Hablitz Named Interim Chair
John J. Hablitz, longtime professor in the UAB School of Medicine, has been named interim chair of the Department of Neurobiology.
“I am honored to have the opportunity to serve as interim chair for the outstanding members of the Neurobiology Department,” Hablitz said.
J. David Sweatt, Ph.D., who has served as Neurobiology department chair the past 10 years, will leave UAB to chair the Department of Pharmacology at Vanderbilt University. Hablitz previously served as interim department chair before Sweatt joined UAB in early 2006. The search for a permanent chair will begin this fall.
“Dr. Hablitz brings a wealth of experience to this interim role, based on his more than 25 years here at UAB,” said Selwyn M. Vickers, M.D., senior vice president for Medicine and dean of the UAB School of Medicine.
Hablitz is a highly regarded scientist in the cellular neurophysiology of epilepsy and synaptic plasticity. His lab uses studies on synaptic transmissions to further understand basic biophysical properties of mammalian central neurons and to explore the pathophysiology of experimental epilepsy.
Hablitz came to UAB in 1989 as a professor of Physiology and Biophysics, and has been a professor and vice chair in the Department of Neurobiology since the department was founded in 1996. He holds additional secondary appointments in the Departments Cell, Developmental and Integrative Biology and Psychology, as well as roles in the UAB Civitan International Research Center, General Clinical Research Center and the Center for Glial Biology in Medicine.
He earned his undergraduate degree from the State University of New York at Plattsburgh in 1968 and his masters (1970) and doctorate (1972) degrees in psychology from the University of Houston before completing postdoctoral training in neurophysiology at the Baylor College of Medicine. He joined the faculty at Baylor in 1974, where he stayed until joining UAB in 1989.
Wadiches Win Mentoring Award
The Graduate Dean’s Excellence
in Mentorship Award recognizes full-time regular UAB faculty members who have demonstrated exceptional commitment as mentors of graduate students and / or postdoctoral fellows.
Susan Bellis, Cell, Developmental, and Integrative Biology
Elizabeth Brown, Pathology
Yabing Chen, Pathology
Deek Cunningham, Occupational Therapy
Jeffrey Engler, Associate Dean, Graduate School
Candace Floyd, Physical Medicine and Rehabilitation
Stuart Frank, Medicine
Amit Gaggar, Medicine
William Geisler, Medicine
Eugenia Kharlampieva, Chemistry
Jacqueline Moss, Nursing
Lisa Schwiebert, Associate Dean, Postdoctoral Education
Jacques Wadiche, Neurobiology
Linda Overstreet Wadiche, Neurobiology
J. Michael Wyss, Cell, Developmental, and Integrative Biology
eBook from Frontiers in Neuroscience
Frontiers in Neuroscience
Wei Li & Xin Xu Published in PNAS
Excitatory synapses are stronger in the hippocampus of Rett syndrome mice due to altered synaptic trafficking of AMPA-type glutamate receptors
Wei Li, Xin Xu, and Lucas Pozzo-Miller
Rett syndrome is the most common intellectual disability in women after Down syndrome (1:10,000 incidence). Different mouse models of intellectual disability and autism exhibit deficits in synaptic plasticity, including impaired long-term potentiation (LTP) in mice lacking methyl-CpG-binding protein 2 (MeCP2); however, the bases of this deficit remain unclear. Using a combination of electrophysiology, time-lapse imaging, cell biology, and biochemistry, we provide direct evidence that naïve hippocampal synapses in Rett mice have all the hallmarks of potentiated synapses. Rett synapses also fail to insert and remove AMPA receptors properly to activated synapses, which freezes them in a nonplastic state. Our findings provide molecular, cellular, and network mechanisms underlying enhanced excitatory synaptic transmission and impaired LTP in Rett mice, identifying previously unidentified molecular targets for therapeutic intervention.
AbstractDeficits in long-term potentiation (LTP) at central excitatory synapses are thought to contribute to cognitive impairments in neurodevelopmental disorders associated with intellectual disability and autism. Using the methyl-CpG-binding protein 2 (Mecp2) knockout (KO) mouse model of Rett syndrome, we show that naïve excitatory synapses onto hippocampal pyramidal neurons of symptomatic mice have all of the hallmarks of potentiated synapses. Stronger Mecp2 KO synapses failed to undergo LTP after either theta-burst afferent stimulation or pairing afferent stimulation with postsynaptic depolarization. On the other hand, basal synaptic strength and LTP were not affected in slices from younger presymptomatic Mecp2 KO mice. Furthermore, spine synapses in pyramidal neurons from symptomatic Mecp2 KO are larger and do not grow in size or incorporate GluA1 subunits after electrical or chemical LTP. Our data suggest that LTP is occluded in Mecp2 KO mice by already potentiated synapses. The higher surface levels of GluA1-containing receptors are consistent with altered expression levels of proteins involved in AMPA receptor trafficking, suggesting previously unidentified targets for therapeutic intervention for Rett syndrome and other MECP2-related disorders.
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Cell Reports - Kavitha Abiraman