SEPTEMBER 20
Our lab uses C. elegans to study the molecular mechanisms of synapse development, focusing on how presynaptic proteins such as neurexins and active zone scaffold molecules interact and assemble. We have found a surprising role for protein-lipid interactions early in the process of synapse assembly. We also use C. elegans to model human patient mutations in presynaptic calcium channels to gain a better understanding of how and why these mutations lead to varied patient manifestations.
SEPTEMBER 27
The Smith lab investigates the molecular mechanisms that underly synaptic inhibition, its plasticity and how it is disrupted in disease. We use advanced microscopy techniques like super-resolution microscopy to analyze the fine details of the synapse, and link these findings to synapse function and diversity, therefore providing a new logic to synaptic inhibition.
OCTOBER 18
Dr. Carrie Esopenko is an Associate Professor in the Brain Injury Research Center at the Icahn School of Medicine at Mount Sinai Hospital in New York City. She is also holds an adjunct faculty appointment at the Traumatic Brain Injury and Concussion Center at the University of Utah, as well as in the Department of Family Medicine and Community Health at Rutgers – Robert Wood Johnson Medical School. She is the principal investigator of a National Institute of Neurological Disorders and Stroke R01-funded multi-site study examining the psychological, cognitive, and neural signatures of IPV-related head trauma. She is the Lead Investigator of the ENIGMA Intimate Partner Violence (IPV) Working Group seeking to increase IPV brain injury research collaborations worldwide, and co-leads ENIGMA Global Knowledge Exchange Network which seeks to provide education and training supports to service providers and advocates working with IPV-related brain injury. Her research focuses on understanding the effects of neurotrauma and mental health conditions across populations, and identifying methods for injury prevention and patient-specific and community-based intervention strategies.
OCTOBER 25
Early life stress increases sensitivity to stress later in life, which may be at the root of increased risk for mental health disorders. Our work seeks to understand the mechanistic underpinnings of this heightened stress sensitivity. Using transgenic mice to label and capture experience-actiated neurons, we show that neurons active during early life stress are more likely to be reactivated during adult stress experience, and that chemogenetically inhibiting these neurons rescues behavioral changes. Heightened cellular reactivity may be due to long-lasting changes in the epigenome that leave chromatin more open and transcriptionally reactive to additional stimuli, particularly in stress-activated neurons. Together, this work supports a biological model in which stress alters chromatin development, leading to increased cellular reactivity and ultimately behavioral sensitivity to future stress.
NOVEMBER 1
Cortical interneurons are the most transcriptionally and morphologically diverse neurons in the brain, characterized in part by their striking degree of synaptic specificity. However, little is known about the extent of their synaptic diversity due to the lack of unbiased methods to extract features of synaptic organization among interneuron subtypes. In this talk, I will introduce an approach we developed that combines imaging and computational extraction of synaptic features from genetically-identified interneuron synapses and their subcellular specificity among postsynaptic targets. A machine-learning approach (1) reveals hundreds of spatial and structural features from each analyzed synapse, (2) constructs a multidimensional data set, consisting of millions of synapses, and (3) uncovers novel synaptic subgroups. By analyzing this dataset, we found that dendrite-targeting synaptic subgroups were clustered onto distinct subdomains of the dendrite along the proximal to distal axis; Soma-targeting subgroups were enriched onto different postsynaptic cell types; Finally, the two main subclasses of interneurons, basket cells and somatostatin interneurons, utilize distinct strategies to enact inhibitory synaptic coverage. Thus, we uncover previously unknown structural and topological features of inhibitory synaptic organization and establishes a conceptual framework for studying inhibitory synaptic diversity in health and disease.
NOVEMBER 15
Social isolation and loneliness has been on the rise for the last 20yrs. Many studies have linked increased rates of isolation and loneliness to dementia, depression, anxiety, and other mental health disorders, but how isolation affects the brain to alter behaviors is unknown. Here, we focus on how isolation impairs learning and memory in the model organism Drosophila. We’ve found that isolation impairs learning and reduces synaptic proteins in the brains of fruit flies. This appears to cause alterations to their neural circuitry that impairs learning by reducing the capacity for synaptic plasticity.
NOVEMBER 22
NOVEMBER 29
Memories for events (i.e., episodic memories) formed in early development differ from those in adulthood in at least two regards. First, these memories tend to be rapidly forgotten (i.e., infantile amnesia). Second, they tend to be less precise than those formed in adulthood (i.e., infantile generalization). My talk will focus on the neurobiological mechanisms that account for these different operating characteristics of episodic memory in the developing brain. With respect to infantile amnesia, we have shown that maturation of cortical circuits is necessary for the formation of enduring event memories. With respect to infantile generalization, our studies reveal that maturation of inhibitory microcircuits in the hippocampus are necessary for the formation of adult-like, precise memories for events.
DECEMBER 6
The amygdalostrital transition zone (ASt) is situated at a crossroads between the amygdala and striatum, but its role in motivated behaviors is poorly understood. We have explored the functional role and genetic identity of this structure, and found the first evidence that the ASt encodes negative valence across behavioral timescales and is essential for orchestrating behavioral fear responses.
JANUARY 17
JANUARY 24
JANUARY 31
FEBRUARY 7
FEBRUARY 14
FEBRUARY 21
FEBRUARY 28
MARCH 7
MARCH 14
MARCH 21
MARCH 28
APRIL 4
APRIL 11
APRIL 25
MAY 2
MAY 9
MAY 16
Dr. Wellington will be introducing a new CFI funded Core Facility that will focus on fluid biomarkers relevant to clinical neurology and fundamental neuroscience.
MAY 23
MAY 30
JUNE 6
JUNE 13