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Molecular neurophysiology

The principal aim of the research conducted in our laboratory is to identify and further clarify cellular and molecular mechanisms that mediate and/or regulate fast and slow synaptic transmission in the brain.

members of the karima chergui lab: Giacomo Sitzia, Karima Chergui, Olga Skiteva, Ning Yao.
Molecular Neurophysiology lab, June 2019: Giacomo Sitzia, Karima Chergui, Olga Skiteva, Ning Yao.

More precisely, our research activities focus on the mechanisms by which afferent inputs and specific neurotransmitter receptors modulate the activity of the different neuronal populations that constitute the basal ganglia and influence their ability to process and integrate incoming information.


We use electrophysiological (whole-cell patch clamp and field potentials recordings) and electrochemical (amperometric detection of dopamine release) approaches in rodent brain slices combined with pharmacological and molecular tools.

Group members

Karima Chergui – Senior lecturer, Research group leader

Giacomo Sitzia – PhD student

Olga Skiteva – Postdoc

Ning Yao – Postdoc


Targeting NMDA receptor dysfunctions in Parkinson's disease

Parkinson's disease is a devastating neurodegenerative disease. It is characterized by severe movement disturbances and is due to a dysfunction of the basal ganglia circuitry as a result of degeneration of dopamine neurons in the substantia nigra. Because glutamatergic neurotransmission is altered in Parkinson's disease, the NMDA type of glutamate receptor and the subunits that compose these receptors are considered attractive drug targets for therapeutic intervention in the disease. Our research aims to determine whether the subunit composition of functional NMDA receptors is altered in different nuclei of the basal ganglia, with a focus on the striatum, in mouse models of Parkinson's disease. The knowledge gained will ultimately provide a better understanding of the pathophysiology of Parkinson's disease and identify novel drug targets.

Recent selected publications

Ketamine and its metabolite (2R,6R)-hydroxynorketamine induce lasting alterations in glutamatergic synaptic plasticity in the mesolimbic circuit.
Yao N, Skiteva O, Zhang X, Svenningsson P, Chergui K
Mol. Psychiatry 2018 10;23(10):2066-2077

Dopamine depletion of the striatum causes a cell-type specific reorganization of GluN2B- and GluN2D-containing NMDA receptors.
Zhang X, Chergui K
Neuropharmacology 2015 May;92():108-15

Induction of cannabinoid- and N-methyl-D-aspartate receptor-mediated long-term depression in the nucleus accumbens and dorsolateral striatum is region and age dependent.
Zhang X, Feng ZJ, Chergui K
Int. J. Neuropsychopharmacol. 2015 Jan;18(4):

Allosteric modulation of GluN2C/GluN2D-containing NMDA receptors bidirectionally modulates dopamine release: implication for Parkinson's disease.
Zhang X, Feng ZJ, Chergui K
Br. J. Pharmacol. 2014 Aug;171(16):3938-45

Allosteric modulation of NMDA receptors alters neurotransmission in the striatum of a mouse model of Parkinson's disease.
Feng ZJ, Zhang X, Chergui K
Exp. Neurol. 2014 May;255():154-60

GluN2D-containing NMDA receptors inhibit neurotransmission in the mouse striatum through a cholinergic mechanism: implication for Parkinson's disease.
Zhang X, Feng ZJ, Chergui K
J. Neurochem. 2014 May;129(4):581-90

Contact us

Karima Chergui

Senior lecturer
Chergui Karima group - Molecular Neurophysiology
Department of Physiology and Pharmacology (FYFA), C3