Tag Archives: behavioral neuroendocrinology

Bad Birds Make Good Birds Feel So Good: It’s In the Genes

Donna Maney's lab found that the more aggressive white-striped morph has a change in the gene for estrogen receptor-alpha that makes expression of this gene more efficient in brain areas important for monogamy, aggression, and parental care.

Donna Maney’s lab found that the more aggressive white-striped morph has a change in the gene for estrogen receptor-alpha that makes expression of this gene more efficient in brain areas important for aggression and parental care.

Donna Maney and colleagues report that

the evolution of complex mating strategies are linked to changes in the gene for the estrogen receptor. Changes in one gene can predispose birds toward a “parental investment strategy” (low levels of competition, high levels of parental care) or a “mating strategy” (high levels of competition, low levels of parental care and exta-pair matings).

That in itself is remarkable, but there is another twist. The birds with the genetic change linked to more aggression and less parental behavior almost invariably mate with birds carrying the other genetic arrangement! We knew that both strategies have their advantages, but now it appears that

the two strategies might be complementary when they occur together in the same couple. One member of the pair is more aggressive and territorial, while the other tends to the nest. In pairs where the male takes on more parental duty, the female is likely to be the one who is more aggressive.

Genes and Behavior

Most people agree that our genes affect some behaviors. Think of Huntington’s disease, in which the devastating loss of motor function, memory, and impulse control are linked to a single gene, HTT. Think about the behavior of different dog breeds. The border collie’s intensity differs from the laid-back demeanor of the Labrador, and both of these tendencies differ from those of the happy yappy terrier. There is no doubt that these behavioral differences came about by selective breeding for specific traits, and that the basis for selective breeding is the heritability of those traits. Heritable traits, those that can be inherited, are affected by genes. No problem, but what about complex social behaviors?

Genes, Hormones, Monogamy, and Parental Care

We know that species differ in their mating strategies. Some species tend toward monogamy in that they show a strong preference for mating with a familiar partner, the parent of their own offspring. In these species, fathers tend to share the parental care of their own offspring, and these behaviors are often incompatible with high levels of aggressive competition. Other species tend toward promiscuity (multiple mating partners and no pair-bonds) and in these species, females tend to bear the burden of offspring care. We know quite a bit about hormonal control of these behaviors in certain species. Hormones are secreted from endocrine glands, and they act by binding to receptors. Hormone-receptor binding stimulates or inhibits the neural circuits that control behavior. In male prairie voles and marmoset monkeys, monogamy is linked to a number of hormones, two of which are oxytocin and vasopressin. Promiscuous species differ from monogamous species in the distribution of these receptors in the brain. One specific gene encodes the vasopressin V1A receptor, and monogamy in male voles is linked to the distribution of brain V1A receptors, which in turn is a consequence of the gene for this receptor. One form of the gene (a polymorphism) is linked with monogamy. How strong is the link between hormone receptor distribution and monogamy? In terms of their vasopressin and oxytocin receptors, monogamous marmoset monkeys look more like monogamous prairie voles than they look like promiscuous species of monkeys! Hormonal influences on monogamy and parental behaviors in birds and mammals are well accepted, and this line of research has provided insights into child neglect and abuse, postpartum depression, and autism.


Donna Maney and her students study song birds that are monogamous, but can be divided into two types, “dads or cads.” They study hormonally-mediated aggressive song and parental behavior in wild birds that form pair bonds with different levels of exclusivity. In biology, we say these species are “monogamous,” but this does not mean they don’t have sex with more than one partner.  In these song birds, they all form pair bonds, but high levels of aggression and territoriality and low levels of offspring care are correlated with more “philandering,” that is, mating with multiple partners. In male birds, sex and aggressive behaviors are linked to hormones like testosterone from the testes and estradiol made from testosterone in the brain. As you will see, this model system affords unique advantages.

Two Morphs of White-throated Sparrow (Dads or Cads)

To link the evolution of behavior to specific genes, we need a snapshot of evolution in action, that is, we need two groups emerging within one population. Maney chose to study two different wild morphs within one population of white-throated sparrows (Zonotrichia albicollis). The morphs differ in their degree of aggressive song and parental care, as well as their propensity for multiple mating partners. As pictured at the top of this post, the tan-striped morph shows more parental behavior, more exclusive pair bonds, and less aggressive song, whereas the white-striped morph forms pair bonds, but also copulates freely with other birds. The white-striped males are less parental. Aggression can be easily measured by recording the species-typical song in response to that of an intruding male. Videos of the aggressive songs and display can be seen in the video here.

The two morphs also differ at chromosome 2, or ZAL2. Sparrows of the white-striped, aggressive morph all have at least one copy of a rearranged chromosome 2, ZAL2m, whereas the tan-striped sparrows never have this inverted chromosome. Donna Maney set out to study gene differences on this inverted chromosome that might explain differences in complex social behavior.

What’s Estrogen Got To Do With It?

In both morphs, the onset of aggressive, territorial song is correlated with increases in testosterone secreted from the testes during the breeding season (spring). Thus, you might suspect that the white-striped morph is more aggressive due to higher levels of testosterone. You would be wrong. When testosterone levels are equalized, the behavioral differences persist. There is something else going on. In the brains of sparrows and many song bird species, testosterone is converted to estradiol. Aggressive song is blocked by treatments that prevent conversion of testosterone to estradiol or by treatments that block estradiol binding to the estrogen receptor-alpha (ER-alpha) (reviewed by Kiran Soma). Receptors for estradiol, in particular ER-alpha, are located in brain areas involved in aggression, including the medial amygdala. Parental behavior is related to ER-alpha in other brain areas, including the medial preoptic area. The differences between the morphs might be related to differences in ER-alpha in the amygdala and preoptic area.

