Jean-François Perrier – University of Copenhagen

Department of Neuroscience > Research Groups > Jean-François Perrier

Jean-François Perrier

Lab Leader:
Associate Professor Jean-François Perrier

Office:
University of Copenhagen
Faculty of Health Sciences
Department of Neuroscience
Maersk Tower, room 07.04.59
Blegdamsvej 3
DK-2200 Copenhagen N
Denmark

Email: perrier@sund.ku.dk
Phone: +45 23812746

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Research

Our lab has a developed a strong expertise in the study of intrinsic properties of individual neurons. By means of technique such as patch clamp recording, pharmacology, two-photon imaging in slice preparations from the central nervous, we are investigating how ion channels generate the electrical activity of neurons and how this contributes to the behavior of neural networks. Our recent results include:

- The identification of the first cellular mechanism responsible for the motor fatigue that occurs in the central nervous system. Motoneurons are the final common output of the central nervous system. Their synaptic activation triggers the contraction of the muscle they innervate. Neurons from the raphe nuclei in the brainstem release serotonin on motoneurons by means of synaptic contacts. Their activation facilitates the activity of motoneurons and thereby muscle contraction. During intense physical activity, serotonin release is increased. A spillover occurs and serotonin reaches extrasynaptic receptors located on the axon initial segment of motoneurons. This inhibits action potential genesis and thereby muscle contraction. In that way serotonin prevents excessive muscle contraction (Cotel et al., 2013).

                     

- The discovery of a new pathway that could prevent the development of temporal lobe epilepsy. The subiculum is a part of the temporal lope of the brain, and this is where temporal lobe epilepsy originates. Calcium flowing through CaV3 channels is responsible for the bursts of activity by pyramidal cells in the subiculum. When the activity of the neurons becomes overly synchronous, it results in abnormal electrical fluctuations, which lead to epileptic seizures. We have found that the activation of serotonin 2C receptors decreases the level of bursting by inhibiting CaV3 channels. This discovery could lead to the development of new principles for treating temporal lobe epilepsy (Petersen et al., 2017).

Key publications

  • Petersen AV, Cotel F, Perrier JF. (2017). Plasticity of the Axon Initial Segment: Fast and Slow Processes with Multiple Functional Roles. Neuroscientist, in press.
  • Petersen AV, Jensen CS, Crépel V, Falkerslev M, Perrier JF (2017). Serotonin Regulates the Firing of Principal Cells of the Subiculum by Inhibiting a T-type Ca2+ Current. Frontiers in Cellular Neuroscience 11
  • D'amico JM, Butler AA, Héroux ME, Cotel F, Perrier JF, JE Butler JE, Gandevia SC, Taylor JL. Human motoneurone excitability is depressed by activation of serotonin 1A receptors with buspirone. The Journal of physiology 595 (5), 1763-1773
  • Perrier JF, Cotel F (2015). Serotonergic modulation of spinal motor control. Current Opinion of Neurobiology, 33: 1-7.
  • Cotel F, Exley R, Cragg SJ, Perrier JF (2013). Serotonin spillover onto the axon initial segment of motoneurons induces central fatigue by inhibiting action potential initiation. Proc Natl Acad Sci U S A. 110(12):4774-9.