subjects. Adrenaline competition studies displayed that adrenaline was a less potent inhibitor of rauwolscine specific binding, the competition curve was steeper and shifted to the right. Computer analysis of this data also revealed two sites of interaction, more of the total number of 2 adrenergic receptors were in the low (2 (L)) and fewer in the higher (2 (H)) affinity state in the PTSD compared to controls. This accounted for a decrease in adrenaline potency. Fewer membrane binding sites and altered ratio of affinity states has been observed in other adrenergic/noradrenergic systems exposed to chronically high levels of endogenous agonist in the CNS. Similarly down regulation and uncoupling of platelet 2 receptors has been demonstrated in clinical states associated with increased circulating catecholamines: congestive heart failure, aging and hypertension. High levels of catecholamines and a secondary down regulation of platelet adrenergic receptors are consistent with an overactive sympathetic nervous system in PTSD. Chronic exposure to agonist decreased the total number of receptors and changed the steady – state between affinity sites (R and R-Ni). The number of receptors present in the membrane and accessible to agonist depends upon a variety of complex intracellular processes. Regulation of receptors in the membrane and receptor-mediated signal transduction is a complex process of receptor internalisation. Following agonist binding the receptor recognition protein is taken into the cell for recycling. A certain percentage of the receptor population is inside the cell. The rate of internalisation is dependant on a variety of factors including agonist concentration, duration of exposure, rate of degradation and rate of phosphorylation.Further dysregulation studies have been carried out to investigate these internalisation processes. It has been found that platelet 2 adrenergic rece...