Just to remind you, Maney and colleagues knew that wild males of the more aggressive, white-striped morphs all have at least one copy of a rearranged copy of chromosome 2 (the rearranged chromosome is called ZAL2m). It turns out, the gene for ER-alpha, called ESR1, is located on this chromosome. Yes. Maney and her colleagues hypothesized that the rearrangement in the chromosome led to a change in ESR1 that led to elevated sensitivity to estradiol, and hence, higher levels of aggression and less parental behavior.

Indeed, Horton et al. found that the white-striped sparrows’ aggression was associated with a more efficient transcription of the gene, ESR1. That is, when the DNA is transcribed to messenger RNA, it occurred at a greater rate in the more aggressive, less parental, white-striped birds. More transcription might led to more translation, and hence more ER-alpha.  This would be expected to render the white-striped birds more sensitive to estradiol’s effects on behavior.

Furthermore, Horton et al., found that in the white-throated morphs, territorial singing and ESR1 expression were higher in a region of the medial amygdala associated with aggression.  Similarly, levels of nest provisioning were predicted by the level of ESR1 expression in the medial preoptic area. Thus, Maney’s group 1) linked a genetic change to a change in behavior, 2) linked a genetic change to a change in efficiency of gene transcription, 3) linked a change in gene expression in a particular brain area to a change in a particular behavior.

Together, these results are consistent with the idea that a genetic change in the gene for the estrogen receptor-alpha has led to the evolution of two different morphs of sparrow that differ in complex social behaviors. These experiments were done using wild birds from natural environments, not just laboratory animals. This and other work on this species was blogged by the awesome, Grrlscientist, at the Guardian. To the best of my knowledge, the Horton et al. article is the first such report in any vertebrate species.

It Takes All Kinds of Birds

Depending on your personal bias, you probably jump to the conclusion that one morph is better than the other, and one morph will win out. Exclusive pair bonds and low levels of aggression might result in more offspring if the offspring receive more parental care. The investment in parental care leads to a pay off in terms of number of reproductively successful offspring.  On the other hand, aggressive, less parental birds can win larger territories and a greater abundance of resources (food and shelter). As this blog documents, the more energy, the greater the reproductive success. Read our latest review for more info on energy and reproduction. I wonder whether the frequency of the different morphs would change depending on the availability of energy in the environment. In any case, this means that in the white-stripe, “Don Draper-like” morph, greater investment in competition for resources might lead to more matings, greater fertility, and higher levels of long-term reproductive success. Maney tells us that these two morphs are not in competition, and probably not about to evolve into two separate species.

In reality, almost all white-throated sparrow breeding pairs consist of one individual with and one without the inverted ZAL2m chromosome. The females also differ in their level of parental investment. In other words, the tan-striped morph invariably mates with the white-striped morph, and the tan-striped male or tan-striped female takes up the slack at the nest. This increases the frequency of heterozygous individuals, and maintains the inverted chromosome ZAL2m in the population. Presumably, there is an evolutionary advantage to both the original version of chromosome 2 and the inverted chromosome ZAL2m, perhaps related to differential parental investment. It’s fascinating that the tan-striped males tend to mate with the more aggressive and territorial females and pick up the slack in the parenting department.

Maney and colleagues and their elegant experiments have shown that in white-throated sparrows, rearrangement of a specific gene, ESR1, is one of the genetic changes that underlies the emergence of two different, complementary life-history strategies.

Human Beings

In birds, voles, and monkeys, the behaviors are measured with precision, and these animals can’t deny, lie about, or exaggerate their sex behaviors. A number of studies have associated human monogamous/promiscuous and parental/nonparental tendencies with genetic polymorphisms, but it’s reasonable to wonder whether monogamy can be studied with any precision in people with such complicated sexuality. When it comes to sex, people are inhibited, shy, disingenuous, priggish, or boastful, rather than factual. Questions about human sexuality might have to wait until sex researchers get a hold of the data compiled by the NSA (that is, data compiled when the agents aren’t spying on their own love interests). Ah, yes. Therein lies a clue.

Well, if humans share anything in common with white-throated sparrows, it would surely be reflected in our musical archives…


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When I’m Sixty Five

Special dedication to

Jacques Balthazart!

quail mating

birthday greetings

bottle of winejuliper

Pictured, a Valentine, a birthday greeting, a bottle of wine, and a Jupiler



Jacques Balthazart is a true leader in behavioral neuroendocrinology, the study of how hormones affect the brain and behavior. His retirement demanded a fitting tribute, but there was a problem. When it comes to international conference organizers, nobody does it better than Jacquesyoung jacques Balthazart. So, who would throw this party? No worries. The Belgian government’s policy requiring mandatory retirement at age 65 turned out to be the catalyst for a nonpareil scientific meeting (throughout this blog, all words underlined are links). It also turned out to be an outrageous birthday party and a creative plan to continue research on his own terms. Last week, the combination of foundational research, cutting-edge science, Belgian beer, and collegiality led to the conference’s new nom de plume: The International Conference Honoring Brilliant Balthazart (ICHBB).

