Neuron
Volume 9, Issue 3, September 1992, Pages 441-448
Journal home page for Neuron

Nitric oxide controls oscillatory activity in thalamocortical neurons

https://doi.org/10.1016/0896-6273(92)90182-DGet rights and content

Abstract

Nitric oxide (NO) is considered a diffusible messenger involved in neuronal communication, although the postsynaptic target cells of NO action and the associated biological function in the CNS are still a matter of controversy. Within the discrete pattern of NO-synthesizing neurons in the brain, NO synthase is specifically colocalized with the cholinergic brain stem-thalamic system, which is thought to regulate the state-dependent activity of the thalamocortical circuit. Here we report evidence indicating that the release of NO onto thalamocortical neurons results in an alteration in voltage dependence of the hyperpolarization-activated cation conductance, probably mediated via the cGMP system. NO selectively dampens oscillatory neuronal activity, indicating a rapidly diffusing signaling mechanism that controls the functional state of the thalamocortical network.

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      NO functions postsynaptically or at presynaptic nerve terminals and plays an important role in the regulation of neurotransmission (Garthwaite, 2008). HCN channels are potential downstream targets of NO/cGMP signaling in deep cerebellar nuclei neurons, trigeminal motoneurons, thalamocortical neurons and hypoglossal motoneurons (Abudara et al., 2002; Pape and Mager, 1992; Wenker et al., 2012; Wilson and Garthwaite, 2010). Using perforated-patch recording technique, it has been shown that application of NO donors induced a reversible increase in the amplitude of Ih, which was attributable to a depolarizing shift in the voltage dependence of HCN channel activation (Wenker et al., 2012; Wilson and Garthwaite, 2010).

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