β1- and β2-adrenoceptor induced synaptic facilitation in rat basolateral amygdala

The expression and characteristics of β-adrenoceptor subtypes (β1 and β2) and their agonist actions on synaptic transmission in the basolateral amygdala (BLA) of the rat were examined using in situ hybridization, quantitative real-time PCR, Western blot analysis and field potential recording. In situ hybridization data revealed an intense distribution of β1-and β2-adrenoceptor mRNA in the BLA. Real-time PCR analysis of rat amygdala revealed significant transcriptional expression levels of both β-adrenoceptors, with β2-adrenoceptors outnumbering β1-adrenoceptors in a ratio of 2.9 to 1. Bath application of the selective β1-adrenoceptor agonist xamoterol hemifumarate (10 µM) facilitated the excitatory field synaptic potential evoked in the BLA by stimulation of the external capsule by 186.5 ± 10.7% of control amplitude. In the presence of the selective β1-adrenoceptor antagonist betaxolol hydrochloride (30 µM), the facilitating effects of field excitatory synaptic potential induced by the agonist were reduced to 126.1 ± 2.3 % of control amplitude in the BLA. Bath application of the selective β2-adrenoceptor agonist salmeterol (15 µM) facilitated the excitatory field synaptic potential evoked in the BLA by stimulation of the external capsule by 167.3 ± 9.7 % of control amplitude. In the presence of the selective β2-adrenoceptor antagonist ICI 118,551 HCl (30 µM), the facilitating effects of field excitatory synaptic potential induced by the agonist were reduced to 121.1 ± 4.1 % of control amplitude in the BLA. These data suggest that β-adrenoceptor mediated synaptic facilitation in the amygdala is mediated by both β1 and β2-adrenoceptor activation.