Past events

The hypothalamo-neurohypophyseal system (HNS) is an evolutionarily conserved neuroendocrine interface through which the brain regulates body homeostasis by means of releasing neuro-hormones (i.e. oxytocin and vasopressin) from the hypothalamus to the blood circulation. The basic components of the HNS are the hypothalamic axonal projections, endothelial blood vessels and astroglial-like cells, termed pituicytes. These three tissue types converge and interact at the ventral forebrain to establish an efficient neuro-vascular interface, which allows the release of neurohormones from the brain to the periphery. In contrast to BBB-containing CNS vessels, neurohypophyseal capillaries are permeable, which enables bypassing the BBB to transfer HNS hormones and blood-borne substances between brain and circulation. I will present our recent molecular and functional analysis that revealed a new role for pituicytes, in establishing a permeable neuro-vascular conduit that bypasses the BBB.

Understanding brain function and dysfunction begins with the knowledge of how neuronal connections are established and organised in functional networks. To address this question my lab is focused in three main questions: 1) How are the mammalian cortical networks built, 2) how do they response to activity and, 3) What are the functional consequences of disrupting the development of cortical circuitries.

Drug addiction is a chronically relapsing disorder characterized by compulsive drug use despite catastrophic personal consequences (e.g., loss of family, job) and even when the substance is no longer perceived as pleasurable. In this talk, I will present results of human neuroimaging studies, utilizing a multimodal approach (neuropsychology, functional magnetic resonance imaging, event-related potentials recordings), to explore the neurobiology underlying the core psychological impairments in drug addiction (impulsivity, drive/motivation, insight/awareness) as associated with its clinical symptomatology (intoxication, craving, bingeing, withdrawal). The focus of this talk is on understanding the role of the dopaminergic mesocorticolimbic circuit, and especially the prefrontal cortex, in higher-order executive dysfunction (e.g., disadvantageous decision-making such as trading a car for a couple of cocaine hits) in drug addicted individuals. The theoretical model that guides the presented research is called iRISA (Impaired Response Inhibition and Salience Attribution), postulating that abnormalities in the orbitofrontal cortex and anterior cingulate cortex, as related to dopaminergic dysfunction, contribute to the core clinical symptoms in drug addiction. Specifically, our multi-modality program of research is guided by the underlying working hypothesis that drug addicted individuals disproportionately attribute reward value to their drug of choice at the expense of other potentially but no-longer-rewarding stimuli, with a concomitant decrease in the ability to inhibit maladaptive drug use. In this talk I will also explore whether treatment (as usual) and 6-month abstinence enhance recovery in these brain-behavior compromises in treatment seeking cocaine addicted individuals. Promising neuroimaging studies, which combine pharmacological (i.e., oral methylphenidate, or RitalinTM) and salient cognitive tasks or functional connectivity during resting-state, will be discussed as examples for using neuroimaging in the empirical guidance for the development of effective neurorehabilitation strategies (including cognitive training) in drug addiction.

Understanding the functional communication across brain has been a long sought-after goal of neuroscientists. However, due to the widespread and highly interconnected nature of brain circuits, the dynamic relationship between neuronal network elements remains elusive. With the development of optogenetic functional magnetic resonance imaging (ofMRI), it is now possible to observe whole-brain level network activity that results from modulating with millisecond- timescale resolution the activity of genetically, spatially, and topologically defined cell populations. ofMRI uniquely enables mapping global patterns of brain activity that result from the selective and precise control of neuronal populations. Advances in the molecular toolbox of optogenetics, as well as improvements in imaging technology, will bring ofMRI closer to its full potential. In particular, the integration of ultra-fast data acquisition, high SNR, and combinatorial optogenetics will enable powerful systems that can modulate and visualize brain activity in real-time. ofMRI is anticipated to play an important role in the dissection and control of network-level brain circuit function and dysfunction. In this talk, the ofMRI technology will be introduced with advanced approaches to bring it to its full potential, ending with examples of dissecting whole brain circuits associated with neurological diseases utilizing ofMRI. Short Bio: Dr. Lee received her Bachelor’s degree from Seoul National University and Masters and Doctoral degree from Stanford University, all in Electrical Engineering. She is a recipient of the 2008 NIH/NIBIB K99/R00 Pathway to Independence Award, 2010 NIH Director’s New Innovator Award, 2010 Okawa Foundation Research Grant Award, 2011 NSF CAREER Award, 2012 Alfred P. Sloan Research Fellowship, 2012 Epilepsy Therapy Project award, 2013 Alzheimer’s Association New Investigator Award, 2014 IEEE EMBS BRAIN young investigator award, and the 2017 NIH/NIMH BRAIN grant award. As an Electrical Engineer by training with Neuroscience research interest, her goal is to analyze, debug, and engineer the brain circuit through innovative technology. 1. Hyun Joo Lee†, Andrew Weitz†, David Bernal-Casas, Ben A. Duffy, Mankin Choy, Alexxai Kravitz, Anatol Kreitzer, Jin Hyung Lee*, Activation of direct and indirect pathway medium spiny neurons drives distinct brain-wide responses, Neuron, 2016;91(2):412-424. 2. Jia Liu†, Ben A. Duffy†, David Bernal-Casas, Zhongnan Fang, Jin Hyung Lee*, Comparison of fMRI analysis methods for heterogeneous BOLD responses in block design studies, Neuroimage, 2017;147:390-408. 3. David Bernal-Casas, Hyun Joo Lee, Andrew Weitz, Jin Hyung Lee*, Studying brain circuit function with dynamic causal modeling for optogenetic fMRI, Neuron, 2017;93:522-532.

Increasing evidence indicates that the brain can control immunity. But how is the brain informed of the state of the immune response? What information is available to the brain regarding the immune system, and how do these essential systems communicate and interact? In this talk, I will try to bridge these gaps. I will demonstrate how specific activity in the brain affects the immune response, and how the peripheral nervous system can convey signals from the brain to the periphery to regulate immunity.

Reversible modulation of neuronal activity is a powerful approach for isolating the roles of specific neuronal populations in circuit dynamics and behavior. Optogenetics enables such experiments, through excitation and inhibition of defined cells within neural circuits. However, in contrast to optogenetic excitation, for which a limited number of optogenetic tools can serve to all but a few experimental needs, tools used for inhibition of neuronal activity still impose stringent constraints on the experimental paradigm. During the seminar I will present data showing that the optimal approach for optogenetic silencing differs between subcellular neuronal compartments, characterize current tools for axonal inhibition and introduce a set of soma-targeted naturally-occurring anion-conducting channelrhodopsins as the potential next generation of inhibitory optogenetic tools for somatodendritic silencing approaches in neuroscience.

Social animals have to know the spatial positions of conspecifics. However, it is unknown how the position of others is represented in the brain. We designed a spatial observational-learning task, in which an observer bat mimicked a demonstrator bat while we recorded hippocampal dorsal-CA1 neurons from the observer bat. A neuronal subpopulation represented the position of the other bat, in allocentric coordinates. About half of these “social place cells” represented also the observer’s own position—that is, were place cells. The representation of the demonstrator bat did not reflect self-movement or trajectory planning by the observer. Some neurons represented also the position of inanimate moving objects; however, their representation differed from the representation of the demonstrator bat. This suggests a role for hippocampal CA1 neurons in social-spatial cognition.