Reduced Brain Norepinephrine and Dopamine Release in Treatment-Refractory Depressive Illness

Abstract

In accordance with the monoamine hypothesis, a deficit in brain norepinephrine and dopamine exists in patients with depressive illness. Moreover, the brains of these patients use an energy source other than glucose, a situation that is normalized following the acute pharmacological blockade of the norepinephrine transporter with the tricyclic antidepressant, desipramine.

Pseudocyesis- A Case Report:-

“…This leads to a decrease in levels of dopamine and norepinephrine activity [6], which corresponds to the findings in various researches that women suffering from pseudocyesis may have dysfunction of catecholaminergic pathways in the central nervous system which are involved in regulation of secretion of anterior pituitary hormones [7] [11]. All this leads to endocrine disorders such as galactorrhea, amenorrhea, hyperprolcatinemia, fetal movements including labor pains approximately around the time of expected delivery date [7].…”

Effects of a α2C-Adrenoreceptor Gene Polymorphism on Neural Responses to Facial Expressions in Depression

“…Notably, healthy a 2C Del322-325-AR carriers also showed (Wong et al, 2000). It also has been hypothesized, however, that chronically increased noradrenaline release into the synaptic cleft that exceeds the capacity of the neuron to return noradrenaline into presynaptic vesicles; however, there can be net neuronal loss of noradrenaline (Eisenhofer et al, 1996;Meredith et al, 1993), which is considered a feature of chronic depression if untreated or unsuccessfully treated (Lambert et al, 2000). We did not observe any between-group differences in performance (accuracy or reaction time) indicating that general attentional, perceptual, or cognitive phenomena did not contribute to the observed neuroimaging differences.…”

Antidepressant-Like Effect of D2/3 Receptor-, but not D4 Receptor-Activation in the Rat Forced Swim Test

“…Mesolimbic dopamine projections are a crucial component in the neural circuitry of reward and/or incentive motivation, both dysfunctional in major depression disorder (Fibiger, 1995;Naranjo et al, 2001). Dopaminergic abnormalities such as reduced dopamine transporter and upregulation of D 2 /D 3 receptors have been found in amygdaloid nuclei in postmortem brain of major depressed patients (Klimek et al, 2002) as well as reduced concentration of homovalinic acid, a dopamine metabolite, in cerebrospinal fluid (Willner, 1983b) and plasma of depressed patients (Lambert et al, 2000). Furthermore, administration of dopamine antagonists as well as drugs that produce depletion of catecholamines (ie reserpine) can elicit symptoms in healthy volunteers that resemble those described in depression such as anhedonia, and lack of volition and energy (Wise et al, 1978;Willner, 1983a), suggesting that reduction in dopamine transmission is an important neurochemical substrate associated with depression.…”