Seminars & Events
Monday, February 11, 2013: Dr. Daphne Soares (University of Maryland College Park) will speak on "The Sensory World of Cavefishes" at 4:45 pm in Goodpaster Hall 195.
Monday, March 4, 2013: Dr. Joe Cheer (University of Maryland Baltimore) will speak on "Endogenous Cannabinoids and the Pursuit of Reward" at 4:45 pm in Goodpaster Hall 195.
Friday, April 12, 2013: Dr. Jill McGaughy (University of New Hampshire) will speak on "The Role of Cortical Norepinephrine in the Ontogeny of Executive Function" at 3:00 pm in Schaefer Hall 106.
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.
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.
Saul, Ronald (2008). Chronic Activation of the Substantia Nigra Nociceptin/ Orphanin Receptor (NOP) Induces Motor Deficits Similar to Parkinson’s Disease: A Behavioral and Motor Assessment Following Chronic UFP-112 Administration into the SNr.
Mentor: Dr. Anne Marie Brady
In an attempt to create a working model of Parkinson’s disease that portrays the motor and non-motor features of the disorder, the nociceptin/ orphanin receptor (NOP) potent agonist UFP-112 was chronically administered into the substantia nigra pars reticulata (SNR). Previous studies have shown stimulation of the SNR NOP receptor decreases dopamine transmission along the nigrostriatal pathway and induces parkinsonian-like motor impairments (Marti et al., 2004b). Following placement of cannulas into the SNR attached to an osmotic pump containing UFP-112 or vehicle alone, both motor behaviors and non-motor behaviors were assessed. Chronic stimulation of the SNr NOP receptor system regulated the nigrostriatal pathway and induced motor performance impairments, but did not disrupt the cognitive and emotional behaviors involved with Parkinson’s disease.