Seminars & Events
Monday, September 19, 2011: Dr. R. Christopher Pierce (University of Pennsylvania) will speak on "Epigenetic Inheritance of a Cocaine Resistance Phenotype" at 4:45 pm in Goodpaster 195.
Friday, November 4, 2011: Dr. Paul Shepard (University of Maryland Baltimore) will speak at 3:00 pm in Schaefer Hall 106.
Friday, November 11, 2011: Dr. Mark Bouton (University of Vermont) will speak at 3:00 pm in Goodpaster Hall 195.
Alumni Highlight
Dr. Erin Johnson '02 recently received her Ph.D. in Neuroscience from the University of Rochester School of Medicine, and was inducted as an alumni member of Nu Rho Psi.
SMP Spotlight
Ron Saul, "Chronic activation of the substantia nigra nociceptin/orphanin receptor induces motor deficits similar to Parkinson's disease," 2008. Saul, the 2008 winner of the Neuroscience Award, infused a drug into the substantia nigra of rats and measured the resulting motor behaviors, mood disturbances, and cognitive abilities.
Scurci, Stephanie (2009). Electrophysiological Study of the Involvement of Nitric Oxide in Long-Term Depression at the Crayfish (Procambarus Clarkii) Neuromuscular Junction. Mentor: Dr. John Ramcharitar
Abstract
The crayfish leg extensor neuromuscular junction (NMJ) consistently exhibits long-term depression (LTD), which is attenuation of excitatory post-synaptic potentials (EPSPs) for an extended period of time induced by a repetitive stimulation. Previous studies at different crayfish muscles have demonstrated that the neurotransmitter nitric oxide (NO) elicits this form of synaptic plasticity. The current study is the first to examine NO involvement at a dually innervated (tonic and phasic) NMJ. In order to isolate LTD at this novel site of study, without the interference of short-term depression (STD), two different frequencies of stimulation were applied. During these experiments, NO production was blocked by L-NAME, a NO synthase inhibitor. We expected inhibition of nitric oxide production to release the neuron from depression causing an increase in EPSP amplitudes. 0.1 Hz stimulation-induced LTD did not recover after a pause in stimulation indicating long-term changes at the synapse. After a pause in 1 Hz stimulations, EPSP amplitude did recover indicating a short-term depression induced by the repetitive stimulation. Application of L-NAME during 0.1 and 1 Hz stimulations caused significant reversal in depression. The significant increase in EPSP amplitude at both stimulation frequencies during L-NAME administration suggests that endogenous NO is responsible for synaptic depression at the NMJ. During L-NAME application, the complete reversal of depression induced by 0.1 Hz stimulations and only partial reversal of depression induced by 1 Hz stimulations indicates that NO affects the induction of LTD only at the extensor NMJ of crayfish Procambarus clarkii.