Jacques is shown above and to the right just moments before the party, and below, just a few days into the party.


Photo by GianCarlo Panzica of Jacques Balthazart, 65,  in a gift hat symbolizing his dual loyalty to Belgium and the U.S.
dave me scottish guy beerjon
ICHBB Conference photos by GianCarlos Panzika

After all, when you are the premier conference organizer, entertainer, and hub of your scientific community, it makes sense that you should plan, host, and orchestrate your own birthday retirement party!

team jacques

“Team Jacques” adapted from a funny photo by Julie Bakker

The first ICHBB was named the International Conference on Hormones Brain and Behavior and held in Bielfeld, Germany in 1982. It was conceived and developed from Jacques’ isolation as one of the few behavioral endocrinologists in Belgium. His uncontrollable desire for scientific interaction led him to invite about 40 premier behavioral endocrinologists from around the world to Bielfeld. To his surprise, they all showed up; it was an unqualified success; and everyone wanted to do it again and again. And again. In subsequent years, Jacques personally nursed the ICHBB in his home town of Liege (in 1984, 1989, and 2014) and affectionately nurtured the conference when it was hosted by others in France, Italy, and Spain.

liege buttfly bushes  2 I learned some things about Jacques’ life that I hope will be shared, remembered, and handed down to our academic offspring! First, necessity is the mother of invention in that some of Jacques’ biggest contributions to science come from his ability to embrace his authentic small-town lifestyle while uniting the world of behavioral neuroendocrinology. He was born, raised, educated, bred, and “retired” in Liege, Belgium, far less a tourist destination than a very pleasant place to grow up, and Jacques truly loves Liege. Many Americans have never even heard of Belgium, let alone, Liege, but one thing is very clear. Liege is “on the map” in the minds of behavioral endocrinologists. This just shows that there is no point in whining about where you work. I know behavioral endocrinologists at big U.S. medical schools, at Yale, or in big universities like UC-Berkeley who feel more isolated than Jacques.

liege night

liege dogs in bar

liege dob in bar 2

Scenes from Liege














This idea was confirmed by plenary speaker, Kathy Olsen, former deputy director of the National Science Foundation, chief scientist for NASA, and associate director and deputy director of science in the executive offices of the President of the United States of America. According to Kathy, there is no one else to blame for putting Liege on the map other than Jacques Balthazart.


Kathy Olsen (right) shown with Vicki Luine and Yasuo Sakuma (left)

In terms of hormones and behavior, Jacques brought the world to Liege. I was surprised to learn that the man we know as the hub of our global science community is very much a local family man. Jacques’ father was a local architect, and his mother worked as a full-time homemaker and mother of two children. Jacques was educated from primary school on up through college in his home town of Liege. It was at the University of Liege that he fell in love with one of his biology professors, the beautiful and enviably fit, Claire (apparently she still runs 10K a day!). In addition to having a successful career in biology, Claire is a super friendly, social, community-oriented woman-about-town. Jacques, on the other hand, is not nearly as involved with his local friends and relatives. Though Claire chides Jacques for not remembering neighbors who have known Jacques his whole life, Jacques, ironically, is the social glue holding together a giant global network of scholars and friends, many of whom traveled far and wide to celebrate Jacques’ birthday. In one of Jacques’ presentations this week, he showed a world map dotted in every continent with markers showing where he has friends who will meet him at the airport.

nicole stripeyriters
Lauren Riters and family (left) and Nicole Cameron with a lot of French stripes (right)


Nicole, Lauren, Lauren’s son, Nancy Forger and Geert DeVries (left) and cannibals on the menu (below)

A Bad Bromance

Everyone in behavioral endocrinology knows that Jacques Balthazart has co-authored numerous landmark articles with Greg Ball, begging the question “How did this fertile collaboration begin?” During the various tributes at the conference, we learned that in 1983, Greg Ball was a graduate student at the Institute for Animal Behavior at Rutgers-Newark, where Jacques Balthazart was a distinguished visitor. Jacques, however, was not impressed with that Greg Ball character!

Jacques recalls Greg as a “lazy, long-haired hippie hanging around drinking coffee and pontificating in the break room all day long in a booming voice that could be heard all over the department.” As they say, first impressions are the best. Well, except the lazy part, because Greg’s and Jacques’ publications together number at least 400, and somewhere between 110-115 of those articles are co-authored by Ball and Balthazart or Balthazart and Ball.

The Ball and Balthazart Bromance was finally consummated (scientifically) a few years later in Germany. Greg Ball, then a postdoc with John Wingfield, was invited to speak at the conference. Greg was put up in a small dormatory-like room with a single bathroom shared by the adjacent room. Greg was brushing his teeth when his new next door neighbor, Jacques Balthazart, burst into the bathroom. “Well, well, well, we meet again!” Only this time, the Greg-Jacques Belgian beer bromance began in earnest (Wait? Who’s Ernest?) From the time of that meeting, Jacques Balthazart and Greg Ball became fast friends and insanely productive collaborators.

Incidentally, you can trace the academic family trees of these characters and that of your own mentor at Neurotree.org. Greg Ball’s tree is probably the most interesting, reaching straight back to Niko Tinbergen and Konrad Lorenz.

