Event Detail (Archived)

Unexpected Interactions in the Basal Ganglia

  • This event already took place in April 2013
  • Carson Family Auditorium (CRC)

Event Details

Type
Special Seminar Series
Speaker(s)
Bernardo Sabatini, M.D., Ph.D., professor of neurobiology, Harvard Medical School; investigator, Howard Hughes Medical Institute
Speaker bio(s)

Animals must learn associations between sensory cues and motor actions that lead to the acquisitions of rewards such as food, water and access to mates. The basal ganglia are a phylogenetically conserved set of subcortical nuclei that are essential for such reward learning and for the generation of coordinated, purposeful movements. Accepted models postulate that the basal ganglia modulate cerebral cortex indirectly via an inhibitory output to the thalamus, thus gating ascending signals from sensory and motor systems. Dr. Sabatini's lab described a direct projection to the cerebral cortex from the globus pallidus, a central nucleus of the basal ganglia. In mice, pallidocortical projection neurons are of two classes, one of which expresses the excitatory neurotransmitter acetylcholine and the other the inhibitor neurotransmitter GABA. Activation of either neuron class in behaving mice mediates net cortical excitation, reflecting differing synaptic targets within cortical microcircuity. Furthermore, pallidocortical projection neurons receive type-2 dopamine receptor sensitive innervation from striatum, revealing a pathway by which therapeutic agents that target these receptors for the treatment of neuropsychiatric disorders can act in the striatum yet modulate frontal cortices. Anatomical tracing in Rhesus macaque monkeys demonstrate structural conservation of the pathway whereas functional imaging in humans reveal highly correlated activity between globus pallidus externus and frontal cortices, as expected for functional conservation. Thus, Dr. Sabatini's lab has revealed an evolutionarily conserved and non-canonical output of the basal ganglia directly to cerebral cortex that controls cognitive centers and may provide the anatomical substrate for the therapeutic action of classical anti-psychotic drugs.
 
Dr. Sabatini earned his Ph.D. in neurobiology from Harvard Medical School and his M.D. from Harvard Medical School and the Massachusetts Institute of Technology, both in 1999. He was a postdoctoral fellow with the Howard Hughes Medical Institute at Cold Spring Harbor Laboratory from 1999 to 2001, where his advisor was Karel Svoboda. He joined the faculty of Harvard Medical School in the department of neurobiology in 2001, where he has been full professor since 2010. Dr. Sabatini became an investigator at the Howard Hughes Medical Institute in 2008. He has received a number of honors, including a Burroughs Wellcome Career Award in Biomedical Sciences, a Searle scholarship, a McKnight Scholar Award and the Society for Neuroscience Young Investigator Award. He has been the Takeda Professor of Neurobiology since 2010. He is an associate editor for the Journal of Neuroscience and is on the advisory board of the Simons Center for the Social Brain, among others. 

Open to
Public
Reception
Refreshments, 3:45 p.m. - 4:00 p.m., Lower Level Greenberg Building (CRC)
Contact
Jill Benz
Phone
(212) 327-7244
Sponsor
Jill Benz
(212) 327-7244
benzj@rockefeller.edu