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J Neurophysiol 97: 3386-3395, 2007. First published March 21, 2007; doi:10.1152/jn.01270.2006
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Modulation of Inhibitory Activity by Nitric Oxide in the Thalamus

Sunggu Yang and Charles L. Cox

Department of Molecular and Integrative Physiology; Department of Pharmacology, College of Medicine; and Beckman Institute, University of Illinois, Urbana-Champaign, Urbana, Illinois

Submitted 4 December 2006; accepted in final form 15 March 2007

The dorsal lateral geniculate nucleus (dLGN) is essential for the transfer of visual information from the retina to visual cortex, and inhibitory mechanisms can play a critical in regulating such information transfer. Nitric oxide (NO) is an atypical neuromodulator that is released in gaseous form and can alter neural activity without direct synaptic connections. Nitric oxide synthase (NOS), an essential enzyme for NO production, is localized in thalamic inhibitory neurons and cholinergic brain stem neurons that innervate the thalamus, although NO-mediated effects on thalamic inhibitory activity remain unknown. We investigated NO effects on inhibitory activity in dLGN using an in vitro slice preparation. The NO donor, SNAP, selectively potentiated the frequency, but not amplitude, of spontaneous inhibitory postsynaptic currents (sIPSCs) in thalamocortical relay neurons. This increase also persisted in tetrodotoxin (TTX), consistent with an increase in GABA release from presynaptic terminals. The SNAP-mediated actions were attenuated not only by the NO scavenger carboxy-PTIO but also by the guanylyl cyclase inhibitor ODQ. The endogenous NO precursor L-arginine produced actions similar to those of SNAP on sIPSC activity and these L-arginine–mediated actions were attenuated by the NOS inhibitor L-NMMA acetate. The SNAP-mediated increase in sIPSC activity was observed in both dLGN and ventrobasal thalamic nucleus (VB) neurons. Considering the lack of interneurons in rodent VB, the NO-mediated actions likely involve an increase in the output of axon terminals of thalamic reticular nucleus neurons. Our results indicate that NO upregulates thalamic inhibitory activity and thus these actions likely influence sensory information transfer through thalamocortical circuits.


Address for reprint requests and other correspondence: C. L. Cox, Department of Molecular and Integrative Physiology, University of Illinois, 2357 Beckman Institute, 405 North Mathews, Urbana, IL 61801 (E-mail: cox2{at}uiuc.edu)




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S. Yang and C. L. Cox
Excitatory and anti-oscillatory actions of nitric oxide in thalamus
J. Physiol., August 1, 2008; 586(15): 3617 - 3628.
[Abstract] [Full Text] [PDF]




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