ABSTRACT
Intracellular calcium (Ca2+) is ubiquitous to cell signaling across all biology. While existing fluorescent sensors and reporters can detect activated cells with elevated Ca2+ levels, these approaches require implants to deliver light to deep tissue, precluding their noninvasive use in freely-behaving animals. Here we engineered an enzyme-catalyzed approach that rapidly and biochemically tags cells with elevated Ca2+ in vivo. Ca2+-activated Split-TurboID (CaST) labels activated cells within 10 minutes with an exogenously-delivered biotin molecule. The enzymatic signal increases with Ca2+ concentration and biotin labeling time, demonstrating that CaST is a time-gated integrator of total Ca2+ activity. Furthermore, the CaST read-out can be performed immediately after activity labeling, in contrast to transcriptional reporters that require hours to produce signal. These capabilities allowed us to apply CaST to tag prefrontal cortex neurons activated by psilocybin, and to correlate the CaST signal with psilocybin-induced head-twitch responses in untethered mice.
ABSTRACT
Postpartum depression (PPD) is a common illness in mothers after childbirth. PPD negatively affect the mother's quality of life and the bond with the infant, which can interfere with the infant's emotional, social, and cognitive development. PPD is caused by various biological and psychosocial factors. The aim of this review is to summarize the latest evidence of the associations between genetic polymorphisms and PPD. PubMed and Scopus were used as the literature search databases for this review. The keywords used were postpartum depression, postnatal depression, genetic, and polymorphism. Twenty-seven articles were reviewed after screening and applying the inclusion criteria. As results, the serotonin gene (5-HTTLPR) and oxytocin genes (OXTR) have the most significant associations with PPD among other genes. Further research on PPD biomarkers should be conducted to diagnose and treat PPD patients.
ABSTRACT
Slow response to the standard treatment for depression increases suffering and risk of suicide. Ketamine, an N-methyl-d-aspartate (NMDA) receptor antagonist, can rapidly alleviate depressive symptoms and reduce suicidality, possibly by decreasing hyperactivity in the lateral habenula (LHb) brain nucleus. Here we find that in a rat model of human depression, opioid antagonists abolish the ability of ketamine to reduce the depression-like behavioral and LHb hyperactive cellular phenotypes. However, activation of opiate receptors alone is not sufficient to produce ketamine-like effects, nor does ketamine mimic the hedonic effects of an opiate, indicating that the opioid system does not mediate the actions of ketamine but rather is permissive. Thus, ketamine does not act as an opiate but its effects require both NMDA and opiate receptor signaling, suggesting that interactions between these two neurotransmitter systems are necessary to achieve an antidepressant effect.
