Zayd M. Khaliq, Ph.D.
Cellular Neurophysiology Unit
Building 35, Room 3C-1002
35 Convent Drive
Bethesda, MD 20892-3700
Dopamine-releasing neurons located in the midbrain play an essential role in movement and reward-based behaviors. Dysfunction of these neurons has been linked to a variety of brain disorders including addiction, schizophrenia, depression and Parkinson's disease. The goal of our research is to understand 1) how voltage-gated ion channels contribute to excitability and action potential firing of dopamine neurons and other neurons that participate in reward circuits, 2) how synaptic inputs interact with intrinsic membrane conductances to produce spiking patterns that are relevant to reward-based learning, 3) and how neuromodulatory inputs influence excitability of these neurons. We address these questions using patch-clamp techniques to record the activity of neurons in brain slices. We combine this approach with imaging, immunohistochemistry and the use of transgenic mice to identify specific populations of neurons within the reward circuit.
Evans RC, Zhu M, Khaliq ZM. Dopamine Inhibition Differentially Controls Excitability of Substantia Nigra Dopamine Neuron Subpopulations through T-Type Calcium Channels. J Neurosci. 2017;37(13):3704-3720.
Hage TA, Sun Y, Khaliq ZM. Electrical and Ca(2+) signaling in dendritic spines of substantia nigra dopaminergic neurons. Elife. 2016;5.
Hage TA, Khaliq ZM. Tonic firing rate controls dendritic Ca2+ signaling and synaptic gain in substantia nigra dopamine neurons. J Neurosci. 2015;35(14):5823-36.
Tarfa RA, Evans RC, Khaliq ZM. Enhanced Sensitivity to Hyperpolarizing Inhibition in Mesoaccumbal Relative to Nigrostriatal Dopamine Neuron Subpopulations. J Neurosci. 2017;37(12):3311-3330.
Philippart F, Khaliq ZM. G<sub>i/o</sub> protein-coupled receptors in dopamine neurons inhibit the sodium leak channel NALCN. Elife. 2018;7.
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This page was last updated on January 3rd, 2019