Peg McCarthy, Greg Ball’s beloved spousal unit, in her plenary lecture, explained that Jacques was a daunting obstacle blocking Greg’s affections for Peg in the initial stages of their courtship. At first, it was clear to Peg that Jacques would always be Greg’s “first wife.” It seemed she could never compete with Jacques. Luckily, Jacques came to adore Peg, and now warmly accepts Peg as a sisterwife. Suffice to say, that if all sisterwives were like Jacques and Peg, we would all be Mormons.

peg and greg

me peg colin
Greg Ball and Peg McCarthy (left) and a nicer pic of Peg with me and Colin Saldanha

world cup

   Celebrating Belgium Moving Up In the World Cup 2014

To Sir Jacques With Love

The entire meeting was infused with enormous gratitude and affection from Jacques’ present and former students, postdocs, collaborators, family, and friends. Greg Ball gave a “What I learned from Jacques” speech that I wish all graduate students could hear. The highlights included

1) PUBLISH all of your data immediately. You never know when or how your results will be useful to other scientists, and none of it will matter if it is not published.

2) Time is precious, so, collect data, and write without fail, regardless of how late you stayed up the night before. No excuses. As Jacques would say, you have one 33 cl (Jupiler) at lunch and then bike back to work!

3) Be brave about methods. If it’s been done, you can do it.

4) Good ideas come from many sources, so, go to meetings and host your own.

5) Good colleagues can be good friends.

jacques at poster jacquest and jeff poster

Jacques and Jeff Blaustein are not at all faking interest in my poster presentation. Photo taken by Vicki Luine.

In any case, there were so many excellent talks and posters at the meeting, demonstrating that Jacques will live on through his scholarship and mentoring as long as human civilization survives. Happily we learned that Jacques will continue working at the University of Liege, without the unpleasant duties of his old position, but instead intensifying focus on the research that he loves. This is one of the benefits of launching the careers of young, outstanding scientists and scholars. Shown below are ICHBB attendees who came to honor Jacques: Dave Grattan, Colin Saldanha, Kiran Soma, Jim Pfaus (with son, Josh), Thierry Charlier, Chuck Roselli and many others in the group photos.

jacques with dave gratten jacques w:colin and kiren

jaques anne etgen

jacques chuck vicki jim









jim thierrymug


Enjoy the next phase, Jacques! Your work is alive and well in all of our research programs. See you soon.

jacques juliper

The above photo of Jacques and the preceding six were taken by GianCarlo Panzica.

There will be more pictures available through the website for the ICHBB. Meanwhile, you will find some links to seminal Balthazart discoveries here and here.

And finally, here’s a funky version of what I’m sure Jacques’ mentees are thinking…


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He’s A Rebel! Paul Heideman visits Lehigh

     This week the Schneider lab had the pleasure of hosting one of our scienImagece heroes, Paul Heideman from The College of William and Mary. He doesn’t wear a leather jacket or anything, and in fact, he looks like a typical white-guy professor. We’re still wondering exactly how he left us so inspired and energized, like we just discovered the thrill of science all over again.

He’s a loner, Dottie, a rebel

     Like most of us, Paul came up the ranks when everyone was advised to learn super cool state-of-the-art molecular techniques, to work on conditional knock-out/knock-in-optogenetic-whatever-the-hell mice, and to focus on cellular mechanism. Did he do this? No. Is he tenured? Yes. Is he funded? Yes, well funded. Is he happy? He seems pretty darn ecstatic.

     Second, he studies the one thing that most biologists avoid like the plague: Individual differences. Most scientists seek to minimize them. They like groups that show little natural variance, and they omit outliers.

      Hating individual differences makes sense in a way. When a drug works to reduce pain or fight infection, you want it to do so reliably in just about everyone. Will a new drug X decrease depression? We want a clean result. We want to see clear differences in depression between the drug-treated and placebo-treated groups. We want as little variation as possible within the groups. Face it. Too much variation within the treated group, and the drug is not going to market.

Vive la diffe’rence!

Image      Paul solved the problem of individual differences by embracing them. He started his career in the field, trying to figure out why some equatorial animals are seasonal breeders and some aren’t.  Fruit bats (a.k.a., flying foxes) that inhabit particular islands in the Philippines breed only in certain seasons, whereas  those on other islands begin their breeding season months later. Presumably, this ensures that offspring are born at the time when they are most likely to survive. But what is the source of the difference?

      To be a seasonal breeder, you need an internal clock, a reliable cue in the environment to set your clock (like the availability of food or the day length), and a sensory system to detect the environmental cue. Also, you need your clock and your senses to be connected to your reproductive system, and ultimately, to your gonads (ovaries or testes). What’s up with a nonseasonal breeder? Is the clock broken or are they deaf to the alarm? Is there a disconnect between the clock and the gonad?

Now What?

Image     Paul was stuck. He just couldn’t figure this out in the field. In order to uncover the internal brain mechanisms, he needed to have animals in the lab. Commercially available lab animals, however, will not do. They gots no variance in the thing he wanted to study. Most lab animals are uniformly year-round breeders. He would have to create a lab population that had the same variation that exists in nature.

     Being a rebel, he did what all of his colleagues were not doing. He trapped wild mice (Peromyscus leucopus) from the wild, brought them to his laboratory, and began crossbreeding. He kept the population large enough to avoid inbreeding (breeding close relatives tends to decrease heritable variation). Now he had a lab population that contained most of the variation that existed in the wild. How would he make use of this to answer his questions about individual differences in seasonality?

