The partial μ opiate agonist buprenorphine protects a sub-population of thalamic reticular neurons following cardiac arrest in rats

Abstract

Extensive loss of neurons occurs from the middle region of the thalamic reticular nucleus (RT) in rats resuscitated after 10 min of cardiac arrest. Administration of the partial μ opiate agonist buprenorphine 45 min after resuscitation produces a small but significant increase in spared neurons along the medial and lateral margins of the middle RT, regions where μ receptors have been localized. Systemic administration of μ agonists may augment endogenous opiate mechanisms that contribute to the relative ischemic resistance of subpopulations of RT neurons.