Institute of Neuroscience Faculty
Professor Emeritus, Department of Psychology
A.B., 1959, Oberlin College
M.A., 1962
Ph.D., 1965, Michigan
Research Interests
Synaptic plasticity; critical periods; neural basis of learningt
Dr. Gordon-Lickey is retired from teaching. He maintains an office in the Roberts lab on the second floor of Heustis Hall.
I am interested in mechanisms that cause functional adaptation of neural circuits in response to novel experience. A good experimental model for studying adaptation is the monocular deprivation effect. In humans and other mammals deprivation of vision in one eye during a developmental critical period causes synaptic changes in the visual cortex that shut off transmission in the sensory pathway originating in the deprived eye. Outside the critical period, monocular deprivation has no effect on transmission in the sensory pathway. The monocular deprivation effect is a very robust phenomenon, it occurs in many mammalian species from mice to humans, and is probably related to many other kinds of functional adaptation that occur during postnatal brain development. The question is, what cellular events can account for the loss of synaptic plasticity when the critical period ends? Glutamate receptors of the NMDA type have been found critical for synaptic plasticity in the hippocampus and elsewhere in the brain.
Barbara Gordon and I are asking whether NMDA receptors are a part of the mechanism of the monocular deprivation effect. In one set of experiments we are carefully charting the developmental expression NMDA receptor subunits in the visual cortex of rats. Development is measured at three levels: mRNA expression, protein abundance and synaptic function. In another set of experiments we are changing the timing of the critical period by rearing rats in total darkness. We then ask whether this change of the timing of the monocular deprivation effect changes the timing of NMDA receptor development. In a third set of experiments we are interfering with the normal expression of NMDA receptor subunits by infecting cells of the visual cortex with viruses that carry NMDA receptor DNA or anti-sense DNA. We predict that disturbance of the expression of the NMDAR proteins will change the capacity for the monocular deprivation effect.
Representative Publications
- Pham TA, Graham SJ, Suzuki S, Barco A, Kandel ER, Gordon B, Lickey ME. (2004) A semi-persistent adult ocular dominance plasticity in visual cortex is stabilized by activated CREB. Learn Mem. 11(6): 738-47.
- Lickey ME, Pham TA, Gordon B. (2004) Swept contrast visual evoked potentials and their plasticity following monocular deprivation in mice. Vision Res. 44 (28): 3381-7.
- Cao, Z., Liu, L., Lickey, M., and Gordon, B. (2000) Development of NR1, NR2A and NR2B mRNA in NR1 immunoreactive cells of rat visual cortex. Brain Res. 868(2): 296-305.
- Cao, Z., Lickey, M.E., Liu, L., Kirk, E., and Gordon, B. (2000) Postnatal development of NR1, NR2A and NR2B immunoreactivity in the visual cortex of the rat. Brain Res. 859(1): 26-37.
- Guire, E.S., Lickey, M.E., and Gordon, B. (1999) Critical period for the monocular deprivation effect in rats: assessment with sweep visually evoked potentials. J. Neurophysiol. 81(1): -128.