The Activation of β2-Adrenergic Receptors in Naïve Rats Causes a Reduction of Blood Glutamate Levels: Relevance to Stress and Neuroprotection

Abstract

This study examines the effects of the activation of β1 and β2-adrenergic receptors on glutamate homeostasis in the blood of naïve rats. Forty five male Sprague-Dawley rats were randomly assigned into one of seven treatment groups that were treated with various β-adrenergic receptor agonist and antagonist drugs. Blood glutamate levels were determined at t=0, 30, 60, 90, and 120min. The activation of β1 and β2-adrenergic receptors via isoproterenol hydrochloride administration produced a marked sustained decrease in blood glutamate levels by 60min after treatment (ANOVA, t=60, 90min: P<0.05, t=120min: P<0.01). Pretreatment with propranolol hydrochloride (a non-selective β-adrenergic receptor blocker) or butaxamine hydrochloride (a selective β2-adrenergic receptor blocker) occluded the isoproterenol-mediated decrease in blood glutamate levels. Propranolol alone had no effect on blood glutamate levels. Selective β1-adrenergic receptor blockade with metoprolol resulted in decreased blood glutamate levels (ANOVA, t=90min: P<0.05, t=120min: P<0.01). Butaxamine hydrochloride alone resulted in a delayed-onset increase in glutamate levels (ANOVA, t=120min: P<0.05). The results suggest that the activation of β2 receptors plays an important role in the homeostasis of glutamate in rat blood.