The Activation of b2-Adrenergic Receptors in Naive Rats Causes a Reduction of Blood Glutamate Levels: Relevance to Stress and Neuroprotection Alexander ZlotnikYael KlinBenjamin F. GruenbaumShaun E. Gruenbaum • Sharon OhayonMathew BoykoEyal SheinerBarak Aricha-Tamir • Academic Article uri icon

abstract

  • This study examines the effects of the activa- tion of b1 and b2-adrenergic receptors on glutamate homeostasis in the blood of naive rats. Forty five male Sprague-Dawley rats were randomly assigned into one of seven treatment groups that were treated with various b-adrenergic receptor agonist and antagonist drugs. Blood glutamate levels were determined at t = 0, 30, 60, 90, and 120 min. The activation of b1 and b2-adrenergic receptors via isoproterenol hydrochloride administration produced a marked sustained decrease in blood glutamate levels by 60 min after treatment (ANOVA, t = 60, 90 min: P \ 0.05, t = 120 min: P \ 0.01). Pretreatment with propran- olol hydrochloride (a non-selective b-adrenergic recep- tor blocker) or butaxamine hydrochloride (a selective b2-adrenergic receptor blocker) occluded the isoprotere- nol-mediated decrease in blood glutamate levels. Pro- pranolol alone had no effect on blood glutamate levels. Selective b1-adrenergic receptor blockade with metoprolol resulted in decreased blood glutamate levels (ANOVA, t = 90 min: P \ 0.05, t = 120 min: P \ 0.01). Butax- amine hydrochloride alone resulted in a delayed-onset increase in glutamate levels (ANOVA, t = 120 min: P \ 0.05). The results suggest that the activation of b2 receptors plays an important role in the homeostasis of glutamate in rat blood.

publication date

  • January 1, 2011