     The next thing he did was brilliant. This base population served as the starting point for a selective breeding program. He started breeding lines of mice that differed in their seasonality. By breeding seasonal males to seasonal females, and unseasonal males to unseasonal females for many generations, he ended up with two groups of animals that differed from each other. They didn’t just differ by accidental inbreeding, or for other unknown reasons. They differed because they were selectively bred for those traits he wanted to study.

     Paul has created and maintained a scientific gold mine. He can expose the two groups to winter conditions, measure their hormones and neuropeptide levels, and figure out what accounts for their differential response to the changing season. He can even sequence their genome and look for differences. He can get answers to questions like “How does evolution change the reproductive system?” “Can natural selection change hormone levels or does it change hormone receptors?” “In nonseasonal animals, is their internal clock broken or are they simply blind to the seasons?”

      To find out the answers, you can check out Paul’s work here and here. Paul writes, “I have worked on multiple populations, but my current mice all come from one population. That’s important to me because I can say that all this variation is just from one little population — and that suggests that other mammals, including humans, might also contain large amounts of variation.”

    I agree and I think it’s especially cool that selection has created wildly different strategies for survival and reproduction within the same species. In this case, you’ve got cautious mice that take the hint that winter is on the way by shutting down the reproductive system in order to conserve energy for survival in the cold. In the same population, you’ve also got flexible mice that will breed willy nilly as long as they can. If the winter is mild, the sexy mice beat the conservatives by producing litters and getting more genes into the next generation. If winter is harsh, the conservatives will win the gamble because they will be the only ones to survive to breed in spring. It takes all kinds. Vive la diffe’rence!

Paul gives a great talk. He gives all of his attention to the students, and he has tons of helpful advice about teaching behavioral endocrinology and science writing. Plus. . .

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Sex and Food and. . . on the Table


oldie but goodie

“Sex and food and. . .” What pops into your mind to finish this sentence? For me it’s “rock and roll” (I substitute food for drugs because I don’t need drugs). If you are more punk than new wave it’s “Food, Sex, and Ewe,” and for the hip hopsters it’s “Sex, Food, and Sports.” The latter is also true for Seinfeld fans. Don’t Google “food and sex” though, you might get distracted.

“Sex-and-food” is the key to life. This grammatical impossibility stems from the fact that in the brain, the desires for sex and food seem to be one and the same, sometimes two sides of the same coin. In my upcoming book “Sex and food and. .” (Oxford University Press), I begin by noting that in every-day language food is sexy and sex is foodie;

“In both word and deed, we express our entangled appetites for food and sex, almost as if we confuse the two. In everyday language, food is sexy and sex is foodie. Chocolate is orgasmic and our lovers are delicious. In The Bible we are told to be fruitful and multiply. In Shakespeare’s Sonnet 118 he uses food metaphors for budding romance, for the “sweetness” of true love, and for the “bitter sauces” of infidelity.”

Just a smidgen of the evidence for the food-sex connection is presented in the table below. These 40-or-so chemical messengers have documented effects on ingestive behavior. They either increase or decrease the amount of food eaten per unit time. The same chemical messengers have clear, repeatable effects on reproductive processes, often including sexual desire and performance. In fact, compounds pushed as anti-obesity drugs by some researchers are being pushed as libido-enhancer by others. Our table reveals information useful for a wide range of scientists, not just those narcissists who feel that all research must have medical application. For more on this topic check out our new preprint now available online (it will be published open access).

TABLE 1. A list of hormones and neuropeptides that influence both food intake and reproduction. From Schneider et al., 2013, When do we eat? Ingestive behavior, survival, and reproductive success, Hormones and Behavior, published online ahead of print.

