Ivett Gabriella, Ph.D., M.A.

I’m Ivett Gabriella, an assistant professor of Psychology at Moreno Valley College. I currently teach Biopsychology (PSYC-2), Introduction to Psychology (PSYC-1), and the Psychology of Human Sexuality (PSYC-11).
I’m originally from Hungary 🇭🇺 and moved to the U.S 🇺🇸. when I was 19 years old to work as a babysitter. My path in higher education has been anything but traditional, which is why I understand that everyone’s journey looks different. I started studying Psychology 𝚿 at Coastline Community College, where I earned my A.A. degree and completed a transfer program. From there, I transferred to California State University, Dominguez Hills (CSUDH), and finally earned my bachelor’s degree at the age of 36. I then continued on to complete a master’s degree in Clinical Psychology at CSUDH.
While completing my studies, I discovered a passion for understanding the brain mechanisms 🧠 that shape behavior, which led me to pursue a Ph.D. in Psychology at the University of California, Riverside, with a focus on behavioral neuroscience. My research explores the neural circuits involved in eating behavior, hunger, satiation, body-weight regulation, and the neurotransmitter systems that influence these processes. I work with rat models and have published research on how different brain regions—including the lateral septum, septohypothalamic nuclei, and lateral hypothalamus—modulate feeding behavior.
Outside the classroom, I love gardening 🌿 and caring for my houseplants—it’s my way of slowing down and staying grounded. I find a lot of joy in watching things grow. Just like plants, every student learns and thrives at their own pace, and I enjoy creating an environment where you can explore, ask questions, and develop your strengths as you grow.

