Nicolas Tritsch

Nicolas_TritschAssistant Professor, Department of Neuroscience & Physiology
Marlene and Paolo Fresco Institute for Parkinson's and Movement Disorders
Neuroscience Institute

450 East 29th St
Alexandria Center, Room 930
New York, NY 10016

Phone: 646-501-2189 (office) 646-501-2191 (lab)
Fax: 646-501-4529
Email: nicolas.tritsch@nyumc.org
Lab Website:http://www.tritschlab.org

Research Summary:

Synaptic mechanisms underlying the control of movement.

The goal of our laboratory is to reveal how the nervous system generates movement, and to determine how disorders of movement control, such as Parkinson’s disease (PD) corrupt this process. We are particularly interested in understanding how a collection of brain nuclei known as the basal ganglia (BG) participates in the selection, execution and reinforcement of voluntary movement at the synaptic, cellular and circuit levels. The BG have been extensively implicated in the control of movement both clinically and experimentally, but the precise neural mechanisms used to enable and learn goal-directed movement remain poorly understood.

Our studies currently focus on elucidating how dopamine-releasing neurons, which play a critical role in the function and plasticity of motor circuits modulate the activity of target neurons within the BG. We have shown that synaptic transmission from dopaminergic neurons is more complex than previously thought, extending beyond the sole release of dopamine. Specifically, we found that dopaminergic neurons silence striatal projection neurons by co-releasing the inhibitory neurotransmitter GABA, and that they modulate the activity of striatal cholinergic interneurons through co-release of dopamine and another neurotransmitter. We apply a variety of experimental approaches, including whole-cell patch-clamp electrophysiology in brain slices and calcium imaging in awake behaving mice. We leverage molecular, genetic, optogenetic and pharmacogenetic tools to precisely identify neural elements and establish their functional necessity and sufficiency. Our research efforts aim to unravel the interplay and net contribution of novel signaling pathways to BG function under physiological as well as pathological conditions.

Selected Publications:

  • Straub C*, Tritsch NX*, Hagan N, Gu C, Sabatini BL (2014) Multiphasic modulation of cholinergic interneurons by nigrostriatal afferents. J Neurosci 34:8557-69. (* co-first authors)
  • Tritsch NX, Oh WJ, Gu C, Sabatini BL (2014) Midbrain dopamine neurons sustain inhibitory transmission using plasma membrane uptake of GABA, not synthesis. eLife 3:e01936.
  • Tritsch NX, Ding JD, Sabatini BL (2012) Dopaminergic neurons inhibit striatal output through non-canonical release of GABA. Nature 490:262-6.
  • Tritsch NX*, Rodriguez-Contreras A*, Crins TT, Wang HC, Borst JG, Bergles DE (2010) Calcium action potentials in hair cells pattern auditory neuron activity before hearing. Nature Neurosci 13:1050-52. (* co-first authors)
  • Tritsch NX, Yi E, Gale JE, Glowatzki E, Bergles DE (2007) The origin of spontaneous activity in the developing auditory system. Nature 450: 50-5.
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