Post-Docs: Jonathan W. Lovelace
Phone: 827-5900 Lab
My research has primarily focused on investigating neurological disorders using both genetic and pharmacological animal models. I am particularly interested in how pathological brain development and neural plasticity can contribute to disorders such as schizophrenia and Fragile X syndrome.
I am currently involved in a project to develop electrophysiological biomarkers in an animal model of Fragile X syndrome (FXS) for translational use in preclinical drug trials. In the lab I utilize methodology for recording and analyzing auditory evoked event related potentials (ERPs) in the cortex of both anesthetized and awake behaving animals. Deficits in auditory processing and hyper sensitivity to sound stimuli are my main focuses of research. The ultimate goal is to develop drug treatment regimens that target various signaling pathways in the brain in order to ameliorate auditory hypersensitivity. The results of our research will then translate directly into clinical trials in patients with FXS.
My dissertation work focused on endocannbinoid (eCB) and behavioral abnormalities in developmental animal models of schizophrenia and adolescent cannabinoid abuse. Endocannbinoid signaling in the brain is known to be important for development of cortical circuits and seems to be particularly vulnerable in the prefrontal cortex during development. The interaction between temporary disruption of plasticity early in development and adolescence may lead to permanent cortical deficits in adult life. This indicates the importance of early intervention in schizophrenia and also eCB signaling as a possible target for new drug therapies as well as growing concerns regarding cannabis abuse in vulnerable individuals during adolescent development.
Matrix metalloproteinase-9 deletion rescues auditory evoked potential habituation deficit in a mouse model of Fragile X Syndrome
Lovelace, J.W., Wen, T., Reinhard, S., Hsu, M.S., Sidhu, H., Ethell, I.M., Binder, D.K., Razak, K.A. (in preparation)
An animal model of female adolescent cannabinoid exposure elicits a long-lasting deficit in presynaptic long-term plasticity.
Lovelace, J.W., Corches, A., Vieira, P.A., Hiroto, A.S., Mackie, K., Korzus, E. 2015. Neuropharmacology. Vol. 99 p 242-255.
Impaired Fear Memory Specificity Associated with Deficient Endocannabinoid-Dependent Long-Term Plasticity.
Lovelace, J.W., Vieira, P.A., Corches, A., Mackie, K., Korzus, E. 2014. Neuropsychopharmacology. Vol. 39: 28p
Prefrontal NMDA receptors gate discriminatory fear learning.
Vieira, P.A., Corches, A., Lovelace, J.W., Westbrook, K.B., Mendoza, M., Korzus, E. 2014 Neurobiology of Learning and Memory. Vol. 119 p 52-62.
Prefrontal consolidation supports the attainment of fear memory accuracy.
Vieira, P., Lovelace, J.W., Corches, A., Rashid, A.J., Josselyn, S.A., Korzus, E. 2014. Learning & Memory. Vol. 21: 8 p.394-405.