Central Synaptic Communication: Neuropeptides, Abused Drugs and Neuropathology
For the past 19 years, our electrophysiology laboratory has sought to understand mechanisms of neuronal function and synaptic communication and the effects of neuropeptides, abused drugs and neuropathological insults on these mechanisms , using extracellular, intracellular and patch recording of neurons in vitro brain slice and freshly-isolated neuronal preparations. We administer drugs, transmitters, cytokines and neurotoxins by superfusion and from micropipettes, and we activate synaptic transmission via stimulating electrodes. The neuropeptides under study include somatostatin, cortistatin, various opioid peptides, nociceptin and neuropeptide Y. These peptides generally have inhibitory actions on central neurons, although with different profiles of actions with respect to neuron type. In addition, several of these peptides have anti-epileptic properties. We also investigate the action and function of several cytokines such as IL-1, IL-6, interferons, and the effects on neuronal function of several neuropathological insults, including those thought to cause dementias, such as beta amyloid and the HIV coat protein gp-120.
A.B., Biology, Harvard University, 1960
Ph.D., Biology, Boston University, 1976
1983-2013 Professor, Molecular and Integrative Neurosciences (MIND), The Scripps Research Institute
Invited speaker, Winter Conference on Brain Research, Snowmass, CO, January 2002 Member, American Society for Neuroscience
Martin, G., Ahmed, S.H., Blank, T., Spiess, J., Koob, G.F., Siggins, G.R. Chronic morphine treatment alters NMDA receptor-mediated synaptic transmission in the nucleus accumbens, J. Neurosci., 19:9081-9089, 1999.
Nie, Z., Madamba, S.G., Siggins, G.R. Ethanol enhances g-aminobutyric acid responses in a subpopulation of nucleus accumbens neurons; role of metabotropic glutamate receptors. J. Pharmacol. Exp. Therap., 293: 654, 2000.
Tallent, M.K., Madamba, S.G., Siggins, G.R. Nociceptin reduces epileptiform events in CA3 hippocampus via presynaptic and postsynaptic mechanisms. J. Neurosci. 21: 6940, 2001.
Krucker, T., Siggins, G.R., McNamara, R.K., Lindsley, K.A., Dao, A., Allison D.W., de Lecea, L., Lovenberg, T.W., Sutcliffe, J.G., Gerendasy D.D. Targeted Disruption of RC3 Reveals a Calmodulin Based Mechanism for Regulating Metaplasticity in the Hippocampus. J. Neurosci., in press, 2002.