Past events

Vocal production and learning rely on the evaluation of auditory feedback. We use the songbird as a model system for exploring how auditory feedback in vocalizing animals is represented by auditory brain areas, and how auditory signals are gated back into premotor areas involved in song production and learning. We expose juvenile zebra finches to distorted auditory feedback and record from neurons in field L, an avian forebrain area thought to be analogous to mammalian primary auditory cortex. Most field L neurons in our ongoing study do not respond to auditory perturbation during singing, despite their motor-related firing being similar to auditory responses to playback of the bird’s own song. We argue that this behaviour of field L neurons is reminiscent of mirror neurons in primate inferior frontal cortex. In adult birds, we demonstrate modulation and gating of auditory and spontaneous cerebral activity by the thalamic nucleus uveaformis (Uva): The normal dependence of premotor-like spike patterns (bursts) on the behavioural state can be reversed by pharmacological manipulation of Uva activity. Our results show that avian thalamic relay neurons have a function that is reminiscent of a mixture of functions attributed to relay and reticular neurons in the mammalian thalamus. In summary, our findings of corollary motor discharges in auditory brain areas and of explicit thalamic gating mechanisms help to advance the understanding of auditory feedback processing and sensorimotor integration for complex learned behaviors.

Dr. Sweatt's seminar will focus on molecular mechanisms underlying learning and memory. Dr. Sweatt uses knockout and transgenic mice to investigate signal transduction mechanisms in the hippocampus, a brain region known to be critical for higher-order memory formation in animals and humans. His talk will describe transcriptional regulation in memory formation, focusing on studies of transcription factors, regulators of chromatin structure, and other epigenetic mechanisms, in order to understand the role of regulation of gene expression in synaptic plasticity and memory.

Background: Opiate addicts entering methadone maintenance treatment exhibit decreased medial frontal cortex activation with occurrence of error (negative) events. The strength of this error-related cortical signal correlated with discrimination performance and moment-to-moment cognitive control. In the clinical setting the strength of this signal predicted individual treatment adherence (e.g., time maintained in treatment before drop-out). While the latter finding suggests a connection between error processing and complex decisions involving choices between immediate and delayed goals, we did not have direct evidence supporting this connection. Methods: Subjects performed both the Go/NoGo task and a delay-discounting task while brain activity was monitored using event-related fMRI. Results: The medial frontal cortex region previously associated with error processing also displayed significant activation during delay discounting. Moreover, the individual strength of brain activation while processing errors correlated with that exhibited during processing decisions between immediate and delayed hypothetical rewards. Supported by NIH grant DA11721 and VA CPPF and MERIT awards.