Dr. Veenema’s research uses mice and rats to examine the roles of vasopressin and oxytocin in regulating social behavior (social play, social recognition, social novelty, social reward) and how sex, age, and early life stress modulate social behavior. The Veenema lab employs a combination of behavioral, molecular, biochemical, and pharmacological techniques to shed light on normal and abnormal human social functioning as observed in autism spectrum disorder, borderline personality disorder, antisocial personality disorder, and schizophrenia.
Veenema is a referee of more than 25 international journals and a member of the Society for Neuroscience, the Federation of European Neuroscience Societies, Society for Behavioral Neuroendocrinology, the Society for Social Neuroscience, the Organization for the Study of Sex Differences, and the International Behavioral Neuroscience Society. She serves on the editorial board of the journals Hormones and Behavior and Social Neuroscience, is a review editor for the journals Frontiers in Behavioral Neuroscience and Frontiers in Endocrinology, and serves as secretary and treasurer for the Society for Social Neuroscience.
Veenema is Associate Professor in Behavioral Neuroscience in the Department of Psychology & Neuroscience at Michigan State University. She studied Biology (specialization in Neuroscience) at the University of Groningen, the Netherlands. In 2003 she received her PhD in Neuroscience at the University of Groningen, The Netherlands with Dr. Jaap M. Koolhaas and Dr. E. Ron de Kloet as her advisors. She did post-doctoral work in the labs of Dr. Inga D. Neumann at the University of Regensburg in Germany and Dr. Geert de Vries at the University of Massachusetts at Amherst. In 2010, she was appointed Assistant Professor in the Department of Psychology at Boston College and received tenure and was promoted to Associate Professor in 2016. Dr. Veenema was recruited by Michigan State University in 2017.
During her PhD, Alexa was supported by a stipend from the Netherlands Organization for Scientific Research. She received two postdoctoral stipends from the Bavarian Research Foundation (Bayerische Forschungsstiftung) and an international research fellowship from the German Research Foundation (Deutsche Forschungsgemeinschaft), and was awarded a NARSAD 2010 Young Investigator Grant from the Brain and Behavior Research Foundation and an NSF Career Award in 2013. Her lab is currently funded by NSF and NIMH.
Industry Expertise (1)
Areas of Expertise (6)
University of Groningen, the Netherlands: MSc, Biology (Neuroscience concentration) 1997
University of Groningen, the Netherlands: PhD, Behavioral Neuroscience 2003
University of Regensburg, Germany: postdoctoral fellow
University of Massachusetts, Amherst: postdoctoral fellow
Dr. Alexa Veenema won the 2019 Undergraduate Research Faculty Mentor of the Year Award for MSU
Michigan State University online
Dr. Alexa Veenema, associate professor of behavioral neuroscience, won the 2019 Undergraduate Research Faculty Mentor of the Year Award for Michigan State University. This annual award recognizes faculty who have demonstrated an outstanding commitment to mentoring undergraduate researchers.
Recent Grants Strengthen Psychology's Focus on Research
The Boston College Chronicle
Assistant Professor Alexa Veenema is the recipient of a five-year National Institutes of Health RO1 award of $1.7 million. The grant will enable her to study the neural circuits underlying social play behavior in juvenile rats and how these neural circuits differ between males and females. Social play is a highly rewarding behavior and has been shown to be important for the development of social skills in humans and rodents, Veenema explained.
The Making of a Bully
The stress protocol only seemed to bear long-term effects in young adolescent rats, however; the same stress protocol on healthy adult rats, failed to produce similar behavioral changes. This suggests that trauma incurred early in life, but not in adulthood, can deeply interfere with the neural programming and physiology, thereby setting the stage for aggressive manifestations in adult life. “These findings are in line with and extend further those using other rodent and non-human primate models in which early life stress, as opposed to stress in adulthood, can cause long-lasting increases in aggressive behaviors,” neuroscientist Alexa Veenema of Boston College wrote in an e-mail.