Research

CURRENT PROJECT___PAST PROJECTS:Receptor-Specific Modulation of Feeding Circuits: GABAergic and Glutamatergic Control Across the Lateral Septum, Septohypothalamic Nuclei, and Lateral Hypothalamus
A Dissertation submitted in partial satisfaction of the requirements for the degree of Doctor of Philosophy
in Psychology by Ivett Gabriella March 2026Link: https://escholarship.org/content/qt20w8d6q2/qt20w8d6q2.pdfConcerns over current rates of obesity and eating disorders warrant investigations of brain circuits controlling feeding. Three related studies examined roles of GABAergic and glutamatergic receptors in feeding in the lateral septum (LS), the septohypothalamic nuclei (SHy), and the lateral hypothalamus (LH).
The first one tested whether Gamma-aminobutyric acid (GABA) receptors in the LS modulate intake. Using microinjections, activation of LS GABAA receptors with muscimol and GABAB receptors with baclofen produced robust, dose-dependent feeding, while GABA receptor antagonists blocked these effects. In addition, Picrotoxin administered at the onset of the dark phase—when rats naturally eat more—reduced spontaneously occurring nocturnal feeding, whereas 2-OH saclofen did not. These results indicate that activation of LS GABAA and GABAB receptors strongly stimulates feeding and suggest endogenous LS GABA acting at GABAA receptors contributes to naturally occurring nocturnal feeding.
The second study explored the understudied SHy region. Adult male rats received central injections of GABAA antagonists (bicuculline or picrotoxin), the GABAB antagonist 2-OH saclofen, or vehicle, with food/water intake and behaviors recorded. Bicuculline and picrotoxin increased food intake during the 2nd and 3rd hours post-injection, while 2-OH saclofen increased intake at 1 hour. All three drugs suppressed resting and increased locomotor activity, indicating heightened arousal. Findings suggest that antagonism of GABAA or GABAB receptors in SHy elicits delayed feeding and increases general arousal, implicating SHy GABA-responsive neurons in feeding neurocircuitry.
The third study examined functional interactions between LS and LH using bilateral cannulas and combinations of GABAergic and glutamatergic agonists/antagonists. LH drug administration (bilateral or contralateral) strongly suppressed feeding induced by LS, while ipsilateral LH injections produced only moderate suppression. Conversely, LS injections could not suppress LH-induced feeding. Results imply LH signals can override LS-initiated feeding, positioning the LH downstream of the LS, potentially via indirect and contralateral pathways.
Collectively, these studies identify GABAergic mechanisms in LS and SHy and LS–LH connectivity as key elements of feeding control circuits. This study provides receptor-specific insights into the septohypothalamic circuit.
___GABA Receptor Antagonism Elicits Feeding in the Septohypothalamic NucleusLink: https://www.frontiersin.org/journals/behavioral-neuroscience/articles/10.3389/fnbeh.2025.1633659/fullCurrent rates of obesity and eating disorders have been steadily increasing, highlighting the importance of understanding the neural circuits of eating. This study explores the potential role of an understudied brain region, the Septohypothalamic Nucleus (SHy), in feeding control. Based on a serendipitous observation, we hypothesized that central injections of GABAA and GABAB antagonists in the SHy would elicit feeding. Adult male Sprague-Dawley rats (n = 39) were microinjected with a vehicle or GABAA receptor antagonists (bicuculline or picrotoxin) or a GABAB receptor antagonist (2-(S)-(+)-2-hydroxy-saclofen [2-OH saclofen]). Food and water intakes were measured 1, 2, 3, and 24 hours after injection, and behavioral responses (sleeping, resting, locomotor and vigorous activity, grooming, eating, drinking) were measured for 1 hour. Results showed increased food intake after bicuculline (p < 0.001) and picrotoxin (p = 0.03) injections during the 2nd and 3rd hours compared to controls. In addition, we found increased food intake 1 hour after 2-OH saclofen injections (p < 0.001). As for other behaviors, all three of the drugs suppressed resting (bicuculline: p < 0.001; picrotoxin < 0.001; 2-OH saclofen: p < 0.01) and increased locomotor activity (bicuculline: p < 0.001; picrotoxin < 0.001; 2-OH saclofen: p = 0.02). Our findings suggest that GABAA or GABAB receptor deactivation by antagonists elicited eating with a delayed effect and increased general arousal in rats. These findings collectively suggest that SHy neurons expressing GABAA and/or GABAB receptors are elements of a neurocircuit that participates in the regulation of feeding.
Keywords: GABA receptors, Septohypothalamuc nuclei, SHy, feeding, eating___Stimulation of GABA Receptors in the Lateral Septum Rapidly Elicits Food Intake and Mediates Natural FeedingLink: https://www.mdpi.com/2076-3425/12/7/848?utmcampaign=releaseissuebrainsciutmmedium=emailutmsource=releaseissueutm_term=titlelink9This study explored the roles of gamma-aminobutyric acid (GABA) receptors within the LS in the control of food intake. Experiments with a rat model (n ≥ 11/group) showed that LS microinjection of the GABAA receptor agonist, muscimol, and the GABAB receptor agonist, baclofen hydrochloride (baclofen), elicited intense, dose-dependent feeding. In contrast, LS pretreatment with the GABAA receptor antagonist, picrotoxin, markedly reduced the muscimol-elicited feeding, and pretreatment injections with the GABAB receptor antagonist, 2-hydroxysaclofen (2-OH saclofen), reduced the baclofen evoked response. Next, we showed that picrotoxin injection at the beginning of the dark phase of the light-dark cycle—when rats show a burst of spontaneous eating—reduced naturally occurring feeding, whereas 2-OH saclofen was ineffective. These results indicate that the activation of LS GABAA and GABAB receptors strongly stimulates feeding and suggests potential roles in feeding control neurocircuitry. In particular, our evidence indicates that endogenous LS GABA and GABAA receptors may be involved in mediating naturally occurring nocturnal feeding.
Keywords: eating; feeding; lateral septum; gamma-aminobutyric acid; GABA receptors; rat model; central injections
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curriculum vitae

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Contact

Ivett Gabriella
University of California, Riverside
Psychology Department
Office Location: LSB 1526
900 University Ave, Riverside, CA
92521