Central “Orexigenic” Peptides Ingestive Effects Reproductive Effects
agouti-related protein (AgRP), HS04, SHU9119 (MCR antagonists) increases food intake in fish (Schjolden et al., 2009), birds (Strader et al., 2003), and mammals (Rossi et al., 1998; Stark, 1998), and food hoarding in hamsters (Day and Bartness, 2004) inhibits gonadotropin secretion in fish (Zhang et al., 2012), inhibits LH in the presence of estradiol in female rats (Schioth et al., 2001; Watanobe et al., 1999), stimulates LH in male mammals (Stanley et al., 1999), ablation of AgRP gene restores fertility in ob/ob mice (Wu et al., 2012)
alarin Increases food intake in male rats (Van Der Kolk et al., 2010) stimulates LH secretion in castrated male rats (Van Der Kolk et al., 2010)
β-endorphin increases food intake in fish (de Pedro et al., 1995b) (reviewed in (Lin et al., 2000)), birds (Deviche and Schepers, 1984; Maney and Wingfield, 1998; Yanagita et al., 2008), and rats (Grandison and Guidotti, 1977; McKay et al., 1981) mediates stress-induced suppression of LH in fish (Ganesh and Chabbi, 2013), birds (Sakurai et al., 1986), inhibits LH secretion and sexual performance (Hughes et al., 1987, 1990; Sirinathsinghji et al., 1983), but might also increase sexual motivation in rats (Mitchell and Stewart, 1990; Torii et al., 1999),
galanin increases food intake in fish (De Pedro et al., 1995a; Lin et al., 2000; Nelson and Sheridan, 2006; Volkoff et al., 2005) and rats (Kyrkouli et al., 1990) stimulates LH secretion in birds (Hall and Cheung, 1991),  steroid-primed rats (Sahu et al., 1987)
galanin-like peptide (GALP) increases food intake in rats (Matsumoto et al., 2002), also decreases food intake in mice (Krasnow et al., 2003) stimulates LH secretion in male mice and rats and in estradiol-treated female rats (Krasnow et al., 2003; Matsumoto et al., 2001; Uenoyama et al., 2008)
gamma aminobutyric acid (GABA) might not mediate hyperphagic effects of orexin in fish (Facciolo et al., 2011); increases food intake in rats (Basso and Kelley, 1999) increases gonadotropin release in fish (Kah et al., 1992); GABA-BR decreases excitability of mouse GnRH-I neurons (Zhang et al., 2009); GABA-AR excitatory for mouse GnRH-I neurons (DeFazio et al., 2002; Moenter and DeFazio, 2005)
melanin-concentrating hormone (MCH) increases food intake in rats (Presse et al., 1996), but decreases food intake in fish (Shimakura et al., 2008) inhibits LH secretion in rats (Tsukamura et al., 2000a)
neuropeptide Y (NPY) increases food intake in fish (de Pedro et al., 2000; Lopez-Patino et al., 1999), frogs (Crespi et al., 2004), snakes (Morris and Crews, 1990), birds (Strader and Buntin, 2001), rats (Stanley and Leibowitz, 1984) and food hoarding in hamsters (Dailey and Bartness, 2009) increases gonadotropin release in fish (Peng et al., 1993), inhibits steroid biosynthesis in frogs (Beaujean et al., 2002), inhibits sex behavior in snakes (Morris and Crews, 1990), inhibits LH in the absence of estradiol, stimulates LH in the presence of estradiol in rats (Crowley et al., 1985; Sahu et al., 1987) (Sahu et al., 1987), inhibits sex behavior in rats (Ammar et al., 2000)
orexin/hypocretin increases food intake in fish (Lin et al., 2000; Volkoff et al., 1999; Volkoff et al., 2005), and rats  (Sakurai et al., 1998), but not in birds (da Silva et al., 2008) inhibits spawning in fish (Hoskins et al., 2008), inhibits LH in rats with little or no estradiol (Furuta et al., 2002), stimulates LH in rats with high  levels of estradiol  (Pu et al., 1998)
gonadotropin inhibiting hormone (GnIH) increases food intake in birds (Tachibana et al., 2005), mice, sheep, and monkeys (Clarke et al., 2012; Johnson et al., 2007; Tachibana et al., 2005) inhibits GnRH and LH secretion and sex behavior in fish (Moussavi et al., 2012), birds (Bentley et al., 2006; Satake et al., 2001) and blocks the LH surge in sheep and inhibits LH secretion in rats and female hamsters (Bentley et al., 2006; Johnson et al., 2007; Kriegsfeld et al., 2006; Smith et al., 2008)
Peripheral “Orexigenic” Hormones Ingestive Effects Reproductive Effects
corticosteroids chronically elevated levels increase food intake in fish (Bernier et al., 2004),  amphibians (Crespi et al., 2004), birds (Astheimer et al., 1992), and rats (Hamelink et al., 1994; McLaughlin et al., 1987; Stevenson and Franklin, 1970) inhibits a wide array of reproductive parameters in fish including parental behavior (Carragher et al., 1989; O’Connor et al., 2009) reviewed by (Milla et al., 2009), inhibits steroid synthesis and spermatogenesis in amphibians (Moore and Zoeller, 1985; Moore and Jessop, 2003), inhibits sex behavior in snakes (Lutterschmidt et al., 2004; Moore and Jessop, 2003), stimulates gonadotropin secretion at low doses in birds (Etches and Cunningham, 1976), inhibits HPG function at chronically high doses in birds (Etches et al., 1984), and mammals (Vreeburg et al., 1988)
ghrelin (gut) increases food intake in fish (goldfish and tilapia), but decreases food intake in rainbow trout (Jonsson, 2013; Jonsson et al., 2010), decreases food intake in birds (Kaiya et al., 2009), increases food intake in rats and mice (Tschop et al., 2000; Wren et al., 2000) and food hoarding in Siberian hamsters (Keen-Rhinehart and Bartness, 2005) stimulates LH release from fish (Grey et al., 2010), inhibits GnRH, LH secretion and sex behavior in rats and mice (Fernandez-Fernandez et al., 2004; Furuta et al., 2001; Shah and Nyby, 2010)
