express the receptor). In view of growing evidence for the role of neurotrophins in the physiology of motor neurons, the above differentiating feature between general somatic and sexually dimorphic motor neurons suggests that p75NGFR may be involved in motor neuron plasticity and may participate in mechanisms by which neurons can protect themselves from degenerative insults.
    [Abstract] [Full Text] [Related] [New Search]