Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P01178 (oxytocin)
 15,767 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Although active learning works, promoting it in large undergraduate science classes is difficult. Here, three students (F. Naji, L. Salci, and G. Hoit) join their teacher (P. K. Rangachari) in describing one such attempt. Two cohorts in a first-year undergraduate biology course explored the molecular underpinnings of human misbehavior. Students were divided into 18 groups and randomly allotted to deal with one of the four deadly sins: sloth, gluttony, lust, and wrath. Students were expected to read primary sources to devise molecular ways to counter these sins. Group progress was monitored over the 12-wk period by the preceptor (P. K. Rangachari) at scheduled intervals. A single randomly selected student was questioned about the work done, and future directions were provided by the preceptor. At the end of the term, randomly selected students defended their group's approaches to the entire class. A final written report was graded. The following multiple target molecules were considered for each sin: gluttony (cholecystokinin, ghrelin, GABA, leptin, peptide YY, neuropeptide Y, and the melanocortin 4 receptor); sloth (dopamine, glutamate, GABA, and orexin); wrath (serotonin, GABA, glutamate, and corticotropin-releasing hormone receptor 2); and lust (prolactin, testosterone, oxytocin, dopamine, and estrogen). Students noted that the project provided a valuable learning experience, and the random selection approach gave students a greater sense of responsibility to their group. The project helped students hone their skills at searching, synthesizing, sharing, and presenting information, fostered group interactions, and provided a solid knowledge base for subsequent courses.
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PMID:The UNSIN project: exploring the molecular physiology of sins. 2238 7

Loss of a partner can have severe effects on mental health. Here we explore the neural mechanisms underlying increased passive stress-coping, indicative of depressive-like behavior, following the loss of the female partner in the monogamous male prairie vole. We demonstrate that corticotropin-releasing factor receptor 2 (CRFR2) in the nucleus accumbens shell mediates social loss-induced passive coping. Further, we show that partner loss compromises the oxytocin system through multiple mechanisms. Finally, we provide evidence for an interaction of the CRFR2 and oxytocin systems in mediating the emotional consequences of partner loss. Our results suggest that chronic activation of CRFR2 and suppression of striatal oxytocin signaling following partner loss result in an aversive emotional state that may share underlying mechanisms with bereavement. We propose that the suppression of oxytocin signaling is likely adaptive during short separations to encourage reunion with the partner and may have evolved to maintain long-term partnerships. Additionally, therapeutic strategies targeting these systems should be considered for treatment of social loss-mediated depression.
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PMID:Oxytocin in the nucleus accumbens shell reverses CRFR2-evoked passive stress-coping after partner loss in monogamous male prairie voles. 2661 73

The paraventricular nucleus of the hypothalamus (PVN) contributes to both autonomic and neuroendocrine function. PVN lesion or inhibition blunts cardiorespiratory responses to peripheral chemoreflex activation, suggesting that the PVN is required for full expression of these effects. However, the role of efferent projections to cardiorespiratory nuclei and the neurotransmitters/neuromodulators that are involved is unclear. The PVN sends dense projections to the nucleus tractus solitarii (nTS), a region that displays neuronal activation following hypoxia. We hypothesized that acute hypoxia activates nTS-projecting PVN neurons. Using a combination of retrograde tracing and immunohistochemistry, we determined whether hypoxia activates PVN neurons that project to the nTS and examined the phenotype of these neurons. Conscious rats underwent 2 h normoxia (21% O2, n = 5) or hypoxia (10% O2, n = 6). Hypoxia significantly increased Fos immunoreactivity in nTS-projecting neurons, primarily in the caudal PVN. The majority of activated nTS-projecting neurons contained corticotropin-releasing hormone (CRH). In the nTS, fibers expressing the CRH receptor corticotropin-releasing factor receptor 2 (CRFR2) were colocalized with oxytocin (OT) fibers and were closely associated with hypoxia-activated nTS neurons. A separate group of animals that received a microinjection of adeno-associated virus type 2-hSyn-green fluorescent protein (GFP) into the PVN exhibited GFP-expressing fibers in the nTS; a proportion of these fibers displayed OT immunoreactivity. Thus, nTS CRFR2s appear to be located on the fibers of PVN OT neurons that project to the nTS. Taken together, our findings suggest that PVN CRH projections to the nTS may modulate nTS neuronal activation, possibly via OTergic mechanisms, and thus contribute to chemoreflex cardiorespiratory responses.
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PMID:Hypoxia activates a neuropeptidergic pathway from the paraventricular nucleus of the hypothalamus to the nucleus tractus solitarii. 3023 Sep 33