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People vulnerable to depression are at increased risk of relapse if they live in highly critical family environments. To explore this link, we used neuroimaging methods to examine cortico-limbic responding to personal criticisms in healthy participants and participants with known vulnerability to major depression. Healthy controls and fully recovered participants with a past history of major depression were scanned while they heard praising, critical, and neutral comments from their own mothers. Prior to scanning, the formerly depressed and the control participants were indistinguishable with respect to self-reported positive, negative, or anxious mood. They also reported similar mood changes after being praised or criticized. However, formerly depressed participants responded to criticism with greater activation in the amygdala and less activation in the dorsolateral prefrontal cortex (DLPFC) and anterior cingulate cortex (ACC) than did controls. During praise and neutral commentary, amygdala activation was comparable in both groups, although lower levels of activation in the DLPFC and ACC still characterized formerly depressed participants. Vulnerability to depression may be associated with abnormalities in cortico-limbic activation that are independent of mood state and that remain even after full recovery. Criticism may be a risk factor for relapse because it activates the amygdala and perturbs the affective circuitry that underlies depression., Psychology

Testicular function is regulated not only by circulating hormones, among which the gonadotrophins play the main role, but also by local factors originating in multiple and complex interactions among cells. In this review, the example of gonadotrophins (LH and FSH) and Transforming Growth Factor beta (TGF beta) was chosen to illustrate the role of interactions between circulating hormones and gonadal growth factors in testicular function control; TGF beta-like activity has been found in the male gonad and we have used a model of cultured purified testicular cells to show that the action of TGF beta on testicular function mainly involves antagonism of the effect of gonadotrophins. Conversely, TGF beta promotes differentiated Leydig and Sertoli cell function. The example of interactions between TGF beta and gonadotrophins reported here shows that locally produced growth factors can regulate the response of testicular cells to gonadotrophins, a finding that extends our concept of reproductive endocrinology to cell-cell interactions.

Ovine prolactin (o-PRL) binding to mammary gland membranes was studied during the estrous cycle in the rat. Groups of rats were decapitated throughout the 4-day estrous cycle at 10 h00 on the days of diestrus I, diestrus II and estrus and at 10 h00, 12 h00, 16 h00 during the day of proestrus. Daily vaginal smears were taken to determine the stage of the estrous cycle which was also controlled by PRL and LH serum levels. Prolactin receptors were quantified in the 100 000 g pellet. For one Scatchard analysis, mammary gland membranes from 5 animals were pooled. Results given are the mean of 4 or 5 pools. Results obtained showed that the apparent affinity constant (KA) remained unchanged during the days of diestrus II and at all the times studied of proestrus and showed a slight but significant decrease on the days of estrus and diestrus I (or metestrus). The binding capacity did not vary from the day of diestrus II to the proestrus 16h00 (11.3 +/- 2.8 fmoles/mg protein) but sharply increased on the day of estrus (190.4 +/- 35.9 fmoles/mg protein). Binding capacity remained elevated on the day of diestrus I. This increase of PRL receptors on the day of estrous would appear to be an important step in preparing mammary gland for pregnancy and lactation.

The aim of this study was to investigate hormonal factors responsible for the huge increase in PRL receptors on the day of estrus in the rat mammary gland. For this purpose, ovariectomized rats were primed with E2 so as to reach a physiological serum concentration of E2 (21.5 +/- 1.2 pg/ml) and high PRL serum values (72.8 +/- 21.9 ng/ml). In these conditions, PRL specific binding and capacity were respectively 22.8 +/- 8.3%/mg protein and 96 +/- 29 fm/mg protein. An injection of either LHRH (500 ng/rat) or LH (60 micrograms LH-RP1/rat) was capable of increasing significantly both PRL specific binding and capacity. Capacity reached the values of 498 +/- 103 and 507 +/- 240 fm/mg protein for LHRH and LH respectively. LHRH action appeared to be mainly mediated through LH secretion, since no difference was found between LHRH and LH. LHRH and LH injections alone were unable to modify PRL binding, suggesting that they only potentiate E2 and PRL action. These results show for the first time that LH is involved in the regulation of PRL receptors in the rat mammary gland.