http://richmond.nimh.nih.gov/richmond.html

http://neuron.nimh.nih.gov/richmond.html

Recent paper: Munetaka Shidara and Barry J. Richmond; Anterior Cingulate: Single Neuronal Signals Related to Degree of Reward Expectancy Science Vol. 296: 1709-1711. May 31, 2002
Full text: http://richmond.nimh.nih.gov/richmond/docs/Science.pdf

ABSTRACT: Evaluating the balance between the amount of work that needs to be done to obtain a reward or achieve a goal is critical step in normal behavior. We study this critical step in behavior by observing how monkeys make use of visual stimuli to predict how many trials of a simple operant task need to be performed to obtain a reward. In line with many long know observations, the number of errors made increase as the visual stimulus indicates that there are more trials remaining, e.g. there are more errors when 3 trials remain than when 2 trials remain. This show that the monkeys have an internal working model of this simple reward schedule task. Recording single neurons in areas of the brain related to dopamine, a transmitter known to play an important role in reward-seeking behavior, we find signals in several brain regions related to the path through the task and the expectancy of the reward. Finally, borrowing techniques from molecular biology we are able to inactivate dopamine 2 (D2) receptor in one region 
of cortex and completely block learning of the association of visual stimuli with reward expectancy.

Research Area: plasticity of the synaptic and intrinsic properties of cortical neurons and circuits      

http://www.bio.brandeis.edu/faculty01/turrigiano.html          

Nature Neuroscience paper:  http://www.nature.com/cgitaf/DynaPage.taf?file=/neuro/journal/v5/n8/abs/nn878.html&dynoptions=doi1046302646

Major depressive disorders, long considered to be of neurochemical origin, have recently been associated with impairments in signaling pathways that regulate neuroplasticity and cell survival. Agents designed to directly target molecules in these pathways may hold promise as new therapeutics for depression. 

http://www.bpkids.org/learning/reference/interviews/004.htm 

4:00 PM

Senior Vice President of Research, Guilford Pharmaceuticals

Seminar Title: "Inhibitors of Glutamate Carboxypeptidase II: A Novel Target for the Treatment of Stroke, ALS and Neuropathic Pain"

Abstract: GCP II is an enzyme that catalyses the hydrolysis of the neuropeptide N-acetyl-aspartyl-glutamate to N-acetyl-aspartate and glutamate. GCP II inhibitors have been shown to  decrease extracellular glutamate, provide neuroprotection following ischemia, attenuate neuropathic pain, reverse peripheral nerve abnormalities following chronic diabetes, and  delay mortality in the mouse SOD transgenic ALS model. These data support GCP II inhibitors as a novel therapeutic approach in diseases wherein excess glutamate is thought to be pathogenic.

http://www.nature.com/cgi-taf/DynaPage.taf?file=/nm/journal/v5/n12/full/nm1299_1396.html