Accession Number:

ADA576663

Title:

Endocannabinoids as a Target for the Treatment of Traumatic Brain Injury

Descriptive Note:

Annual rept. 4 Oct 2011-3 Oct 2012

Corporate Author:

LOUISIANA STATE UNIV HEALTH SCIENCES CENTER NEW ORLEANS DEPT OF PHARMACOLOGY

Personal Author(s):

• Molina, Patricia E.

Report Date:

2012-11-01

Pagination or Media Count:

15.0

Abstract:

Results from studies conducted during this funding period provides further evidence that TBI results in neuroinflammination and altered neuroendocrine and neurobehavioral deficits that persist 72hrs following the injury. Our findings indicate that interventions aimed at modulation of the endocannabinoid EC system targeting degradation of 20arachidonoyl glycerlol 2- AG and N-arachidonoyl ethanolamine AEA effectively reduce neuroinflammination and blood barrier leak while preserving neurobehavioral function post-TBI. Studies examined the extent to which these interventions prevent the rise in proinflammatory cytokine expression, neutrophil influx, blood brain barrier permeability, neurological and neurobehavioral impairments following TBI produced by lateral fluid percussion. Inhibition of EC degradation results in significant protection 24hrs post-TBI produced by lateral fluid percussion. Inhibition of EC degradation results in significant protection 24hrs post- TBO in blood brain barrier integrity, as well as significant reduction in sensory and motor damage 24-72hrs post-injury.

Descriptors:

• *BLOOD BRAIN BARRIER
• *NEUROLOGY
• *TRAUMATIC BRAIN INJURIES
• BEHAVIOR
• BRAIN
• DAMAGE
• DEFICIENCIES
• DEGRADATION
• ENDOCRINE GLANDS
• INHIBITION
• PERMEABILITY
• REDUCTION
• TARGETS
• WOUNDS AND INJURIES

Subject Categories:

• Medicine and Medical Research

Distribution Statement:

APPROVED FOR PUBLIC RELEASE