The Characterization of β Adrenoceptor Subtypes in the Rat Amygdala and Hippocampus

Abstract

(-)-[125I]Iodocyanopindolol [-]ICYP), is a ligand with high specific activity and nearly equal affinity for beta 1 and beta 2 adrenoceptors in a variety of tissues. Unfortunately, (-)ICYP also has affinity for 5HT1B serotonin receptors. To get an accurate estimate of beta adrenoceptors in the rat amygdala and hippocampus, (-)ICYP binding studies were done with membranes from these limbic structures in the presence of 10 microM serotonin to prevent the binding of (-)ICYP to serotonin receptors. Under these conditions. (-)ICYP binding to amygdaloid and hippocampus membrane preparations is saturable and reversible. Scatchard analyses revealed in both regions a single class of binding sites with an equilibrium dissociation constant (KD) of 18.5 pM for the amygdala and 19.6 pM for the hippocampus. The hippocampus has a significantly lower density of binding sites (Bmax) than amygdala (51.6 vs 62.3 fmol/mg membrane protein, p less than .05). The two brain regions do not differ with respect to kinetic reactions in that both show comparable slow association and dissociation rates. However, the dissociation reactions do reveal two affinity states for the binding sites in both areas. Detailed competition analyses with beta adrenoceptor subtype selective drugs (ICI-89406 and ICI-118551) show that in both regions about 70% of the beta adrenoceptor population is of the beta 1 subtype with the remainder being beta 2 subtype.

Adrenoceptor subtype‐specific acceleration of the hypoxic depression of excitatory synaptic transmission in area CA1 of the rat hippocampus

“…However, we saw no effect of β 2 ‐AR stimulation on the depressant effects of hypoxia. This is consistent with their reduced abundance in the rat hippocampus where they make up 30% of β‐ARs, as opposed to β 1 ‐ARs which comprise the remaining 70% (Tiong & Richardson, 1990). Instead, β 1 ‐AR activation accelerates the hypoxic inhibition of excitatory synaptic transmission but only under conditions when the release of adenosine is compromised.…”

Involvement of Noradrenergic Neurotransmission in the Stress- but not Cocaine-Induced Reinstatement of Extinguished Cocaine-Induced Conditioned Place Preference in Mice: Role for β-2 Adrenergic Receptors

“…The role of beta-2 AR in stress- and anxiety-related processes is unclear. However, beta-2 AR are found throughout the rat brain, including in the BNST (Rainbow, et al 1985) and the amygdala (Tiong and Richardson, 1990), sites where non-selective antagonism of beta AR has been shown to attenuate stressor-induced cocaine seeking (Leri, et al 2002) and where beta-2 AR have been implicated in affective, but not sensory or somatic, elements of pain (Deyama, et al 2008) or opiate withdrawal (Watanabe, et al 2003). Confirmation that central but not peripheral beta-2 AR activation is required for stress-induced reinstatement will require further investigation.…”

Beta receptor-mediated modulation of the late positive potential in humans

“…In the mammalian brain, most β-receptors are of the β1 subtype (Zill et al 2003). Evidence from animal studies indicates that this is also the most abundant subtype in the amygdala (Tiong and Richardson 1990). The polymorphism we focused on is the β1-receptor polymorphism G1165C (Borjesson et al 2000; Maqbool et al 1999).…”