Article Text

ENDOGENOUS CANNABINOID SYSTEM ACTIVATION IN NEONATAL FOCAL CEREBRAL ISCHEMIC INJURY IN RAT PUPS
  1. M R Rogido1,
  2. J A MartinezOrgado2,
  3. R Pazos2,
  4. T C Wen1,
  5. A Sola1,
  6. J Romero2
  1. 1Atlantic Neonatal Research Institute, Morristown Memorial Hospital, Morristown, NJ, USA
  2. 2Laboratorio de Apoyo A la Investigacion, Fundacion Hospital Alcorcon, Madrid, Spain

Abstract

The endogenous cannabinoid system is neuroprotective both in vitro and in vivo in the adult animal, and it could also protect the developing brain. However, its role has not been determined in perinatal ischemia.

Objective To study the expression of cannabinoid receptors CB1 and CB2 and the enzyme Fatty Acid Amide Hydrolase (FAAH) in a model of perinatal stroke.

Methods P7 Wistar rat pups were subjected to permanent focal cerebral ischemia (FCI) as previously described (Wen, 2003) and sacrificed at 1, 3 or 7 days alter FCI. The brains were fixed and cryoprotected. Nissl staining for neurons and immunohistochemistry for astrocytes (GFAP), CB1, CB2 and FAAH expression were performed using a polyclonal rabbit antibody and an anti-rabbit goat antibody and Alexa 488 or 546.

Results FCI caused a well defined ipsilateral injury with an almost absence of neurons and intense glial reaction. We observed an increase in neuronal population in the penumbra starting on day 3 post FCI. The expression of CB1 in neurons increased very early, 24 hours post FCI. Reactive astrocytes showed an increased expression of FAAH 7 days after FCI and CB2 in the penumbra.

Conclusions An ischemic episode to the developing brain causes early and sustained increase in the expression of CB1 and a later increase in the expression of CB2 and FAAH. These findings suggest a relevant role of the endogenous cannabinoid system in general and of the CB2 receptors in particular, in the natural response to an ischemic lesion.

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