insulin (pancreas) chronically elevated levels increase body weight, adiposity, and food intake in birds (Nir and Levy, 1973), rats (Booth and Brookover, 1968; Friedman, 1977; Friedman et al., 1982; Houpt, 1974) systemic treatment inhibits LH secretion at doses that increase food intake in hamsters not allowed to overeat (Wade et al., 1991), inhibits LH secretion in sheep treated peripherally with saline but not with glucose (Clarke et al., 1990)
motilin (gut) increases food intake in fasted rats (Garthwaite, 1985) inhibits LH secretion in rats (Tsukamura et al., 2000b)
progesterone (gonads, adrenals) reverses the weight reducing effects of estradiol on body weight and food intake in rodents (Hervey and Hervey, 1966, 1969; Zucker et al., 1972) synergizes with estradiol to stimulate female sexual performance in rats (Dempsey et al., 1936), enhances estradiol feedback on LH in female rats (Chappell and Levine, 2000), mimics testosterone in male rats (Witt et al., 1995)
testosterone (gonads, adrenals) increases food intake and growth in rats (Siegel et al., 1981) stimulates sexual motivation in females (de Jonge et al., 1986; Everitt and Herbert, 1970) and sexual performance in male rats (Davidson, 1966; Davidson and Bloch, 1969)
Central “Anorectic” Peptides Ingestive Effects Reproductive Effects
α-melanocyte stimulating hormone (α-MSH), melanotan- II (MT-II), PT-141 decreases food intake in fish (Kang et al., 2011; Schjolden et al., 2009), amphibians (Carpenter and Carr, 1996), birds (Kawakami et al., 2000; Tachibana et al., 2007),  and rats (Vergoni et al., 1986), and food hoarding in Siberian  hamsters (Keen-Rhinehart and Bartness, 2007a; Shimizu et al., 1989) enhances electric organ discharge in  electric fish (Markham et al., 2009), Stimulates LH secretion and sex behavior in rats (Alde and Celis, 1980; Thody et al., 1981)
Cocaine and amphetamine-regulated transcript (CART) decreases food intake in fish (Volkoff et al., 2005), birds (Tachibana et al., 2003), rats (Kristensen et al., 1998) stimulates GnRH secretion in rats (Lebrethon et al., 2000; Parent et al., 2000)
Cholecystokinin (CCK) decreases food intake in fish (Himick and Peter, 1994; Volkoff et al., 2005), birds (Tachibana et al., 2012), rats (Gibbs et al., 1973) and food hoarding in Siberian hamsters (Bailey and Dela-Fera, 1995; Figlewicz et al., 1989; Teubner and Bartness, 2010) stimulates GnRH and LH secretion in rats (Ichimaru et al., 2003; Kimura et al., 1983)CCK in the medial preoptic areas is required for estradiol-induced lordosis in rats (Dornan et al., 1989; Holland et al., 1997)
Corticotropin releasing hormone (CRH) decreases food intake in fish (De Pedro et al., 1993; Matsuda et al., 2008), amphibians (Crespi et al., 2004), birds (Denbow et al., 1999; Furuse et al., 1997), rats (Heinrichs and Richard, 1999; Levine et al., 1983; Morley and Levine, 1982; Negri et al., 1985) and food hoarding in rats (Cabanac and Richard, 1995) reviewed by (Carr, 2002) inhibits spawning in fish (Mousa and Mousa, 2006), inhibits LH secretion and lordosis in rats (Olster and Ferin, 1987) and sex behavior in Syrian hamsters (Jones et al., 2002)
Dopamine (DA) decreases food intake in fish (Leal et al., 2013), rats (Heffner et al., 1977), increases food hoarding in rats (Borker and Mascarenhas, 1991; Kelley and Stinus, 1985), and reward (Wise, 2004) inhibits gonadotropin secretion in fish (Omeljaniuk et al., 1989), stimulates sexual arousal, motivation and reward in birds (Cornil et al., 2005), rats and hamsters (Agmo and Picker, 1990; Meisel and Mullins, 2006)
Glucagon-like peptide (GLP-I) decreases food intake in fish (Silverstein et al., 2001), birds (Tachibana et al., 2006), rats (Turton et al., 1996) stimulates LH secretion (Beak et al., 1998)
Gonadotropin releasing hormone (GnRH I or II) decreases food intake in fish (Hoskins et al., 2008; Nishiguchi et al., 2012), and female musk shrews (Kauffman and Rissman, 2004b) stimulates LH secretion in fish (Moussavi et al., 2012), birds (Chowdhury and Yoshimura, 2004), stimulates LH secretion and sex behavior in amphibians and reptiles (Alderete et al., 1980; Licht et al., 1984), rats and sheep and sex behavior in shrews and mice (Kauffman and Rissman, 2004a; Kauffman et al., 2005) (Temple et al., 2003) (Moss and McCann, 1975) (Clarke and Cummins, 1982)
Insulin-like Growth Factor -1 (IGF-I in CNS) ICV treatment decreases food intake in diabetic, but not normal rats (Lu et al., 2001), required for post-fast hyperphagia in rats (Todd et al., 2007) restores LH surge amplitude in middle-aged rats (Todd et al., 2010), required for the LH surge, estrous behavior, estrous cycles in rats (Etgen and Acosta-Martinez, 2003; Quesada and Etgen, 2002; Todd et al., 2007), and for sex behavior in rats (Etgen and Acosta-Martinez, 2003)
Kisspeptin decreases food intake in mice (Stengel et al., 2011) stimulates GnRH and LH secretion in fish (Moussavi et al., 2012; Tena-Sempere et al., 2012), stimulates testicular expression of ER-a in frogs (Chianese et al., 2013), rats (Gottsch et al., 2004; Irwig et al., 2004)
Norepinephrine decreases food intake in birds (Denbow, 1983) and stimulates food intake in rats (Ritter and Epstein, 1975) inhibits LH secretion in rats (Iwata et al., 2011), stimulates sex behavior in birds (Cornil et al., 2005) and rats (Nock and Feder, 1979)
