Columbia University Medical Center

DEPARTMENT OF NEUROSCIENCE

Samuel M. Schacher, PhD

Samuel M. Schacher, PhD
  • Department of Neuroscience
  • Department of Psychiatry
    Division of Neurobiology and Behavior
  • Professor of Neuroscience (in Psychiatry)

Neural circuits controlling behavior have three fundamental properties:  Individual components of the circuit form connections with specific partners with appropriate synaptic baselines that can have the capacity to be modified for long durations by activity-dependent mechanisms. 

My lab is interested in understanding the cellular and molecular mechanisms that regulate these properties of a behaviorally relevant neural circuit – the sensori-motor synapse – in the marine mollusk Aplysia.  Sensory neurons form synapses with specific motor neurons that mature and maintain a synaptic baseline that can be modified in a bidirectional manner for short and long durations by activity known to produce long-lasting bidirectional changes in behavior.  We have found that interactions of cell adhesion molecules, activation of sequential cascades of specific signaling pathways involving the timely secretion of neurotrophin-like peptides with autocrine and paracrine actions contribute to these various phases of synapse development and maturation and long-term plasticity associated with behavioral adaptations.   We wish to understand how the timely activations of these pathways produce specific regulation of gene transcription/activation, local and cell-wide protein translation, and the network of interacting processes that balance the strength of synapses in a mature neural circuit.

Primary Lab Locations

Kolb Research Annex

40 Haven Avenue
Room 817
New York, NY 10032

Phone:
(646) 774-7326
Email:
sms2@cumc.columbia.edu

Research Interests

Neurobiology of Learning and Memory
Synapses and circuits
Axon Pathfinding and Synaptogenesis
cellular/molecular/developmental neuroscience

Lab Members

Publications

  • Hernandez AI, Wolk J, Hu JY, Schwartz JH, Schacher S (2009).  Poly- (ADP-ribose) Polymerase-1 is necessary for long-term facilitation in Aplysia.  J Neurosci. 29: 29:9553-9562.
  • Hu JY, Chen Y, Bougie JK, Sossin WS, Schacher S (2010). Aplysia cell adhesion molecule and a novel protein kinase C activity in the postsynaptic neuron are required for presynaptic growth and initial formation of specific synapses. J Neurosci 30:8353– 8366.
  • Hu JY, Baussi O, Levine A, Chen Y, Schacher S (2011). Persistent long-term synaptic plasticity requires activation of a new signaling pathway by additional stimuli. J Neurosci 31:8842-8850.
  • Schacher S, Hu JY (2014) The less things change, the more they are different: the contributions of long-term synaptic plasticity and homeostasis to memory.  Learn Mem 21:128-134.
  • Hu JY, Schacher S (2014).  Persistent long-term facilitation at an identified synapse becomes labile with activation of short-term heterosynaptic plasticity.  J Neurosci 34:4776-4785.
  • Hu JY, Levine A, Sung Y, Schacher S (2014). cJun and CREB2 in the postsynaptic neuron contribute to persistent long-term facilitation at a behaviorally relevant synapse. J Neurosci 34: in press.