The University of Illinois at Urbana-Champaign
407 South Goodwin Avenue, 427 Burrill Hall
Learning, memory, and plasticity
Psychiatric and neurological illness
Activity-dependent regulation of GIRK and Kv7 potassium channels and their impacts on homeostatic plasticity and epileptogenesis:
Homeostatic plasticity maintains neuronal firing and synaptic strength within physiological limits and is how neurons cope with loss or increase in activity. Although much has been learned about homeostatic synaptic plasticity, much less is known about homeostatic intrinsic excitability, including the molecular mechanism mediating this plasticity. My first project was to examine how high-frequency epileptic seizures dysregulate G protein-activated inward rectifying potassium channels (GIRK). We found that prolonged seizures induce caspase3-dependent cleavage of GIRK subunits, leading to a loss of surface expression and current and a reduction in binding to Gβγ which is critical for gating (Baculis et al.,2017). My current project is to examine activity-dependent regulation of Kv7 and NaV channels at the axonal initial segment (AIS), the key site for action potential generation. Our lab has previously found that with chronic activity blockade there is a downregulation of potassium channel genes as well as an increase in intrinsic excitability or the likelihood to fire action potential given a certain current injection. I am currently using immunohistochemistry and high-resolution imaging to examine Kv7 and NaV at the AIS during homeostatic scaling of intrinsic excitability in hippocampal neuron in dissociated and organotypic slice culture. I am also developing a novel transgenic mouse line in which activity blockade can be inducible in forebrain excitatory neurons.
2004 to 2008: Watchung Hills Regional High School – Graduated with Honors
2008 to 2013: Temple University – B.S., Neuroscience, minor in psychology
2016 to present: University of Illinois at Urbana-Champaign – Neuroscience graduate program
Awards and Honors
National Science Foundation Research Traineeship program
NRT-UtB: Training the Next Generation of Researchers in Engineering and Deciphering of Miniature Brain Machinery (MBM), University of Illinois at Urbana-Champaign
TA: MCB 461 Cell & Molecular Neuroscience
1. Baculis, B., Diaz, M. and Fernando Valenzuela, C. (2015). Third trimester-equivalent ethanol exposure increases anxiety-like behavior and glutamatergic transmission in the basolateral amygdala. Pharmacology Biochemistry and Behavior, 137, pp.78-85.
2. Topper, L., Baculis, B. and Valenzuela, C. (2015). Exposure of neonatal rats to alcohol has differential effects on neuroinflammation and neuronal survival in the cerebellum and hippocampus. Journal of Neuroinflammation, 12(1).
3. Baculis, B. and Valenzuela, C. (2015). Ethanol exposure during the third trimester equivalent does not affect GABAA or AMPA receptor-mediated spontaneous synaptic transmission in rat CA3 pyramidal neurons. Journal of Negative Results in BioMedicine, 14(1).
4. Welch, J., Mayfield, J., Leibowitz, A., Baculis, B. and Valenzuela, C. (2016). Third trimester-equivalent ethanol exposure causes micro-hemorrhages in the rat brain. Neuroscience, 324, pp.107-118.
5. Baculis, B., Weiss, A., Pang, W., Jeong, H., Lee, J., Liu, D., Tsai, N. and Chung, H. (2017). Prolonged seizure activity causes caspase dependent cleavage and dysfunction of G-protein activated inwardly rectifying potassium channels. Scientific Reports, 7(1).
6. Bird, C., Baculis, B., Mayfield, J., Chavez, G., Ontiveros, T., Paine, D., Marks, A., Gonzales, A., Ron, D. and Valenzuela, C. (2018). The brain-derived neurotrophic factor VAL68MET polymorphism modulates how developmental ethanol exposure impacts the hippocampus. Genes, Brain and Behavior, p.e12484.