Postpartum and Depression Status are Associated With Lower [11C]raclopride BPND in Reproductive-Age Women

Abstract

The early postpartum period is associated with increased risk for affective and psychotic disorders. Because maternal dopaminergic reward system function is altered with perinatal status, dopaminergic system dysregulation may be an important mechanism of postpartum psychiatric disorders. Subjects included were non-postpartum healthy (n ¼ 13), postpartum healthy (n ¼ 13), nonpostpartum unipolar depressed (n ¼ 10), non-postpartum bipolar depressed (n ¼ 7), postpartum unipolar (n ¼ 13), and postpartum bipolar depressed (n ¼ 7) women. Subjects underwent 60 min of [ 11 C]raclopride-positron emission tomography imaging to determine the nondisplaceable striatal D 2/3 receptor binding potential (BP ND ). Postpartum status and unipolar depression were associated with lower striatal D 2/3 receptor BP ND in the whole striatum (p ¼ 0.05 and p ¼ 0.02, respectively) that reached a maximum of 7-8% in anteroventral striatum for postpartum status (p ¼ 0.02). Unipolar depression showed a nonsignificant trend toward being associated with 5% lower BP ND in dorsal striatum (p ¼ 0.06). D 2/3 receptor BP ND did not differ significantly between unipolar depressed and healthy postpartum women or between bipolar and healthy subjects; however, D 2/3 receptor BP ND was higher in dorsal striatal regions in bipolar relative to unipolar depressives (p ¼ 0.02). In conclusion, lower striatal D 2/3 receptor BP ND in postpartum and unipolar depressed women, primarily in ventral striatum, and higher dorsal striatal D 2/3 receptor BP ND in bipolar relative to unipolar depressives reveal a potential role for the dopamine (DA) system in the physiology of these states. Further studies delineating the mechanisms underlying these differences in D 2/3 receptor BP ND , including study of DA system responsivity to rewarding stimuli, and increasing power to assess unipolar vs bipolarrelated differences, are needed to better understand the affective role of the DA system in postpartum and depressed women.

N-3 (Omega-3) Polyunsaturated Fatty Acids in the Pathophysiology and Treatment of Depression: Pre-Clinical Evidence

“…This decrease in expression of ventral striatal D 2 receptors concurs with the hypoactivity of the mesolimbic dopamine system that is hypothesized to occur in depression, and is also consistent with the decreases in the density of the D 2 receptor found rat models of depression such as learned helplessness, chronic mild stress-induced anhedonia, and the socially-isolated Flinders sensitive line rat [76–78]. Although no alterations in the number of D 2 receptors the ventral striatu, of postmortem depressed patients [79], a PET imaging study found lower D 2/3 dopamine receptor density in the striatum of depressed women [80]. Thus, the effects of a reduction of DHA in the brain of the adult rat are consistent with rodent models of depression, and perhaps also with depressed humans.…”

Chronic Interferon-α Decreases Dopamine 2 Receptor Binding and Striatal Dopamine Release in Association with Anhedonia-Like Behavior in Nonhuman Primates

“…Increased DA synthesis and release may downregulate D2Rs and decrease subsequent DA synthesis through end product inhibition (Carlsson et al, 1976). Of note, reduced striatal D2R binding has been reported in patients with depression (Moses-Kolko et al, 2012). Although it is unknown whether decreased D2R binding reflects a change in pre-or postsynaptic receptors, both types of receptors are thought to be important in regulation of DA synthesis (Anzalone et al, 2012).…”

Relationship of Monoamine Oxidase-A Distribution Volume to Postpartum Depression and Postpartum Crying

“…However, there are several imaging studies of PPD that include subjects with previous MDEs. Changes reported include reduced occipital cortex GABA levels, reduced D 2 receptor binding in the ventral striatum in postpartum irrespective of PPD, and reduced 5-HT 1A receptor binding in the orbitofrontal, subgenual, and mesiotemporal cortex in a sample of unipolar and bipolar PPD (Epperson et al, 2006;Moses-Kolko et al, 2008, 2012. As with many complex psychiatric illnesses, it is generally believed that a number of neuropathological changes contribute to the symptoms of PPD and it is plausible that some of these markers reflect specific vulnerability to PPD, MDE in general, or both conditions.…”