Ph.D., University of Rochester
M.S., University of Rochester
B.S., Cornell University
Dr. Eileen Lynd-Balta is a neuroscientist whose research focuses on elucidating neurochemical profiles in the brain. Her main research interest is to characterize alterations in the hippocampal formation associated with temporal lobe epilepsy.
Dr. Lynd-Balta's main research interest is to characterize changes in the hippocampal formation associated with temporal lobe epilepsy. This includes looking at patterns of cell loss and synaptic reorganization.
Human epidemiological studies suggest that a neurological insult (febrile seizure, head trauma, infection, or an ischemic event) before the sixth year of life, predisposes a subset of the population to the subsequent development of intractable seizures. Following the insult, alterations occur during a latency period, and it is these changes that cause the development of epileptogenic networks in the brain. Our research goal is to elucidate underlying mechanisms of altered brain structure and function and use that knowledge for therapeutic and/or preventative measures to maintain the integrity of vulnerable neural circuits. Aberrant glutamatergic neurotransmission has been implicated as a putative cause in the genesis and maintenance of TLE. Using sclerotic hippocampal specimens procured from children with TLE, we showed that glutamate receptor up-regulation precedes mossy fiber sprouting (Lynd-Balta et al., 2004). Our interest in the glutamatergic neurons affected in epileptic seizures prompted studies in the kainate model of epilepsy to localize COX-2 immunoreactivity. In particular, we are examining the role inflammation may play in the degenerative changes associated with epilepsy. Marked enhanced COX-2 protein immunostaining was found primarily in olfactory-limbic regions and we were able to characterize a neuroanatomical seizure substrate extending from the olfactory bulb to the entorhinal cortex and hippocampus (Joseph et al., 2006). Along with glutamate neurotransmission, ATP is co-released from synaptic terminals and can act as a chemical messenger by binding to one of many purinergic receptor subtypes, i.e. P2X and P2Y. Glia can exert a powerful influence on neural activity and integrity. We were the first to localize P2X7 receptor immunostaining in microglia in vivo following seizures in the rat brain (Rappold et al, 2006). In identifying cell death, gliosis, and changes in neurochemical profiles, we now appreciate that neuroinflammatory processes and synaptic reorganization are integral components of epileptogenesis and seizure activity.
- Freeman, E. and Lynd-Balta, E. Developing Information Literacy Skills Early in an Undergraduate Curriculum. College Teaching (accepted).
- Lynd-Balta, E. Using literature and innovative assessments to ignite interest and cultivate critical thinking skills in an undergraduate neuroscience course, CBE- Life Sciences Education 5(2): 167-174, 2006.
- Joseph, S.A., Lynd-Balta, E., O’Banion, M.K., Rappold, P.M., Daschner, J. Allen, A., and
- Padowski, J. Enhanced cyclooxygenase-2 expression in olfactory-limbic forebrain following kainate-induced seizures, Neuroscience 140: 1051-1065, 2006.
- Rappold, P.M., Lynd-Balta, E., Joseph, S.A. P2X7 receptor immunoreactive profile confined to resting and activated microglia in the epileptic brain, Brain Research 1089: 171-178, 2006.
- Erklenz-Watts, M., Westbay, T.D., and Lynd-Balta, E. An Alternative Professional Development Program: Lessons Learned. College Teaching 54(3): 275-280, 2006.
- Lynd-Balta, E., Erklenz-Watts, M., Freeman, C., and Westbay, T.D. Linking Pedagogical Theory to Practice in College Science. Journal of College Science Teaching XXXV(4), January-February: 18-24, 2006.
- Murphy, M.L. and Lynd-Balta, E. PANDAS – A subset of Pediatric OCD. OCD Newsletter, 18(6): 18, 2004.
- Lynd-Balta, E., Pilcher, W.H., and Joseph S.A. Glutamate receptor alterations precede mossy fiber sprouting in young children with temporal lobe epilepsy. Neuroscience 126(1): 105-114, 2004.
- Joseph, S.A. and Lynd-Balta, E. Evidence for an anatomical substrate of hyperexcitability in human temporal lobe epilepsy: glutamate receptor alterations and reorganized circuitry. Functional Neurology, 16(4):347-365, 2001.