ORTIZ LAB
Behavioral Neuroscience Lab



our goals
The goal of our research is to examine how mechanisms (oxytocin, vasopressin, and other neurotransmitters) regulate social behavior. We accomplish this by integrating microfluidics (brain-on-chip) technology. We can keep brain slices alive on a 3D printed chip and examine neural activity when given a specific neurotransmitter/drug. The animal models we use are the prairie vole and mice.

microfluidics
[ mahy-kroh-floo-id-iks ]
noun
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the science of the behavior of fluids at very small volumes or flowing in very small channels typically measured in tens of micrometers, as in microminiaturized devices: used in many technologies, including those involved in DNA analysis, immunoassays, chemical synthesis, and optics.
e keep a slice of brain tissue alive and examine activity via ex vivo calcium imaging
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Current Research Projects
Oxytocin (OT) signaling in the endopiriform nucleus (EPN)
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The EPN is a region not well studied, that contributes to sensory social integration. The disruption of the processes responsible for integrating and processing social stimuli is involved in various behavioral disorders, including autism and schizophrenia. OT has been shown to play a role in sensory-social integration. The EPN is rich in OT receptors and we wish to examine a dose-dependent function of OT within the EPN, with and without the function of oxytocin receptor. We can do this by chemically silencing OT receptor function, while administering OT..and observe brain slice activation.
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Drug-Interaction Dynamics
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With our brain-on-a-chip technology, we can examine how practically any substance activates (or silences) any brain region. We are interested in measuring the brain activity of a region responsible for reward, the nucleus accumbens (Nac). We wish to examine how the nonapeptide, dopamine, changes NAc activity over time. We have the power to keep the brain alive in our chip for over 10+ hours (for now) and can see if there is a phasic-shift in the regulation of dopamine receptors.​
Nature vs. Nurture​
We have an animal model that shows differences in social behavior based on parental population. We have crossbred KS and IL voles and noticed that hybrid offspring follow a specific pattern of social behavior (for example, male hybrids with a less social mom and a more social dad follow the mom's behavior/neural patterning). We can harness this information and use it to examine the role of nature and nurture in regions critical for social behavior.
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Light Sheet Microscope Fabrication
Light sheet microscopy (LSM), also known as selective plane illumination microscopy (SPIM), is an advanced imaging technique that enables high-resolution, three-dimensional visualization of biological samples with minimal phototoxicity. Unlike traditional fluorescence microscopy, which illuminates the entire sample, LSM uses a thin sheet of light to selectively excite fluorophores in a single plane, reducing photobleaching and improving optical sectioning. This approach allows for rapid imaging of live specimens over extended periods, making it particularly valuable for developmental biology, neuroscience, and tissue engineering. We are making a light sheet microscope using 3D printed parts and open-source tools.​
Endocannabinoidome and Circadian Rythm
Alzheimer’s disease (AD) is a progressive neurodegenerative disorder marked by β-amyloid accumulation, neuroinflammation, calcium dysregulation, and widespread circadian rhythm disruption, with growing evidence suggesting these processes interact early in disease progression. The suprachiasmatic nucleus (SCN), the brain’s master circadian clock, relies on tightly regulated calcium oscillations and CLOCK gene activity, both of which are impaired in AD and may contribute to sleep and homeostatic dysfunction. Microglia, the brain’s innate immune cells, respond to AD pathology by adopting disease-associated states that can both clear amyloid and exacerbate neurodegeneration through excessive inflammation and phagocytosis. Components of the endocannabinoidome are expressed in the SCN and microglia, and are implicated in AD pathology. This project examines how endocannabinoid metabolites and inflammation interact to alter the SCN and help identify potential mechanistic links relevant to AD progression.
