ptors are desensitised to agonist in PTSD. It appears that chronic agonist administration uncouples the receptor and second messenger resulting in an accelerated mechanism for down regulation, that is a higher percentage of membrane receptors are taken out of the membrane and internalised following any agonist exposure. In PTSD there appears to be a more rapid and extensive apparent internalisation following agonist incubation which is also accompanied by a large increase in the ratio R is less likely to react with Ni. Chronic exposure to increased agonist level results in an receptor – effector system less capable of responding to agonist increases associated to subsequent stressors that is the platelet 2 adrenergic receptor-effector system was “overloaded” and easily ”fatigued”. It is clear that permanent intraneuronal changes which lead to alterations in expression of receptor proteins do take place with agonism in mature neuronal systems. This can be related to the molecular bases for memory and learning, in this regard the dissociative and flashback symptoms of PTSD can be conceptualised as physiological memories. (GILLER et al. 1990). This demonstrates the ability of an individual receptor to alter transmission rates long term resulting in actual dysregulation.The catecholamine neurotransmitters adrenaline and noradrenaline mediate their physiological responses through the family of adrenergic receptors. Three subfamilies of adrenergic receptors have been identified: 1 2 and . Within these subfamilies are subtypes including the subtypes of 2 adrenergic receptors: 2A 2B 2C. During an investigation on the mechanisms of down-regulation in the adrenergic subtypes, an endogenous agonist noradrenaline was used in one of the procedures. Rat 2B adrenergic subtypes were transfected into a Chinese hamster ovary cell line. When ...
