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In most mammals, exclusive care of offspring is the responsibility of the mother – males are rarely involved in direct offspring care. This sex difference in responsiveness to young offspring is mediated in many rodents, in part, by exposure to high levels of the androgen hormone, testosterone, in males during the first few days of their life. One species that is a prominent exception to this general mammalian rule of exclusive maternal care is the prairie vole, Microtus ochorogaster. Prairie vole fathers are extensively involved in all aspects of offspring care, with the obvious exception of nursing behavior. Lansing, French, and Lonstein tested the hypothesis that male prairie voles have lower levels of testosterone during this critical postnatal period, and this lack of 'masculinization' leads to higher levels of offspring care by fathers. Contrary to expectations, the research group demonstrated that neonatal males exhibit significantly higher levels of testosterone than their female littermates in the first five days after birth, similar to rodent species in which paternal care is low or absent. In fact, on the first day after birth, testosterone levels in neonatal prairie voles are as high as those found in breeding adult males. Therefore, the high levels of care provided by fathers in the prairie vole appear to be mediated by testosterone-independent mechanisms.
In most primate species, including humans, exposure of developing fetuses to high levels of male-like hormones (androgens) masculinizes both external genitalia in sex-specific patterns, and sex-typical play patterns. Primate fetuses that are exposed to higher levels of prenatal androgens exhibit higher levels of rough-and-tumble play, and choose male-typical play objects. We monitored gestational levels of androgens in pregnant female marmoset monkeys, and looked for associations with postnatal play patterns. Unlike humans and rhesus monkeys, juveniles born to mothers with higher gestational levels of androgen hormones received fewer play initiations from other group members overall, received fewer play initiations from siblings, engaged in less overall play with siblings, and initiated fewer play bouts with male siblings. High levels of aggressive-like play in juveniles (and aggression in adulthood) may be incompatible with prosocial behavior that is critical for pair-bond formation and parental care in marmosets. Therefore, marmosets may employ mechanisms by which increased exposure to gestational androgens can facilitate both physical and behavioral characteristics that favor a monogamous and biparental social structure.
UNO Neuroscience majors were featured in the College of Arts and Sciences 2012 Newsletter. Link to article.
Rosemary Strasser, a UNO faculty member in the Neuroscience Program, was a co-author on a recent paper in the international journal Age. The study evaluated the impact of variation in early testosterone exposure on lifespan in the house sparrow, a common North American songbird. A summary of the paper follows below, and a link to the paper can be found here:http://tinyurl.com/6qd7ezu
The presence or absence of certain hormones during prenatal development can organize the brain and influence the future behavior of offspring. Many mothers "program" the development of their offspring through the transmission of maternal steroid hormones to their young. These early maternal hormones can have long-lasting effects on the growth, development, behavior, and survival of their young. Birds are an excellent model system to study these maternal effects because the mothers naturally vary the amount of steroid hormones they deposit into their eggs and the young develop outside the mother. In many bird species, the concentration of these maternal steroids, mostly androgens like testosterone, can "organize" the brain and influence the behavior of the offspring well into adulthood. In a recent publication, we report that injections of a physiological dose of testosterone (T) into yolks of freshly laid eggs of a small, seasonally breeding songbird, the house sparrow (Passer domesticus), increased survivorship during the first years of life. In addition, survival effects of developmental T exposure were sex-dependent, with males generally having a higher risk of death their first year. T treatment resulted in higher body mass at 3–4months of age which subsequently influenced mortality risk. This study suggest that although testosterone-enhanced survivorship could potentially increase lifetime reproductive success, there is a “cost” associated with this. Specifically, testosterone may increase mortality risk from extrinsic factors in young male house sparrows by altering adult sexual and aggressive behavior, by increasing the risk of exposure to infectious disease, predation, and injury, or by alterations in physiology early in life that could, in turn, affect health, physiological function and survivorship later in life.
Tony Wilson, a UNMC faculty member with an Courtesy Appointment with the Neuroscience Program at UNO, and Beth Heinrichs-Graham, an M.A. student in psychobiology at UNO, have recently published a paper in the journal Human Brain Mapping exploring the relationship between brain function in a unique brain circuit called the default-mode network, and attention deficit disorder. A brief summary follows, and a copy of the original paper can be found here.