Journal Articles (3)
Nicholas B. Worley, Kelly M. Dumais, Jingting C. Yuan, Laura E. Newman, Andrea G. Alonso, Tessa C. Gillespie, Nicholas J. Hobbs, S. Marc Breedlove, Cynthia L. Jordan, Remco Bredewold, Alexa H. Veenema
Oxytocin (OT) often regulates social behaviours in sex‐specific ways, and this may be a result of sex differences in the brain OT system. Adult male rats show higher OT receptor (OTR) binding in the posterior bed nucleus of the stria terminalis (pBNST) than adult female rats. In the present study, we investigated the mechanisms that lead to this sex difference. First, we found that male rats have higher OTR mRNA expression in the pBNST than females at postnatal day (P) 35 and P60, which demonstrates the presence of the sex difference in OTR binding density at message level. Second, the sex difference in OTR binding density in the pBNST was absent at P0 and P3, but was present by P5. Third, systemic administration of the oestrogen receptor (ER) antagonist fulvestrant at P0 and P1 dose‐dependently reduced OTR binding density in the pBNST of 5‐week‐old male rats, but did not eliminate the sex difference in OTR binding density. Fourth, pBNST‐OTR binding density was lower in androgen receptor (AR) deficient genetic male rats compared to wild‐type males, but higher compared to wild‐type females. Finally, systemic administration of the histone deacetylase inhibitor valproic acid at P0 and P1 did not alter pBNST‐OTR binding density in 5‐week‐old male and female rats. Interestingly, neonatal ER antagonism, AR deficiency, and neonatal valproic acid treatment each eliminated the sex difference in pBNST size. Overall, we demonstrate a role for neonatal ER and AR activation in setting up the sex difference in OTR binding density in the pBNST, which may underlie sexual differentiation of the pBNST and social behaviour.
Caroline J.W. Smith, Brett T. DiBenedictis, Alexa H. Veenema
Vasopressin (AVP) and oxytocin (OXT) regulate social behavior by binding to their canonical receptors, the vasopressin V1a receptor (V1aR) and oxytocin receptor (OTR), respectively. Recent studies suggest that these neuropeptides may also signal via each other’s receptors. The extent to which such cross-system signaling occurs likely depends on anatomical overlap between AVP/OXT fibers and V1aR/OTR expression. By comparing AVP/OXT fiber densities with V1aR/OTR binding densities throughout the rat social behavior neural network (SBNN), we propose the potential for cross-system signaling in four regions: the medial amygdala (MeA), bed nucleus of the stria terminalis (BNSTp), medial preoptic area, and periaqueductal grey. We also discuss possible implications of corresponding sex (higher in males versus females) and age (higher in adults versus juveniles) differences in AVP fiber and OTR binding densities in the MeA and BNSTp. Overall, this review reveals the need to unravel the consequences of potential cross-system signaling between AVP and OXT systems in the SBNN for the regulation of social behavior.
Remco Bredewold, Nara F. Nascimento, Grace S. Ro, Shannon E. Cieslewski, Christina J. Reppucci & Alexa H. Veenema
Social play is a highly rewarding behavior displayed mostly during the juvenile period. We recently showed that vasopressin V1a receptor (V1aR) blockade in the lateral septum (LS) enhances social play in male juvenile rats, but reduces it in females. Here, we determined whether the LS-AVP system modulates dopamine (DA) and/or norepinephrine (NE) neurotransmission in the LS to regulate social play behavior in sex-specific ways. Using microdialysis combined with retrodialysis, we demonstrated that both LS-AVP administration and social play exposure increased extracellular LS-DA release in females, but not in males. Pharmacological blockade of LS-DA receptors reduced social play in both sexes, but required a higher dose in females. This suggests that baseline LS-DA release is sufficient for social play in males, while increased LS-DA release is necessary for social play in females. Administration of a V1aR antagonist into the LS inhibited the social play-induced increase in extracellular LS-DA release in females. Furthermore, co-administration of the DA agonist apomorphine prevented the LS-V1aR blockade-induced decrease in social play in females. This suggests that LS-V1aR blockade reduces social play in females by dampening the rise in LS-DA release. Extracellular LS-NE release was enhanced in response to pharmacological manipulations of the LS-AVP system and to social play in males and/or females, but pharmacological blockade or stimulation of LS-NE receptors did not alter social play in either sex. Overall, we define a mechanism by which the LS-AVP system alters LS-DA neurotransmission differently in males than females resulting in the sex-specific regulation of juvenile social play behavior.