Seminars & Events

Thursday, September 11, 2014: Dr. Bevil Conway (Wellesley College) will speak on his research in visual neuroscience and color at 4:30 pm in Goodpaster Hall 195.

Monday, October 27, 2014: Dr. Todd Gould (University of Maryland Baltimore) will speak on "Genes to behaviors to treatments in bipolar disorder" at 4:45 pm in Goodpaster Hall 195

Friday, December 5, 2014:  Dr. Brian Mathur (University of Maryland Baltimore) will speak on "Braking bad: Aberrant inhibitory neurotransmission in addiction" at 3:00 pm in Goodpaster Hall 195.


Alumni Highlight

Check out Jordan Gaines Lewis '11's award-winning blog, Gaines on Brains.




SMP Spotlight

Katie Gluskin and Jeff Haus present their SMP
Katie Gluskin and Jeff Haus, "Entorhinal Cortex Lesions, Habituation, and Latent Inhibition," 2013. Gluskin and Haus, the 2013 co-winners of the Neuroscience Award, infused a neurotoxin into the entorhinal cortex of rats to induce a lesion, and measured the resulting habituation and latent inhibition behavior within a fear conditioning paradigm.


Bailey, A.M., Enos, J., and Medley, V.  (2009, October).  Damage to nucleus basalis magnocellularis (nBM) cholinergic target areas produce different effects on the acquisition of learning set.  Poster presented at the Society for Neuroscience Annual Meeting, Chicago, IL.


Lesions to the nucleus basalis magnocellularis (nBM) using either quisqualic acid or 192 IgG-saporin produce differing effects on the acquisition of learning set. Specifically, quisqualic acid lesions produce severe and long lasting impairments but 192 IgG-saporin lesions produce transient effects on learning set acquisition. One possible explanation for acquisition differences involves altered neuronal activity in the cholinergic target areas of the nBM. We examined two main cholinergic targets of the nBM, namely the amygdala and the prefrontal cortex (PFC). Rats with either NMDA (20 µg/µl) lesions to the basolateral amygdala (n=10) or NMDA (20 µg/µl) lesions to the anterior cingulate PFC (n=6) were tested on an olfactory learning set formation task as well as operant delayed non-matching to-position (DNMTP) and open field activity. The rats with amygdala lesions were additionally tested on a fear conditioning task. Lesions to the PFC significantly impaired acquisition of learning set as measured by chance performance on Trial 2 (M = 56.17%, SD = 7.47). Rats with PFC lesions did not differ from sham animals on the DNMTP task (p > .05) or in activity counts in an open field (p > .05). However, rats with NMDA lesions to the amygdala were significantly higher than chance (50% correct) on Trial 2 (p .05) or percentage correct on the DNMTP task (p > .05). NMDA lesions to the amygdala did, however, significantly decrease time spent freezing to an aversive CS+ in the fear conditioning task (p < .05). In total, the results imply that learning set acquisition differences following either quisqualic acid or 192 IgG-saporin lesions to the nBM are not likely due to damage to the cholinergic projection to the amygdala but may be associated with altered PFC activity.