Research Interests

In my group we utilize biochemical and pharmacological approaches to study synaptic physiology and the actions of drugs and natural substances at synaptic targets in mammalian brain.

Our studies demonstrate that certain drugs acting at CB1 receptors, as well as endocannabinoids (e.g. anandamide, 2-AG and NADA) and structurally related lipids (e.g. cis-oleamide, a putative initiator of sleep), bind to and inhibit voltage-gated sodium channels. These substances also inhibit the release of glutamic acid and GABA from synaptosomes when evoked by sodium channel activation. The pharmacological profiles we observe are strikingly similar to those of depressant drugs which target sodium channels such as anticonvulsants, antiarrhythmics and neuroprotectants. The sodium channel represents one of the more abundant excitatory ion channels in the brain and our results suggest potential for negative modulation by these lipid molecules at this complex.

Another important focus of my laboratory is on the synaptic role of ethanolamine. Just recently we have discovered that ethanolamine and other endogenous amino alcohols have the ability to 1) increase the ATP-dependent membrane potential of synaptic vesicles, 2) enhance intravesicular uptake of the L-glutamate surrogate [3H]-D-aspartate and 3) facilitate basal and evoked release of [3H]-D-aspartate transmitter from synaptosomes. Our experiments therefore indicate that ethanolamine may function in the regulation of synaptic vesicle filling. These findings may also be relevant to neuropathophysiological conditions (epilepsy and ischemia) where production of ethanolamine is altered.

Former students and researchers from my laboratory have gone on to do higher degrees, or to do postdoctoral research, or have obtained jobs in industry or government.