Academic Appointments

  • Basic Life Science Research Associate, Biology

Honors & Awards

  • Ruth Kirschstein National Research Service Award, National Institutes of Health (2012-2015)
  • National Science Foundation Graduate Research Fellowship, NSF (2004-2007)

Professional Education

  • Ph.D., University of California, San Francisco, Neuroscience (2010)
  • BS, University of Wisconsin-Madison, Zoology & Psychology (2001)

All Publications

  • Electrical synapses connect a network of gonadotropin releasing hormone neurons in a cichlid fish PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA Ma, Y., Juntti, S. A., Hu, C. K., Huguenard, J. R., Fernald, R. D. 2015; 112 (12): 3805-3810


    Initiating and regulating vertebrate reproduction requires pulsatile release of gonadotropin-releasing hormone (GnRH1) from the hypothalamus. Coordinated GnRH1 release, not simply elevated absolute levels, effects the release of pituitary gonadotropins that drive steroid production in the gonads. However, the mechanisms underlying synchronization of GnRH1 neurons are unknown. Control of synchronicity by gap junctions between GnRH1 neurons has been proposed but not previously found. We recorded simultaneously from pairs of transgenically labeled GnRH1 neurons in adult male Astatotilapia burtoni cichlid fish. We report that GnRH1 neurons are strongly and uniformly interconnected by electrical synapses that can drive spiking in connected cells and can be reversibly blocked by meclofenamic acid. Our results suggest that electrical synapses could promote coordinated spike firing in a cellular assemblage of GnRH1 neurons to produce the pulsatile output necessary for activation of the pituitary and reproduction.

    View details for DOI 10.1073/pnas.1421851112

    View details for Web of Science ID 000351477000061

    View details for PubMedID 25775522

  • Tol2-Mediated Generation of a Transgenic Haplochromine Cichlid, Astatotilapia burtoni PLOS ONE Juntti, S. A., Hu, C. K., Fernald, R. D. 2013; 8 (10)
  • Sexually Dimorphic Neurons in the Ventromedial Hypothalamus Govern Mating in Both Sexes and Aggression in Males CELL Yang, C. F., Chiang, M. C., Gray, D. C., Prabhakaran, M., Alvarado, M., Juntti, S. A., Unger, E. K., Wells, J. A., Shah, N. M. 2013; 153 (4): 896-909


    Sexual dimorphisms in the brain underlie behavioral sex differences, but the function of individual sexually dimorphic neuronal populations is poorly understood. Neuronal sexual dimorphisms typically represent quantitative differences in cell number, gene expression, or other features, and it is unknown whether these dimorphisms control sex-typical behavior exclusively in one sex or in both sexes. The progesterone receptor (PR) controls female sexual behavior, and we find many sex differences in number, distribution, or projections of PR-expressing neurons in the adult mouse brain. Using a genetic strategy we developed, we have ablated one such dimorphic PR-expressing neuronal population located in the ventromedial hypothalamus (VMH). Ablation of these neurons in females greatly diminishes sexual receptivity. Strikingly, the corresponding ablation in males reduces mating and aggression. Our findings reveal the functions of a molecularly defined, sexually dimorphic neuronal population in the brain. Moreover, we show that sexually dimorphic neurons can control distinct sex-typical behaviors in both sexes.

    View details for DOI 10.1016/j.cell.2013.04.017

    View details for Web of Science ID 000318844000017

    View details for PubMedID 23663785

  • Tol2-mediated generation of a transgenic haplochromine cichlid, Astatotilapia burtoni. PloS one Juntti, S. A., Hu, C. K., Fernald, R. D. 2013; 8 (10)


    Cichlid fishes represent one of the most species-rich and rapid radiations of a vertebrate family. These ∼2200 species, predominantly found in the East African Great Lakes, exhibit dramatic differences in anatomy, physiology, and behavior. However, the genetic bases for this radiation, and for the control of their divergent traits, are unknown. A flood of genomic and transcriptomic data promises to suggest mechanisms underlying the diversity, but transgenic technology will be needed to rigorously test the hypotheses generated. Here we demonstrate the successful use of the Tol2 transposon system to generate transgenic Astatotilapia burtoni, a haplochromine cichlid from Lake Tanganyika, carrying the GFP transgene under the control of the ubiquitous EF1α promoter. The transgene integrates into the genome, is successfully passed through the germline, and the widespread GFP expression pattern is stable across siblings and multiple generations. The stable inheritance and expression patterns indicate that the Tol2 system can be applied to generate A. burtoni transgenic lines. Transgenesis has proven to be a powerful technology for manipulating genes and cells in other model organisms and we anticipate that transgenic A. burtoni and other cichlids will be used to test the mechanisms underlying behavior and speciation.

    View details for DOI 10.1371/journal.pone.0077647

    View details for PubMedID 24204902

  • The androgen receptor governs execution but not programming of male sexual and territorial behaviors NEURON Juntti, S. A., et al 2010; 66: 260-272
  • A genetic approach to dissect sexually dimorphic behaviors HORMONES AND BEHAVIOR Juntti, S. A., Coats, J. K., Shah, N. M. 2008; 53 (5): 627-637


    It has been known since antiquity that gender-specific behaviors are regulated by the gonads. We now know that testosterone is required for the appropriate display of male patterns of behavior. Estrogen and progesterone, on the other hand, are essential for female typical responses. Research from several groups also indicates that estrogen signaling is required for male typical behaviors. This finding raises the issue of the relative contribution of these two hormonal systems in the control of male typical behavioral displays. In this review we discuss the findings that led to these conclusions and suggest various genetic strategies that may be required to understand the relative roles of testosterone and estrogen signaling in the control of gender-specific behavior.

    View details for DOI 10.1016/j.yhbeh.2007.12.012

    View details for Web of Science ID 000256283100004

    View details for PubMedID 18313055