The default-mode network (DMN) is a group of brain structures that are active when a person engages in processes such as self-reflection or mind wandering. The DMN includes the medial prefrontal cortex (MPFC), the posterior cingulate/precuneus cortices (PCC), and the mediolateral inferior parietal cortices bilaterally (RIPL and LIPL). Dysfunction in these areas may be associated with Attention Deficit/Hyperactivity Disorder, a disorder characterized by inattention and hyperactivity/impulsivity. One consistent finding is that there is reduced functional connectivity between the MPFC and the PCC cortices in patients with ADHD during the resting-state. This study evaluates neurophysiological function within cortices of the DMN during a period of awake rest using magnetoencephalography (MEG) in unmedicated and medicated adults with ADHD (predrug/postdrug), as well as group of adults without ADHD. Findings included a global reduction of high-frequency activity in the DMN in unmedicated adults with ADHD, and a particularly robust decrease of neuronal activity in the MPFC of adults with ADHD that was frequency-nonspecific. The unmedicated patients also exhibited significantly stronger activation in posterior nodes (LIPL and RIPL) than the anterior MPFC at lower frequencies. The administration of ADHD medication suppressed the cross-frequency gamma coupling and significantly normalized 8–14 Hz alpha activity in the MPFC of adults with ADHD. However, neuronal activity in all other frequency bins remained abnormal. This study improves knowledge of the DMN as it is the first to demonstrate broadband (not just low-frequency) abnormalities in patients with ADHD, as well as provides insight into the frequency-specific pharmacological effects of ADHD medication on adults with ADHD.
Dr. Bruce Chase, Professor of Biology and a member of the Neuroscience faculty, was recently a co-author on a scientific paper that describes a potential link between a genetic mutation and the neurodegenerative condition known as Parkinson’s disease, or Parkinsonism. He summarizes the 
work below:
Most cases of Parkinson's Disease are sporadic and have an unknown cause. However, a few percent of cases result from dominant or recessive mutations. Studying these rare inherited mutations has led to the identification of about a dozen genes. In turn, their analysis has led to substantial insights into the causes of Parkinson's Disease. The first gene to be identified was that for alpha-synuclein. Alpha-synuclein accumulates in most forms of Parkinson's disease as well as in several other neurodegenerative disorders, including Alzheimer Disease. This paper presents an analysis of a Swedish kindred with an A53T alpha-synuclein mutation. By comparing the genetic region containing the alpha-synuclein gene in the Swedish kindred to that in Greek kindreds that also have the A53T mutation, it shows that the A53T mutation has arisen independently in different human lineages. This supports the idea that the A53T mutation itself, and not some other nearby genetic variant, causes disease. By comparing the parkinsonian phenotype in the Swedish kindred to that seen in other kindreds, this paper also shows that the A53T mutation is associated with different parkinsonian phenotypes in different individuals. One possible explanation for this is that phenotypic differences arise from genetic variation at genes other than alpha-synuclein. Understanding how differences at other genes can modify a parkinsonian phenotype holds promise for developing therapeutic interventions that can delay or prevent the onset of sporadic Parkinson's disease.
A link to the full-text article can be found here:
http://tinyurl.com/3nzfoss
The black tufted-ear marmoset is helping the psychobiology lab of Dr. Jeffrey French at UNO understand the ways in which hormones and social interactions can influence health and well-being.
Maternal gestational androgen levels in female marmosets (Callithrix geoffroyi) vary across trimesters but do not vary with the sex ratio of litters. General and comparative endocrinology 2010;165(2):309-14.French Jeffrey A; Smith Adam S; Birnie Andrew K
Maternal hormones can dramatically modify offspring phenotypes via organizational actions on morphological and behavioral development. In placental mammals, there is the possibility that some portion of hormones in maternal circulation may be derived from 
fetal origin. We tested the possibility that maternal androgens in pregnant female marmosets reflected, in part, contributions from male fetuses by comparing levels of urinary androgens across pregnancy in females carrying varying numbers of male offspring. We monitored urinary androgen excretion in 18 pregnancies from five female white-faced marmosets (Callithrix geoffroyi). Androgen levels rose significantly in the first trimester of pregnancy, reached a peak in the middle of the second trimester, and then declined gradually until parturition. At no point in pregnancy were levels of urinary androgens higher in females carrying litters that had 50% or more males than in females carrying litters that were less than 50% male. Levels of maternal androgens were not associated with litter size, the number of males in the litter, or with the proportion of the litter that was male. The high levels of androgen in pregnant females are therefore likely of strictly maternal origin, and any modification of fetal growth and development can be considered a 'maternal effect'.