Oxytocin decreases food intake in birds (Jonaidi et al., 2003), rats (Olson et al., 1991) stimulates GnRH and LH secretion sex behavior in rats (Rettori et al., 1997; Whitman and Albers, 1995)
Secretin decreases food intake in  rats (Cheng et al., 2011a) stimulates LH secretion in rats (Babu and Vijayan, 1983)
Serotonin (5HT) decreases food intake in birds (Denbow et al., 1982), rats (Blundell, 1977) stimulates LH in the presence of estradiol in rats (Coen and MacKinnon, 1979) Inhibits LH secretion in the absence of estradiol in rats (Coen et al., 1980) (Koh et al., 1984)
Thyrotropin releasing hormone decreases food intake in rats (Vijayan and McCann, 1977) and Siberian hamsters (Steward et al., 2003) stimulates LH secretion in pituitary in vitro not in vivo in rats (Fujihara and Shiino, 1983), and indirectly by effects on thyroid hormones in rats (Barrett et al., 2007)
Urocortin decreases food intake in fish, amphibians, birds, and rats (Spina et al., 1996) stimulates LH secretion in ewes (Holmberg et al., 2001), inhibits LH secretion in rats (Li et al., 2005; Nemoto et al., 2010), directly inhibits Leydig cell function in rats (Rivier, 2008)
Peripheral “Anorectic” Hormones Ingestive Effects Reproductive Effects
Adiponectin (adipocytes) decreases food intake in rats (Bassi et al., 2012), increases food intake in mice (Kubota et al., 2007), decreases body weight and increases energy expenditure, insulin sensitivity, and ffa oxidation without effect on food intake in rats (Fruebis et al., 2001; Qi et al., 2004) implicated in embryo implantation and fetal development in pigs and women (Palin et al., 2012), inhibits ovarian steroidogenesis in cows (Lagaly et al., 2008), inhibits GnRH and LH in rats and in GnRH cell cultures (Cheng et al., 2011b; Lu et al., 2008)
Adrenocorticotropic hormone (ACTH) decreases food intake in rats (Vergoni et al., 1986) stimulated LH secretion in female rats inhibits LH secretion in male rats (indirect via adrenals) (Mann et al., 1985; Putnam et al., 1991)
Bombesin (gut) decreases food intake in fish (Volkoff et al., 2005), birds (Savory and Hodgkiss, 1984; Tachibana et al., 2010), and rats (Gibbs et al., 1979) stimulates LH secretion in rats (Babu and Vijayan, 1983)
Cholecystokinin (gut) decreases food intake in fish (Volkoff et al., 2005), birds (Savory and Hodgkiss, 1984), and hoarding in Siberian hamsters (Gibbs et al., 1973; Qian et al., 1999; Teubner and Bartness, 2010) simulates LH secretion in rats (Perera et al., 1993); Inhibits lordosis duration in rats (Mendelson and Gorzalka, 1984), but see central effects in Table 1.1
Estradiol (gonads, adrenals, adipocytes, brain) decreases body weight and food intake in fish (Leal et al., 2009), lizards (Shanbhag and Prasad, 1992), obese but not lean hens (Jaccoby et al., 1995; Jaccoby et al., 1996), rats (Nunez et al., 1980; Roepke et al., 2010; Roy and Wade, 1977; Zucker, 1969) and food hoarding in Syrian hamsters (Klingerman et al., 2010) stimulates sexual receptivity and vitellogenesis and has negative feedback on LH in fish, frogs, lizards and birds (Chakraborty and Burmeister, 2009; Cheng, 1973; Crews, 1975; Gavaud, 1986; Gibbins and Robinson, 1982a, b; Licht et al., 1985; Liley, 1972; Mason and Adkins, 1976; McCreery and Licht, 1984; Redshaw et al., 1969; Shanbhag and Prasad, 1992; Yu et al., 1981), and stimulates LH surges in female rats (Chazal et al., 1974) and female sex behavior in rats (Dempsey et al., 1936; Powers, 1970), increases courtship and sexual behaviors in hamsters (Ciaccio and Lisk, 1973; Ciaccio et al., 1979; Takahashi et al., 1985)
Insulin (ICV treatment) decreases food intake in rats and baboons (Chavez et al., 1995; Woods et al., 1979) stimulates LH pulses in rats, pigs, and diabetic sheep and non diabetic ovariectomized sheep (Bucholtz et al., 2000; Cox et al., 1987; Daniel et al., 2000; Kovacs et al., 2003; Miller et al., 1995), inhibits LH in ad libitum-fed ovariectomized lambs (Hileman et al., 1993)
Insulin-like growth factor increases body weight gain at superphysiological concentrations (Gruaz et al., 1997) does not accelerate reproductive development in female rats (Gruaz et al., 1997)
Leptin (adipocytes, liver) decreases body weight, adiposity, and food intake in fish (Crespi and Denver, 2006; Murashita et al., 2008), and mice (Campfield et al., 1995; Halaas et al., 1995; Pelleymounter et al., 1995) and food hoarding in Syrian hamsters (Buckley and Schneider, 2003) while increasing energy expenditure mammalian leptin increases gonadotropin secretion in fish (Peyon et al., 2003; Peyon et al., 2001), delays the summertime regression of the testes in lizards (Putti et al., 2009), delays fasting-induced cessation of egg laying, follicular regression, and follicle wall apoptosis in chickens (Paczoska-Eliasiewicz et al., 2003), reverses the effects of metabolic challenges on gonadotropin secretion in mice (Ahima et al., 1996; Barash et al., 1996), estrous cycles, and steroid-induced sex behavior (the latter only in ad libitum fed female hamsters) (Schneider et al., 2007; Schneider et al., 1997; Wade et al., 1997)
Resistin transient decreases in food intake in rats (Tovar et al., 2005) promotes ovarian steroid secretion in rats (Maillard et al., 2011)

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