The Jasmin laboratory, at the Cedars-Sainai Medical Center conducts basic science research in two areas:

• Pains due to dysfunction of the CNS
• Remyelination of the CNS

Anatomy & Pharmacology of Pain Behavior (nociception)

• Cortical control of pain and analgesia:
  This project investigates the role of a specific area of the cortex, the rostal agranular insular cortex (RAIC) in nociception. The RAIC is a prefrontal cortex area where opioidergic and dopaminergic neurotransmission have a profound effect on pain behaviors and activation of spinal nociceptive neurons. The corresponding area in humans has been also associated with pain perception in imaging studies. We are currently studying the role GABAergic transmission in the RAIC.
  This project is funded by the NIH.
  

  Ohara, Peter T., Alberto Granato, Theodore M. Moallem, Bai-Ren Wang, Yves Tillet, Luc Jasmin. Dopamine input to GABAergic neurons in the rostral agranular insular cortex. Journal of Neurocytology (in press).

  Jasmin, L. S.D Rabkin, A. Granato, A. Boudah, P.T. Ohara  Analgesia and hyperalgesia from GABA-mediated modulation of the cerebral cortex, Nature 424 , 316-320 (2003)

  
  
• Noradradrenergic mechanisms of nociception:
  This project involves modeling fibromyalgia , a painful disorder present in 2% of the population. To do so, we are reproducing in the rodent the biochemical anomalies encountered in the CNS of fibromyalgia patients, mainly the decreased central noradrenaline and increased central nerve growth factor (NGF).
  This project is funded by the NIH.
  

  Jasmin, L, A. Boudah, P.T. Ohara (2003) "Long-term effects of decreased noradrenergic CNS innervation on pain behavior and opioid antinociception". Journal of Comparative Neurology, May 19;460(1):38-55.

  Jasmin L., D. Tien, D. Weinshenker, R.D. Palmiter, P.G. Green, G. Janni & P.T. Ohara (2002) “The NK1 receptor mediates both the hyperalgesia and the resistance to morphine in mice lacking noradrenaline” Proc Natl Acad Sci U S A, 99(2):1029-1034.

CNS-modulated peripheral inflammation

• We have developed a rat model of neurogenic inflammation of the bladder (cystitis) produced by a central nervous system disease. The main features of this neurogenic cystitis mirror those of human interstitial cystitis, a painful chronic bladder disease. We have additionally observed a clear sex difference in the degree of cystitis, and are currently studying the influence of sex hormones on the inflammation.
  

  Jasmin, L., Janni, G., and Rabkin, S.D. (2000) CNS induced neurogenic cystitis is associated with bladder mast cell degradation in the rat. J Urol. 164, 852-855.

  Jasmin, L., Janni,G. H. J. Manz, and S. D. Rabkin (1998) Activation of CNS circuits producing a neurogenic cystitis: evidence for centrally induced peripheral inflammation. J Neurosci 18 (23), 10016-29.

  
  

Schwann cell remyelination of the CNS

• We are studying the mechanisms of Schwann cell remyelination of the spinal cord using a new model of spinal demyelination in the rodent. In this model, rats undergo a massive demyelination of the spinal cord followed by a diffuse primary remyelination by Schwann cells and complete neurological recovery and finally a secondary remyelination by oligodendrocytes. We are examining the origin of Schwann cells entering the spinal cord, and the mechanisms by which a Schwann cell, after having myelinated a central axon, is normally induced to demyelinate and leave (desheath) the axon.
  This project is funded by the National Multiple Sclerosis Society.
  

  Jasmin, L. and Ohara, P.T. (2002) "Remyelination within the CNS: do schwann cells pave the way for oligodendrocytes? "Neuroscientist, Jun;8(3):198-203.

  Jasmin, L., Janni, G., Lappi, D.A., and Ohara, P.T. (2000) Schwann cells are removed from the spinal cord after effecting recovery from paraplegia. J Neurosci 20, 9215-9223.