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.