Synapses are specialized junctions between excitable (neuron-neuron or neuron-muscle) and non-excitable cells (immune cells). At the synapses, neurotransmitter receptor ion channels play key role in transducing the chemical signals secreted by the presynaptic cells to electrical signals in the post-synaptic cells and regenerate the nerve impulses. Electro-chemical signals at the nascent synapses is critical for synapse formation during embryonic development.

During synaptic development, structure, function, and subunit stoichiometry of many ion channel receptors undergo changes which manifest as changes in synaptic current. This is a key universal phenomenon known as maturation of synaptic receptors. My lab is keen to understand the cellular and biophysical basis of this key milestone during development in central and ganglionic neurons. To this end, we have been investigating the biophysical properties of ion channels, ranging from neurotransmitter 'binding' to the receptor, 'gating', and 'desensitization' as well as the sequence of intracellular events that eventually trigger the necessary gene expression and turnover of receptors at the synapses.

Publications

Tapan K Nayak, *Auerbach A (2013). Asymmetric transmitter binding sites of fetal muscle acetylcholine receptors shape their synaptic response. Proc. Natl. Acad. Sci. U.S.A., 110(33): 13654-59. Link
Tapan K Nayak, Bruhova I, Chakrabarty S, Gupta S, Zheng W, *Auerbach A. (2014). Functional differences between neurotransmitter binding sites of muscle acetylcholine receptors. Proc. Natl. Acad. Sci. U.S.A., 111(49): 17660-05. Link
Tapan K Nayak, Chakrabarty S, Zheng W, *Auerbach A. (2016). Structural correlates of affinity in fetal versus adult endplate nicotinic receptors. Nature Communications 7:11352. Link

Our Research Areas

Mechanism of ligand binding and channel gating

Mechanism of allosteric communication in AChRs

Synaptic maturation

Allosteric modulators as therapeutic candidates

Role of intracellular ion channels in Autophagy

Allostery in GPCRs

Neuronal AChRs in chronic neuropathic pain