Oral Contraceptives Modulate the Relationship Between Resting Brain Activity, Amygdala Connectivity and Emotion Recognition - A Resting State fMRI Study.

Recent research into the effects of hormonal contraceptives on emotion processing and brain function suggests that hormonal contraceptive users show (a) reduced accuracy in recognizing emotions compared to naturally cycling women, and (b) alterations in amygdala volume and connectivity at rest. To date, these observations have not been linked, although the amygdala has certainly been identified as core region activated during emotion recognition. To assess, whether volume, oscillatory activity and connectivity of emotion-related brain areas at rest are predictive of participant's ability to recognize facial emotional expressions, 72 participants (20 men, 20 naturally cycling women, 16 users of androgenic contraceptives, 16 users of anti-androgenic contraceptives) completed a brain structural and resting state fMRI scan, as well as an emotion recognition task. Our results showed that resting brain characteristics did not mediate oral contraceptive effects on emotion recognition performance. However, sex and oral contraceptive use emerged as a moderator of brain-behavior associations. Sex differences did emerge in the prediction of emotion recognition performance by the left amygdala amplitude of low frequency oscillations (ALFF) for anger, as well as left and right amygdala connectivity for fear. Anti-androgenic oral contraceptive users (OC) users stood out in that they showed strong brain-behavior associations, usually in the opposite direction as naturally cycling women, while androgenic OC-users showed a pattern similar to, but weaker, than naturally cycling women. This result suggests that amygdala ALFF and connectivity have predictive values for facial emotion recognition. The importance of the different connections depends heavily on sex hormones and oral contraceptive use.

Optimization of whole-brain rabies virus tracing technology for small cell populations.

The lateral hypothalamus (LH) is critically involved in the regulation of homeostatic energy balance. Some neurons in the LH express receptors for leptin (LepRb), a hormone known to increase energy expenditure and decrease energy intake. However, the neuroanatomical inputs to LepRb-expressing LH neurons remain unknown. We used rabies virus tracing technology to map these inputs, but encountered non-specific tracing. To optimize this technology for a minor cell population (LepRb is not ubiquitously expressed in LH), we used LepRb-Cre mice and assessed how different titers of the avian tumor virus receptor A (TVA) helper virus affected rabies tracing efficiency and specificity. We found that rabies expression is dependent on TVA receptor expression, and that leakiness of TVA receptors is dependent on the titer of TVA virus used. We concluded that a titer of 1.0-3.0 × 107 genomic copies per µl of the TVA virus is optimal for rabies tracing. Next, we successfully applied modified rabies virus tracing technology to map inputs to LepRb-expressing LH neurons. We discovered that other neurons in the LH itself, the periventricular hypothalamic nucleus (Pe), the posterior hypothalamic nucleus (PH), the bed nucleus of the stria terminalis (BNST), and the paraventricular hypothalamic nucleus (PVN) are the most prominent input areas to LepRb-expressing LH neurons.

Limbic control over the homeostatic need for sodium.

The homeostatic need for sodium is one of the strongest motivational drives known in animals. Although the brain regions involved in the sensory detection of sodium levels have been mapped relatively well, data about the neural basis of the motivational properties of salt appetite, including a role for midbrain dopamine cells, have been inconclusive. Here, we employed a combination of fiber photometry, behavioral pharmacology and c-Fos immunohistochemistry to study the involvement of the mesocorticolimbic dopamine system in salt appetite in rats. We observed that sodium deficiency affected the responses of dopaminergic midbrain neurons to salt tasting, suggesting that these neurons encode appetitive properties of sodium. We further observed a significant reduction in the consumption of salt after pharmacological inactivation of the nucleus accumbens (but not the medial prefrontal cortex), and microstructure analysis of licking behavior suggested that this was due to decreased motivation for, but not appreciation of salt. However, this was not dependent on dopaminergic neurotransmission in that area, as infusion of a dopamine receptor antagonist into the nucleus accumbens did not alter salt appetite. We conclude that the nucleus accumbens, but not medial prefrontal cortex, is important for the behavioral expression of salt appetite by mediating its motivational component, but that the switch in salt appreciation after sodium depletion, although detected by midbrain dopamine neurons, must arise from other areas.