Ionic mechanisms of neuronal excitability

Information in the nervous system is transmitted by electrical signals (action potentials) within neurons and by chemical signals between neurons. The research interests of this lab are in studying the biophysical properties of voltage- and ligand-gated ion channels intrinsic to neurons, as well as in understanding the physiological consequences of the different patterns of activity characteristic of specific neurons.

We are currently studying neurons of the cerebellum, a brain region that participates in controlling movements. Projects in the lab focus on the ionic mechanisms of high-frequency firing in Purkinje neurons, the transmission of synaptic signals from Purkinje to cerebellar nuclear cells, and the response of cerebellar nuclear cells to different patterns of synaptic input. These types of studies will be useful for the development of accurate computer models of neuronal activity, as well as for cellular-level interpretations of systems-level studies of cerebellar function.

e-mail Dr. Raman
ph: 847.467.7912
fax: 847.491.5211

Selected References:

• Aman TK, Grieco-Calub TM, Chen C, Rusconi R, Slat EA, Isom LL, Raman IM. (2009). Regulation of persistent Na current by interactions between beta subunits of voltage-gated Na channels. J Neurosci. 29(7):2027-42.

• Pugh JR, Raman IM. (2009). Nothing can be coincidence: synaptic inhibition and plasticity in the cerebellar nuclei. Trends Neurosci. Jan 27. [Epub ahead of print]

• Pugh JR, Raman IM. (2008). Mechanisms of potentiation of mossy fiber EPSCs in the cerebellar nuclei by coincident synaptic excitation and inhibition. J Neurosci. 28(42):10549-60. [Full Text].

• Aman T.K., Raman I.M. (2007). Subunit dependence of Na channel slow inactivation and open channel block in cerebellar neurons. Biophysical Journal. 92(6):1938-51. [Full Text].

• Pugh J.R., Raman I.M. (2006). Potentiation of mossy fiber EPSCs in the cerebellar nuclei by NMDA receptor activation followed by postinhibitory rebound current. Neuron. Jul 6;51(1):113-23 [Full Text].

• Levin S.I., Khaliq Z.M., Aman T.K., Grieco T.M., Kearney J.A., Raman I.M., Meisler M.H. (2006). Impaired motor function in mice with cell-specific knockout of sodium channel Scn8a (NaV1.6) in cerebellar purkinje neurons and granule cells. Journal of Neurophysiology 96(2):785-93. [Full Text].

• Khaliq Z.M., Raman I.M. (2006). Relative contributions of axonal and somatic Na channels to action potential initiation in cerebellar Purkinje neurons. Journal of Neuroscience. 26(7):1935-44. [Full Text].

• Grieco, T.M., Malhotra, J.D., Chen, C., Isom, L.L., and Raman, I.M. (2005). Open-channel block by the cytoplasmic tail of sodium channel beta 4 as a mechanism for resurgent sodium current. Neuron. 45: 233-244. [Full Text].

• Khaliq, Z.M. and Raman, I.M. (2005). Axonal propagation of simple and complex spikes in cerebellar Purkinje neurons. Journal of Neuroscience. 25(2): 454-63. [Full Text].

• Pugh, J.R. and Raman, I.M. (2005). GABAA receptor kinetics in the cerebellar nuclei: Evidence for detection of transmitter from distant release sites. Biophysical Journal. 88 (3): 1740-54. [Full Text].

• Telgkamp, P., Padgett, D.E., Ledoux, V.A., Woolley, C.S., Raman, I.M. (2004). Maintenance of high-frequency transmission at Purkinje to cerebellar nuclear synapses by spillover from boutons with multiple release sites. Neuron. 41(1): 113-26.[Full Text].

• Grieco, T.M., Raman, I.M. (2004). Production of resurgent current in NaV1.6-null Purkinje neurons by slowing sodium channel inactivation with beta-pompilidotoxin. Journal of Neuroscience. 24(1): 35-42. [Full Text].

• Khaliq, Z.M., Gouwens, N.W., Raman, I.M. (2003). The contribution of resurgent sodium current to high-frequency firing in Purkinje neurons: an experimental and modeling study. Journal of Neuroscience. 23(12): 4899-912. [Full Text].

• Telgkamp, P., Raman, I.M. (2002). Depression of inhibitory synaptic transmission between Purkinje cells and neurons of the cerebellar nuclei. Journal of Neuroscience. 22(19): 8447-57. [Full Text].

Other Links:

• link to more detailed research description

• Northwestern University Institute for Neuroscience