Froemke Laboratory
The brain has the remarkable capacity to change as we learn and have new
experiences. Our lab studies the mechanisms and benefits of this neuroplasticity in
two main types of subjects: new parents and neuroprosthetic device users. Our
research has revealed when, where, and how the neurohormone oxytocin acts in
the brain to help new mothers recognize the importance of baby cries, and how
oxytocin also enables cooperative behaviors between co-parents- including how
experienced parental animals might help or teach other animals how to be
successful caregivers. In collaboration with the NYU Langone Department of
Otolaryngology, we have studied how cochlear implants interface with the nervous
system to provide a new electrical hearing sense to profoundly deaf subjects.
In both cases, we have studied the diversity of individual experiences and
behaviors. What contributes to individual variation in social behaviors? When
someone is struggling to care for themselves or others, what mechanisms are
available to help shift their behavior to improve mental and physical wellness? The
mammalian oxytocin system interacts with many other neurochemical systems in
the body and brain. Our lab has studied how applied neuromodulation can open
windows of opportunity for changes to synapses and neural networks, and we have
designed large-scale 24/7 behavioral monitoring systems to make life-long
documentaries of how short-term interventions can lead to enduring improvements.
Locus coerulus activity improves cochlear implant performance
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The Klann Lab
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The research in our laboratory is focused on the regulation of protein
synthesis in the brain and how it is involved in learning and memory. We
also study how dysregulated protein synthesis contributes to aberrant
behavior in mouse models of fragile X syndrome, intellectual disability,
autism spectrum disorder, and neurodegenerative disease.
We use a number of experimental approaches, including genetic,
molecular, biochemical, electrophysiological, optical, imaging, and
behavioral experiments. We have recently begun examining dysregulated
protein synthesis in iPSC-derived neurons from patients with fragile X
syndrome, MEHMO syndrome, EEF1A2 syndrome, and frontotemporal
dementia.
Finally, we generate molecular tools to study protein synthesis in specific
cell types in order to understand how protein synthesis impacts circuit
function during memory formation and how these circuits are altered in
mouse models of neurodevelopmental and neurodegenerative disease.
These studies include examining mRNA and protein expression to find
alterations in disease models and to identify potential therapeutic targets
for treatment of these brain disorders. For example, our work as resulted
in clinical trials for drugs that target an enzyme called S6K1 for the
treatment of fragile X syndrome.
Autism- and epilepsy-assocated EEF1A2 mutations lead to translational dysfunction
We investigated the neuron-specific translation factor, eukaryotic Elongation Factor 1a2 (eEF1A2), which when mutated in patients results in autism, epilepsy, and intellectual disability. We characterized three EEF1A2 patient mutations and demonstrate that all three mutations decrease de novo protein synthesis, alter neuronal morphology, and decrease tRNA availability, thus altering the actin cytoskeleton.
This supports the hypothesis that eEF1A2 acts as a bridge between protein synthesis and the actin cytoskeleton, which is essential for proper neuron development and function.
Cell-type specific dysfunction of cortico-striatal circulatry drives repetition in fragile X mice
Individuals with fragile X syndrome (FXS) are frequently diagnosed with autism, including increased risk for restricted and repetitive behaviors. Using a multidisciplinary approach, we dissected the contribution of two populations of striatal medium spiny neurons (SPNs) in the expression of repetitive behaviors in FXS model mice and reported that dysregulated protein synthesis at cortico-striatal synapses is a molecular culprit of the synaptic and autism-associated motor phenotypes displayed by FXS model mice. Cell-type-specific translational profiling of the FXS mouse striatum reveals differentially translated mRNAs, providing critical information concerning potential therapeutic targets.
The Carter Lab
Our lab studies neural circuits in the mammalian brain that underlie cognition,
emotion, and motivation. We focus on the frontal cortex, thalamus, and striatum,
whose dysfunction is linked to diverse neuro-psychiatric disorders, including
schizophrenia, anxiety, and depression. We broadly study how different
populations of neurons communicate in their local and long-range networks, and
how specific types of cells and synapses are regulated by dopamine and other
neuromodulators. We are particularly interested in how these networks are
impacted by both rewarding and aversive experiences at critical windows during
development. Our experiments combine advanced anatomy, electro-physiology,
two-photon microscopy, optogenetics, and animal behavior. We also take
advantage of genetic tools, including viruses and transgenic animals, to examine
and manipulate specific neurons and connections.
Our recent work has extended to the insular cortex, part of frontal cortex that is
important for perception of bodily states, known as interoception. This relatively
unexplored region encodes feeding-related signals such as hunger and taste,
and processes motivational signals including reward and aversion. We are using
the tools that we have advanced over the past decade to study how insular
cortex is wired with the rest of the brain. We are particularly interested in how
neurons and connections mature over development from adolescence to
adulthood. Our long-term goal is to determine how these circuits are disrupted by
stressful experiences, and to assess how circuit perturbations contribute to
aberrant behaviors such as eating disorders. This is exciting new area of
research for the lab is being pioneered by a talented new MD/PhD student,
Stephanie Tetrick.
