Dr. Michael Long

Michael Long is the Thomas and Susanne Murphy Professor of Neuroscience at the NYU School of Medicine. He completed his graduate studies with Barry Connors at Brown University where he investigated the role of electrical synapses in the mammalian brain. During his postdoctoral work with Michale Fee at MIT, Long began to study the songbird model system to uncover the cellular and network properties that give rise to learned vocal sequences. Since beginning his laboratory in 2010, Long has focused his attention on the neural circuits underlying skilled movements, often in the service of vocal interactions. To accomplish this, the Long lab has taken a comparative approach, examining relevant mechanisms in the songbird, a newly characterized neotropical rodent, and humans. In addition to federal funding, the Long lab has also received support from NYSCF, the Rita Allen Foundation, the Klingenstein Foundation, and the Herschel-Weill Foundation.

Long Lab

Abstract:  Vocal communication is central to our everyday lives, facilitating social exchange. Despite significant recent discoveries, the neural mechanisms underlying coordinated vocal exchanges remain poorly understood. We examine the brain processes involved in interactive vocal behaviors, focusing on forebrain circuitry in the songbird and the rodent, and we relate these to emerging human studies that employ a range of methods to manipulate and monitor cortical areas relevant for speech.

Carla Rothlin Rothlin Ghosh Lab

Abstract: Cell death is an invariant feature throughout our lifespan, starting with extensive scheduled cell death during morphogenesis and continuing with death under homeostasis in adult tissues. Additionally, cells become victims of accidental, unscheduled death following injury and infection. Cell death in each of these occasions triggers specific and specialized responses in the living cells that surround them or are attracted to the dying/dead cells. These responses sculpt tissues during morphogenesis, replenish lost cells in homeostasis to maintain tissue/system function, and repair damaged tissues after injury. Wherein lies the information that sets in motion the cascade of effector responses culminating in remodeling, renewal or repair? I will attempt to provide a framework for thinking about cell death in terms of the specific effector responses that accompanies various modalities of cell death. I will discuss an integrated three-fold “cell death code” consisting of information intrinsic to the dying/dead cell, the surroundings of the dying cell and the identity of the responder. I will propose that this can provide a foundation for the prediction of resolving and non-resolving inflammation.